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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Apoetm1Unc
targeted mutation 1, University of North Carolina
MGI:1857129
Summary 180 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Apoetm1Unc/Apoetm1Unc B6.129P2-Apoetm1Unc MGI:3758858
hm2
Apoetm1Unc/Apoetm1Unc B6.129P2-Apoetm1Unc/J MGI:2384131
hm3
Apoetm1Unc/Apoetm1Unc B6.Cg-Apoetm1Unc Faslpr MGI:3799495
hm4
Apoetm1Unc/Apoetm1Unc either: B6.129P2-Apoetm1Unc/J or (involves: 129P2/OlaHsd * C57BL/6J * ICR) MGI:3717197
hm5
Apoetm1Unc/Apoetm1Unc involves: 129P2/OlaHsd MGI:3718006
hm6
Apoetm1Unc/Apoetm1Unc involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 MGI:3764959
hm7
Apoetm1Unc/Apoetm1Unc involves: 129P2/OlaHsd * C57BL/6 MGI:3714936
hm8
Apoetm1Unc/Apoetm1Unc involves: 129P2/OlaHsd * C57BL/6 * DBA MGI:4358709
hm9
Apoetm1Unc/Apoetm1Unc involves: 129P2/OlaHsd * C57BL/6 * FVB/N MGI:3822450
ht10
Apoetm1Unc/Apoe+ involves: 129P2/OlaHsd * C57BL/6 MGI:3836194
ht11
Apoeshl/Apoetm1Unc involves: 129P2/OlaHsd * KOR MGI:3716843
cn12
Apoetm1Unc/Apoetm1Unc
Nck1tm1Paw/Nck1tm1Paw
Nck2tm3Paw/Nck2tm3Paw
Tg(Cdh5-cre/ERT2)1Rha/0
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6 MGI:7316557
cn13
Apoetm1Unc/Apoetm1Unc
Atictm1c(EUCOMM)Hmgu/Atictm1c(EUCOMM)Hmgu
Gt(ROSA)26Sortm1(cre/ERT2)Tyj/Gt(ROSA)26Sor+
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6J * C57BL/6N MGI:7511828
cn14
Apoetm1Unc/Apoetm1Unc
Atictm1c(EUCOMM)Hmgu/Atictm1c(EUCOMM)Hmgu
X/Tg(Myh11-icre/ERT2)1Soff
involves: 129P2/OlaHsd * 129S4/SvJaeSor * C57BL/6J * C57BL/6N * FVB/N MGI:7511826
cn15
Apoetm1Unc/Apoetm1Unc
Ddit3tm1.1Irt/Ddit3tm1.1Irt
Taglntm2(cre)Yec/Tagln+
involves: 129P2/OlaHsd * 129S6/SvEvTac * C57BL/6J MGI:5781094
cn16
Apoetm1Unc/Apoetm1Unc
Gja5tm1Mchn/Gja5tm1Mchn
Tg(TIE2-lacZ)182Sato/0
involves: 129P2/OlaHsd * BALB/c * C57BL/6 MGI:4818410
cn17
Apoetm1Unc/Apoetm1Unc
Smarcd1tm1.1Jddl/Smarcd1tm1.1Jddl
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129P2/OlaHsd * C57BL/6 * DBA MGI:5912277
cn18
Apoetm1Unc/Apoetm1Unc
Svep1tm1c(EUCOMM)Hmgu/Svep1tm1c(EUCOMM)Hmgu
Tg(Myh11-icre/ERT2)1Soff/0
involves: 129P2/OlaHsd * C57BL/6N * FVB/N MGI:7516351
cn19
Apoetm1Unc/Apoetm1Unc
Klf15tm2Jain/Klf15tm2Jain
Tg(Tagln-cre)1Jjl/0
involves: 129P2/OlaHsd * FVB/N MGI:5552967
cx20
Apoetm1Unc/Apoetm1Unc
Cdkn1atm1Tyj/Cdkn1atm1Tyj
B6.129-Apoetm1Unc Cdkn1atm1Tyj MGI:4420802
cx21
Apoetm1Unc/Apoetm1Unc
Cx3cl1tm1Sgs/Cx3cl1tm1Sgs
B6.129-Apoetm1Unc Cx3cl1tm1Sgs MGI:3527869
cx22
Apoetm1Unc/Apoetm1Unc
Cx3cr1tm1Zm/Cx3cr1+
B6.129-Apoetm1Unc Cx3cr1tm1Zm MGI:3618279
cx23
Apoetm1Unc/Apoetm1Unc
Cx3cr1tm1Zm/Cx3cr1tm1Zm
B6.129-Apoetm1Unc Cx3cr1tm1Zm MGI:3618277
cx24
Apoetm1Unc/Apoetm1Unc
Ifngtm1Ts/Ifngtm1Ts
B6.129-Apoetm1Unc Ifngtm1Ts MGI:4938323
cx25
Apoetm1Unc/Apoetm1Unc
Pecam1Gt(OST16303)Lex/Pecam1Gt(OST16303)Lex
B6.129-Apoetm1Unc Pecam1Gt(OST16303)Lex MGI:3822293
cx26
Apoetm1Unc/Apoetm1Unc
Cxcl10tm1Adl/Cxcl10tm1Adl
B6.129-Cxcl10tm1Adl Apoetm1Unc MGI:4938324
cx27
Apoetm1Unc/Apoetm1Unc
Thbdtm1.1(THBD)Sltz/Thbdtm1.1(THBD)Sltz
B6.129(FVB)-Thbdtm1.1(THBD)Sltz Apoetm1Unc MGI:5462232
cx28
Apoetm1Unc/Apoetm1Unc
Hsd11b1tm1Lex/Hsd11b1tm1Lex
B6.129-Hsd11b1tm1Lex Apoetm1Unc MGI:5502603
cx29
Apoetm1Unc/Apoetm1Unc
Il1r1tm1Imx/Il1r1tm1Imx
B6.129-Il1r1tm1Imx Apoetm1Unc MGI:4939466
cx30
Apoetm1Unc/Apoetm1Unc
Nceh1tm1Ishi/Nceh1tm1Ishi
B6.129-Nceh1tm1Ishi Apoetm1Unc MGI:4359427
cx31
Apoetm1Unc/Apoetm1Unc
Nos3tm1Plh/Nos3tm1Plh
B6.129-Nos3tm1Plh Apoetm1Unc MGI:4367467
cx32
Apoetm1Unc/Apoetm1Unc
Cd44tm1Mak/Cd44+
B6.129P2-Cd44tm1Mak Apoetm1Unc MGI:4942389
cx33
Apoetm1Unc/Apoetm1Unc
Cd44tm1Mak/Cd44tm1Mak
B6.129P2-Cd44tm1Mak Apoetm1Unc MGI:4942387
cx34
Apoetm1Unc/Apoetm1Unc
Nos3tm1Unc/Nos3tm1Unc
B6.129P2-Nos3tm1Unc Apoetm1Unc MGI:3794764
cx35
Apoetm1Unc/Apoetm1Unc
Serpine1tm1Mlg/Serpine1tm1Mlg
B6.129-Serpine1tm1Mlg Apoetm1Unc MGI:3811066
cx36
Apoetm1Unc/Apoetm1Unc
Ccr2tm1Ifc/Ccr2tm1Ifc
B6.Cg-Apoetm1Unc Ccr2tm1Ifc MGI:4833679
cx37
Apoetm1Unc/Apoetm1Unc
Cdh18Tg(GFAP-APOE_i4)1Hol/0
B6.Cg-Apoetm1Unc Cdh18Tg(GFAP-APOE_i4)1Hol/J MGI:3784302
cx38
Apoetm1Unc/Apoetm1Unc
Ccr2tm1Ifc/Ccr2tm1Ifc
Cx3cl1tm1Lira/Cx3cl1tm1Lira
B6.Cg-Apoetm1Unc Cx3cl1tm1Lira Ccr2tm1Ifc MGI:4833678
cx39
Apoetm1Unc/Apoetm1Unc
Faslpr/Faslpr
B6.Cg-Apoetm1Unc Faslpr MGI:3800213
cx40
Apoetm1Unc/Apoetm1Unc
Phactr1tm1.2Gdo/Phactr1tm1.2Gdo
B6.Cg-Apoetm1Unc Phactr1tm1.2Gdo MGI:7713059
cx41
Apoetm1Unc/Apoetm1Unc
Pik3cgtm1Dwu/Pik3cgtm1Dwu
B6.Cg-Apoetm1Unc Pik3cgtm1Dwu MGI:4358191
cx42
Apoetm1Unc/Apoetm1Unc
Tg(CMV-Serpine1)1Dgi/0
B6.Cg-Apoetm1Unc Tg(CMV-Serpine1)1Dgi MGI:3810982
cx43
Apoetm1Unc/Apoetm1Unc
Tg(EIF1AX-Aldh2*E487K)101Oht/Tg(EIF1AX-Aldh2*E487K)101Oht
B6.Cg-Apoetm1Unc Tg(EIF1AX-Aldh2*E487K)101Oht MGI:5699095
cx44
Apoetm1Unc/Apoetm1Unc
Tg(GFAP-APOE_i3)37Hol/0
B6.Cg-Apoetm1Unc Tg(GFAP-APOE_i3)37Hol MGI:3784381
cx45
Apoetm1Unc/Apoetm1Unc
Tg(GFAP-APOE_i4)22Hol/0
B6.Cg-Apoetm1Unc Tg(GFAP-APOE_i4)22Hol MGI:3784306
cx46
Apoetm1Unc/Apoetm1Unc
Tg(GFAP-APOE_i4)#Hol/0
B6.Cg-Apoetm1Unc Tg(GFAP-APOE_i4)#Hol MGI:3784380
cx47
Apoetm1Unc/Apoetm1Unc
Arhgef26tm1.1Kbur/Arhgef26tm1.1Kbur
B6.Cg-Arhgef26tm1.1Kbur Apoetm1Unc MGI:5500052
cx48
Apoetm1Unc/Apoetm1Unc
Crptm1Hjf/Crptm1Hjf
B6.Cg-Crptm1Hjf Apoetm1Unc MGI:4947400
cx49
Apoetm1Unc/Apoetm1Unc
Fabp4tm1Brsp/Fabp4tm1Brsp
Fabp5tm1Hota/Fabp5tm1Hota
B6.Cg-Fabp4tm1Brsp Fabp5tm1Hota Apoetm1Unc MGI:3815438
cx50
Apoetm1Unc/Apoetm1Unc
Faslgld/Faslgld
B6.Cg-Faslgld Apoetm1Unc MGI:5514345
cx51
Apoetm1Unc/Apoetm1Unc
Tg(GFAP-APOE_i3)37Hol/0
B6.Cg-Tg(GFAP-APOE_i3)37Hol Apoetm1Unc/J MGI:3784303
cx52
Apoetm1Unc/Apoetm1Unc
Glg1Gt(RST092)Byg/Glg1+
B6J.129P2-Apoetm1Unc Glg1Gt(RST092)Byg MGI:5699561
cx53
Apoetm1Unc/Apoetm1Unc
Msr1tm1Csk/Msr1tm1Csk
either: (involves: 129P2/OlaHsd * 129X1/SvJ * C57BL/6J * ICR) or (involves: 129P2/OlaHsd * 129X1/SvJ * 129/Sv * ICR) MGI:2177115
cx54
Apoetm1Unc/Apoetm1Unc
Hptm1Alev/Hptm1Alev
involves: 129 MGI:3790694
cx55
Apoetm1Unc/Apoetm1Unc
Egr1tm1Jmi/Egr1tm1Jmi
involves: 129 * C57BL/6 MGI:4821395
cx56
Apoetm1Unc/Apoetm1Unc
Lpltm1Sem/Lpltm1Sem
involves: 129P2/OlaHsd MGI:4354296
cx57
Apoetm1Unc/Apoetm1Unc
Tg(APPV717F)109Ili/Tg(APPV717F)109Ili
involves: 129P2/OlaHsd MGI:3721542
cx58
Apoetm1Unc/Apoetm1Unc
Cd36tm1Mfe/Cd36tm1Mfe
involves: 129P2/OlaHsd * 129S1/Sv * C57BL/6 MGI:4888254
cx59
Apoetm1Unc/Apoetm1Unc
Clutm1Jakh/Clutm1Jakh
Tg(APPV717F)109Ili/Tg(APPV717F)109Ili
involves: 129P2/OlaHsd * 129S2/SvPas MGI:3721541
cx60
Apoetm1Unc/Apoetm1Unc
Ncf1tm1Shl/Ncf1tm1Shl
involves: 129P2/OlaHsd * 129S2/SvPas MGI:4438110
cx61
Apoetm1Unc/Apoetm1Unc
Scarb1tm1Kri/Scarb1tm1Kri
involves: 129P2/OlaHsd * 129S2/SvPas * BALB/c * C57BL/6 MGI:5558016
cx62
Apoetm1Unc/Apoetm1Unc
Itgb3tm1Hyn/Itgb3tm1Hyn
involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6 MGI:4439279
cx63
Apoetm1Unc/Apoetm1Unc
Fut4tm1Jbl/Fut4tm1Jbl
Fut7tm1Jbl/Fut7tm1Jbl
involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6 MGI:3652962
cx64
Apoetm1Unc/Apoetm1Unc
Scarb1tm1Kri/Scarb1tm1Kri
involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6 MGI:3799448
cx65
Apobec1tm1Chan/Apobec1tm1Chan
Apoetm1Unc/Apoetm1Unc
involves: 129P2/OlaHsd * 129S4/SvJae MGI:3850552
cx66
Apoetm1Unc/Apoetm1Unc
Ccr1tm1Gao/Ccr1tm1Gao
involves: 129P2/OlaHsd * 129S4/SvJae MGI:5317889
cx67
Apoetm1Unc/Apoetm1Unc
Ccr2tm1Ifc/Ccr2+
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 MGI:4831159
cx68
Apoetm1Unc/Apoetm1Unc
Ccr2tm1Ifc/Ccr2tm1Ifc
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 MGI:4831158
cx69
Apoetm1Unc/Apoetm1Unc
Timp1tm1Pds/Y
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 MGI:3652791
cx70
Apoetm1Unc/Apoetm1Unc
Ttpatm1Far/Ttpatm1Far
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 MGI:3653653
cx71
Apoetm1Unc/Apoetm1Unc
Ttpatm1Far/Ttpa+
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 MGI:3653676
cx72
Apoetm1Unc/Apoetm3(APOE_i4)Yhg
Zbtb20Tg(PDGFB-APPSwInd)20Lms/0
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * DBA/2 MGI:5427502
cx73
Apoetm1Unc/Apoetm2(APOE_i3)Yhg
Zbtb20Tg(PDGFB-APPSwInd)20Lms/0
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * DBA/2 MGI:5427501
cx74
Apoetm1Unc/Apoetm1Unc
Soat1tm1Far/Soat1tm1Far
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6J MGI:3761832
cx75
Apoetm1Unc/Apoetm1Unc
Soat2tm1Far/Soat2tm1Far
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6J MGI:3762636
cx76
Angptl3tm1Lex/Angptl3tm1Lex
Apoetm1Unc/Apoetm1Unc
involves: 129P2/OlaHsd * 129S5/SvEvBrd * C57BL/6 MGI:3849583
cx77
Apoetm1Unc/Apoetm1Unc
Cyp4f13Gt(OST14770)Lex/Cyp4f13Gt(OST14770)Lex
involves: 129P2/OlaHsd * 129S5/SvEvBrd * C57BL/6 MGI:6455724
cx78
Apoetm1Unc/Apoe+
Cyp4f13Gt(OST14770)Lex/Cyp4f13Gt(OST14770)Lex
involves: 129P2/OlaHsd * 129S5/SvEvBrd * C57BL/6 MGI:6455725
cx79
Apoetm1Unc/Apoetm1Unc
Mmp9tm1Tvu/Mmp9tm1Tvu
involves: 129P2/OlaHsd * 129S6/SvEvTac MGI:4367614
cx80
Apoetm1Unc/Apoetm1Unc
Spp1tm1Blh/Spp1+
involves: 129P2/OlaHsd * 129S6/SvEvTac * Black Swiss * C57BL/6J MGI:4361697
cx81
Apoetm1Unc/Apoetm1Unc
Spp1tm1Blh/Spp1tm1Blh
involves: 129P2/OlaHsd * 129S6/SvEvTac * Black Swiss * C57BL/6J MGI:4361696
cx82
Apoetm1Unc/Apoetm1Unc
Cyp19a1tm1Esi/Cyp19a1tm1Esi
involves: 129P2/OlaHsd * 129S6/SvEvTac * C57BL/6 MGI:5428435
cx83
Apoetm1Unc/Apoetm1Unc
Lipgtm1Tq/Lipgtm1Tq
involves: 129P2/OlaHsd * 129S6/SvEvTac * C57BL/6J MGI:3785086
cx84
Apoetm1Unc/Apoetm1Unc
Dp(17Nfkbil1-Or2h1)1Cogr/0
involves: 129P2/OlaHsd * 129S6/SvEvTac * C57BL/6J MGI:5451045
cx85
Apoetm1Unc/Apoetm1Unc
Ldlrtm1Her/Ldlrtm1Her
involves: 129P2/OlaHsd * 129S7/SvEvBrd MGI:4367224
cx86
Apobtm2Sgy/Apobtm2Sgy
Apoetm1Unc/Apoetm1Unc
Lepob/Lepob
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6 MGI:5819053
cx87
Soat1tm1Ishi/Soat1tm1Ishi
Apoetm1Unc/Apoetm1Unc
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6 MGI:3582202
cx88
Apobec1tm1Ishi/Apobec1tm1Ishi
Apoetm1Unc/Apoetm1Unc
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6 MGI:3710350
cx89
Apoetm1Unc/Apoetm1Unc
Spp1tm1Rit/Spp1tm1Rit
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6 MGI:4361863
cx90
Apoetm1Unc/Apoetm1Unc
Spp1tm1Rit/Spp1+
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6 MGI:4361864
cx91
Apoetm1Unc/Apoetm1Unc
Nos2tm1Mrl/Nos2tm1Mrl
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6 MGI:4837860
cx92
Apobtm1Sgy/Apobtm1Sgy
Apoetm1Unc/Apoetm1Unc
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6 MGI:5882610
cx93
Apobtm2Sgy/Apobtm2Sgy
Apoetm1Unc/Apoetm1Unc
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6 MGI:5882611
cx94
Apoetm1Unc/Apoetm1Unc
Ldlrtm1Her/Ldlrtm1Her
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6J MGI:3789482
cx95
Apoetm1Unc/Apoetm1Unc
Rag2tm1Fwa/Rag2+
involves: 129P2/OlaHsd * 129S/SvEv MGI:3789200
cx96
Apoetm1Unc/Apoetm1Unc
Rag2tm1Fwa/Rag2tm1Fwa
involves: 129P2/OlaHsd * 129S/SvEv MGI:3789198
cx97
Apoetm1Unc/Apoetm1Unc
Il1rntm1Dih/Il1rntm1Dih
involves: 129P2/OlaHsd * 129S/SvEv * C57BL/6 MGI:3789134
cx98
Apoetm1Unc/Apoetm1Unc
Sprr3tm1.1Ppy/Sprr3tm1.1Ppy
involves: 129P2/OlaHsd * 129S/SvEv * C57BL/6J * SJL MGI:5776478
cx99
Apoetm1Unc/Apoetm1Unc
Klf15tm1Jain/Klf15tm1Jain
involves: 129P2/OlaHsd * 129X1/SvJ MGI:5552968
cx100
Apoetm1Unc/Apoetm1Unc
Pon1tm1Lus/Pon1tm1Lus
involves: 129P2/OlaHsd * 129X1/SvJ * C57BL/6J MGI:2654938
cx101
Apoetm1Unc/Apoetm1Unc
Npc1m1N/Npc1m1N
involves: 129P2/OlaHsd * BALB/c MGI:3785902
cx102
Apoetm1Unc/Apoetm1Unc
Cbstm1Unc/Cbstm1Unc
Tg(Mt1-CBS)25Waku/0
involves: 129P2/OlaHsd * C3H * C57BL/6 MGI:5796685
cx103
Apoetm1Unc/Apoetm1Unc
Csf1op/Csf1op
involves: 129P2/OlaHsd * C3HeB/Fe * C57BL/6 MGI:3836254
cx104
Apoetm1Unc/Apoetm1Unc
Ath29C57BL/6J/?
involves: 129P2/OlaHsd * C3H/HeJ * C57BL/6J MGI:3766466
cx105
Apoetm1Unc/Apoetm1Unc
Ptgdrtm1Dgen/Ptgdrtm1Dgen
involves: 129P2/OlaHsd * C57BL/6 MGI:5473362
cx106
Apoetm1Unc/Apoetm1Unc
Ccr5tm1Blck/Ccr5tm1Blck
involves: 129P2/OlaHsd * C57BL/6 MGI:5317846
cx107
Apoetm1Unc/Apoetm1Unc
Ccr5tm1Kuz/Ccr5tm1Kuz
involves: 129P2/OlaHsd * C57BL/6 MGI:5317842
cx108
Apoetm1Unc/Apoetm1Unc
Svep1em1Nost/Svep1em1Nost
involves: 129P2/OlaHsd * C57BL/6 MGI:7516347
cx109
Apoetm1Unc/Apoetm1Unc
Tlr4tm1Aki/Tlr4tm1Aki
involves: 129P2/OlaHsd * C57BL/6 MGI:3588777
cx110
Apoetm1Unc/Apoetm1Unc
Tg(Eno2-APP*751)10Cord/0
involves: 129P2/OlaHsd * C57BL/6 MGI:3784391
cx111
Apoetm1Unc/Apoetm1Unc
Tg(APPV717F)109Ili/0
involves: 129P2/OlaHsd * C57BL/6 MGI:3784385
cx112
Apoetm1Unc/Apoetm1Unc
Il10tm1Cgn/Il10tm1Cgn
involves: 129P2/OlaHsd * C57BL/6 MGI:4460235
cx113
Apoetm1Unc/Apoetm1Unc
Tg(APPV717F)109Ili/0
Tg(GFAP-APOE_i3)37Hol/0
involves: 129P2/OlaHsd * C57BL/6 * CBA MGI:3784384
cx114
Apoetm1Unc/Apoetm1Unc
Tg(Prnp-Abca1)EHol/0
involves: 129P2/OlaHsd * C57BL/6 * CBA MGI:3801012
cx115
Apoetm1Unc/Apoetm1Unc
Tg(Eno2-APP*751)10Cord/0
Tg(GFAP-APOE_i3)37Hol/0
involves: 129P2/OlaHsd * C57BL/6 * CBA MGI:3784390
cx116
Apoetm1Unc/Apoetm1Unc
Tg(Eno2-APP*751)10Cord/0
Cdh18Tg(GFAP-APOE_i4)1Hol/0
involves: 129P2/OlaHsd * C57BL/6 * CBA MGI:3784389
cx117
Apoetm1Unc/Apoetm1Unc
Tg(APPV717F)109Ili/0
Tg(GFAP-APOE_i2)14Hol/0
involves: 129P2/OlaHsd * C57BL/6 * CBA MGI:3784387
cx118
Apoetm1Unc/Apoetm1Unc
Tg(APPV717F)109Ili/0
Tg(GFAP-APOE_i4)#Hol/0
involves: 129P2/OlaHsd * C57BL/6 * CBA MGI:3784383
cx119
Apoetm1Unc/Apoetm1Unc
Serpind1tm1Moto/Serpind1+
involves: 129P2/OlaHsd * C57BL/6 * CBA MGI:3713848
cx120
Apoetm1Unc/Apoetm1Unc
Lcattm1Hgc/Lcattm1Hgc
involves: 129P2/OlaHsd * C57BL/6 * DBA MGI:4358706
cx121
Apoetm1Unc/Apoetm1Unc
Tg(CAG-IL1RN)2Cga/?
involves: 129P2/OlaHsd * C57BL/6 * DBA/1 * FVB MGI:3789132
cx122
Apoetm1Unc/Apoetm1Unc
Tg(CAG-IL1RN)1Cga/?
involves: 129P2/OlaHsd * C57BL/6 * DBA/1 * FVB MGI:3789130
cx123
Abca1tm1Jdm/Abca1tm1Jdm
Abcg1tm1Dgen/Abcg1tm1Dgen
Apoetm1Unc/Apoetm1Unc
involves: 129P2/OlaHsd * C57BL/6 * DBA * DBA/1LacJ MGI:5451015
cx124
Apoetm1Unc/Apoetm1Unc
Tg(NOS3)2Crom/0
involves: 129P2/OlaHsd * C57BL/6 * FVB MGI:2653578
cx125
Apoetm1Unc/Apoetm1Unc
Tg(NOS3)3Crom/0
involves: 129P2/OlaHsd * C57BL/6 * FVB MGI:2653579
cx126
Apoetm1Unc/Apoe+
Tg(APPV717I)1130Kha/0
involves: 129P2/OlaHsd * C57BL/6 * FVB/N MGI:3722317
cx127
Apoetm1Unc/Apoetm1Unc
Tg(Cyp21a1-Apoe)614Fet/0
involves: 129P2/OlaHsd * C57BL/6 * FVB/N MGI:3822447
cx128
Apoetm1Unc/Apoetm1Unc
Tg(Cyp21a1-Apoe)619Fet/0
involves: 129P2/OlaHsd * C57BL/6 * FVB/N MGI:3822449
cx129
Apoetm1Unc/Apoetm1Unc
Tg(APPV717I)1130Kha/0
involves: 129P2/OlaHsd * C57BL/6 * FVB/N MGI:3722316
cx130
Apoetm1Unc/Apoetm1Unc
Nfe2l2tm1Mym/Nfe2l2tm1Mym
involves: 129P2/OlaHsd * C57BL/6J MGI:4420430
cx131
Apoetm1Unc/Apoetm1Unc
Thbs4tm1Olsa/Thbs4tm1Olsa
involves: 129P2/OlaHsd * C57BL/6J MGI:7628726
cx132
Apoetm1Unc/Apoetm1Unc
Hhipl1tm1a(KOMP)Wtsi/Hhipl1tm1a(KOMP)Wtsi
involves: 129P2/OlaHsd * C57BL/6J * C57BL/6N MGI:6477559
cx133
Apoetm1Unc/Apoetm1Unc
Tg(APOC1)1Bres/0
involves: 129P2/OlaHsd * C57BL/6J * CBA/J MGI:2653531
cx134
Apoetm1Unc/Apoetm1Unc
Tg(Eno2-APOE_i4)1Rabr/0
involves: 129P2/OlaHsd * C57BL/6J * ICR MGI:3717195
cx135
Apoetm1Unc/Apoetm1Unc
Tg(Eno2-APOE_i3)1Rabr/0
involves: 129P2/OlaHsd * C57BL/6J * ICR MGI:3717196
cx136
Ay/a
Apoetm1Unc/Apoetm1Unc
Ccr2tm1Mae/Ccr2tm1Mae
involves: 129P2/OlaHsd * C57BL/6J * KK/TaJcl MGI:5297861
cx137
Ay/a
Apoetm1Unc/Apoetm1Unc
involves: 129P2/OlaHsd * C57BL/6J * KK/TaJcl MGI:5297860
cx138
Apoetm1Unc/Apoetm1Unc
Svep1tm1a(EUCOMM)Hmgu/Svep1+
involves: 129P2/OlaHsd * C57BL/6N MGI:7516350
cx139
Apoetm1Unc/Apoetm1Unc
Tg(MSR1-Plau)1Ddi/0
involves: 129P2/OlaHsd * C57BL/6 * SJL MGI:3690213
cx140
Apoetm1Unc/Apoetm1Unc
Leprdb/Leprdb
involves: 129P2/OlaHsd * C57BLKS/J MGI:3775795
cx141
Apoetm1Unc/Apoetm1Unc
Tg(Eno2-APOE_i4)1Rabr/0
involves: 129P2/OlaHsd * ICR MGI:3718008
cx142
Apoetm1Unc/Apoetm1Unc
Tg(Eno2-APOE_i3)1Rabr/0
involves: 129P2/OlaHsd * ICR MGI:3718007
cx143
Apoetm1Unc/Apoetm1Unc
Tnfrsf11btm1Eac/Tnfrsf11btm1Eac
involves: 129S4/SvJaeSor * C57BL/6 MGI:3852641
cx144
Apoetm1Unc/Apoetm1Unc
Pla2g15tm1Ytan/Pla2g15tm1Ytan
involves: 129S/SvEv * B6.129P2-Apoetm1Unc/J MGI:3576623
cx145
Apoetm1Unc/Apoetm1Unc
Cst3tm1Karl/Cst3tm1Karl
involves: 129S/SvEv * C57BL/6 MGI:3621887
cx146
Apoetm1Unc/Apoetm1Unc
Cav1tm1Mls/Cav1tm1Mls
involves: 129/Sv * 129P2/OlaHsd * C57BL/6J * SJL MGI:4418046
cx147
Apoetm1Unc/Apoetm1Unc
Lgals3tm1Poi/Lgals3tm1Poi
involves: 129/Sv * C57BL/6 * SJL MGI:3789127
cx148
Albq4A/J/Albq4A/J
Apoetm1Unc/Apoetm1Unc
involves: A/J * C57BL/6J MGI:3794639
cx149
Albq4A/J/Albq4C57BL/6J
Apoetm1Unc/Apoetm1Unc
involves: A/J * C57BL/6J MGI:3794640
cx150
Apoetm1Unc/Apoetm1Unc
Gofm2C57BL/6J/?
involves: C3H/HeJ * C57BL/6J MGI:3707035
cx151
Apoetm1Unc/Apoetm1Unc
Gofm1C57BL/6J/?
involves: C3H/HeJ * C57BL/6J MGI:3707034
cx152
Apoetm1Unc/Apoetm1Unc
Tnfsf4Ath1-C57BL/6J/Tnfsf4Ath1-C57BL/6J
involves: C3H/HeJ * C57BL/6J MGI:3819480
cx153
Apoetm1Unc/Apoetm1Unc
Athsq3C3H/HeJ/Athsq3C3H/HeJ
involves: C3H/HeJ * C57BL/6J MGI:3819478
cx154
Apoetm1Unc/Apoetm1Unc
Ath33C3H/HeJ/Ath33C3H/HeJ
involves: C3H/HeJ * C57BL/6J MGI:3819477
cx155
Apoetm1Unc/Apoetm1Unc
Ath32C57BL/6J/Ath32C57BL/6J
involves: C3H/HeJ * C57BL/6J MGI:3819476
cx156
Apoetm1Unc/Apoetm1Unc
Ath29C57BL/6J/Ath29C57BL/6J
involves: C3H/HeJ * C57BL/6J MGI:3819481
cx157
Apoetm1Unc/Apoetm1Unc
Nhdlq12C3H/HeJ/Nhdlq12C57BL/6J
involves: C3H/HeJ * C57BL/6J MGI:3769560
cx158
Apoetm1Unc/Apoetm1Unc
Nhdlq11C3H/HeJ/Nhdlq11C3H/HeJ
involves: C3H/HeJ * C57BL/6J MGI:3769557
cx159
Apoetm1Unc/Apoetm1Unc
Nhdlq11C3H/HeJ/Nhdlq11C57BL/6J
involves: C3H/HeJ * C57BL/6J MGI:3769556
cx160
Apoetm1Unc/Apoetm1Unc
Trigq4C3H/HeJ/Trigq4C57BL/6J
involves: C3H/HeJ * C57BL/6J MGI:3769550
cx161
Apoetm1Unc/Apoetm1Unc
Trigq4C3H/HeJ/Trigq4C3H/HeJ
involves: C3H/HeJ * C57BL/6J MGI:3769549
cx162
Apoetm1Unc/Apoetm1Unc
Hdlq91C3H/HeJ/?
involves: C3H/HeJ * C57BL/6J MGI:3769548
cx163
Apoetm1Unc/Apoetm1Unc
Pnhdlc1C57BL/6J/Pnhdlc1C57BL/6J
involves: C3H/HeJ * C57BL/6J MGI:3769564
cx164
Apoetm1Unc/Apoetm1Unc
Pnhdlc6C3H/HeJ/?
involves: C3H/HeJ * C57BL/6J MGI:3769566
cx165
Apoetm1Unc/Apoetm1Unc
Hdlq19C57BL/6J/Hdlq19C57BL/6J
involves: C3H/HeJ * C57BL/6J MGI:3769547
cx166
Apoetm1Unc/Apoetm1Unc
Hdlq86C3H/HeJ/?
involves: C3H/HeJ * C57BL/6J MGI:3769546
cx167
Apoetm1Unc/Apoetm1Unc
Hdlq86C3H/HeJ/Hdlq86C3H/HeJ
involves: C3H/HeJ * C57BL/6J MGI:3769545
cx168
Apoetm1Unc/Apoetm1Unc
Hdl5C57BL/6J/Hdl5C57BL/6J
involves: C3H/HeJ * C57BL/6J MGI:3769543
cx169
Apoetm1Unc/Apoetm1Unc
Trigq3C3H/HeJ/Trigq3C3H/HeJ
involves: C3H/HeJ * C57BL/6J MGI:3769568
cx170
Apoetm1Unc/Apoetm1Unc
Cath1C3H/HeJ/Cath1C57BL/6J
involves: C3H/HeJ * C57BL/6J MGI:3769542
cx171
Apoetm1Unc/Apoetm1Unc
Cath1C57BL/6J/Cath1C57BL/6J
involves: C3H/HeJ * C57BL/6J MGI:3769541
cx172
Apoetm1Unc/Apoetm1Unc
Trigq3C3H/HeJ/?
involves: C3H/HeJ * C57BL/6J MGI:3769569
cx173
Apoetm1Unc/Apoetm1Unc
Ath30C57BL/6J/Ath30C57BL/6J
involves: C3H/HeJ * C57BL/6J MGI:3819474
cx174
Apoetm1Unc/Apoetm1Unc
Ath31C57BL/6J/Ath31C57BL/6J
involves: C3H/HeJ * C57BL/6J MGI:3819475
cx175
Apoetm1Unc/Apoetm1Unc
Athsq3C57BL/6J/Athsq3C57BL/6J
involves: C3H/HeJ * C57BL/6J MGI:5613592
cx176
Apoetm1Unc/Apoetm1Unc
Gofm4C3H/HeJ/?
involves: C3H/HeJ * C57BL/6J MGI:3707039
cx177
Apoetm1Unc/Apoetm1Unc
Nhdlq12C57BL/6J/Nhdlq12C57BL/6J
involves: C3H/HeJ * C57BL/6J MGI:3769561
cx178
Apoetm1Unc/Apoetm1Unc
Gofm3C57BL/6J/?
involves: C3H/HeJ * C57BL/6J MGI:3707037
cx179
Apoetm1Unc/Apoetm1Unc
Gofm2C3H/HeJ/?
involves: C3H/HeJ * C57BL/6J MGI:3707036
cx180
Apoetm1Unc/Apoetm1Unc
Faslpr/Faslpr
MRL.Cg-Apoetm1Unc Faslpr MGI:3799494


Genotype
MGI:3758858
hm1
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Genetic
Background
B6.129P2-Apoetm1Unc
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• mice maintained on a high fat diet and infected with Leishmania major generate more IL-4 and IL-5 producing CD4+ T cells compared to wild-type mice
• the immune response of mice fed a high fat diet to Leishmania major infection is skewed towards a Th2-type response
• in an adoptive transfer experiment, the proliferation of Tg(TcrLCMV)2Aox CD45.2+ cell in mice fed a high fat diet and receiving then immunized with GP61-80 peptide with CpG is reduced compared to in wild-type mice similarly treated
• dendrictic cells mount reduced IL-12p40 and TNF-alpha responses to stimulation with zymosan, poly(I:C), LPS, imiquimod, and a combination of anti-CD40 antibodies and CpG compared to wild-type mice but similar to wild-type mice fed a high fat diet
• in mice fed a high fat diet, dendritic cell production of IL-12p40, IL-6 and TNF-alpha after 35 to 40 weeks, but not after 6 to 10 weeks, is severely impaired compared to wild-type cells in response to CpG/anti-CD-40 stimulation
• CD8alpha-, but not CD8alpha+, dendritic cells are defective in their ability to produce IL-12p40
• dendritic cells from mice on a high fat diet are severely impaired in their ability to produce Il-12p40, -12p70, -6, and TNF-alpha compared to dendritic cells from wild-type mice on a high fat diet
• however, CD8alpha+ dendritic cells produce normal amounts of Il-12p70 and -12p40
• mice fed a high fat diet and co-stimulated with CpG or LPS have fewer IL-12p40-producing CD8alpha- dendritic cells (4.6+/-1.1%) than wild-type mice fed a high fat diet (15.3+/-2.4%)
• however, the immune responses of bone marrow derived dendritic cells from mice fed a high fat diet or splenic dendritic cells from mice fed a regular diet are normal
• mice maintained on a high fat diet and infected with Leishmania major produce more IL-4 and IL-5 producing CD4+ T cells compared to wild-type mice
• the immune response of mice fed a high fat diet to Leishmania major infection is skewed towards a Th2-type response
• mice maintained on a high fat diet or regular chow and infected with Leishmania major exhibit an increased swelling and parasitic burden at the site of infection (footpad)

homeostasis/metabolism
• plasma leptin levels are low at both 6 and 18 months
• mice have increased levels of circulating oxidized lipids compared to wild-type mice
• mice develop severe cholesterolemia when receiving a high fat diet from 6 to 30 weeks (elevated levels are detected at 6, 15, and 30 weeks)

behavior/neurological
• mice consume food slower in a new environment than Tg(GFAP-APOE_i4)#Hol Apoetm1Unc/Apoetm1Unc and wild-type mice
• mice require more time to habituate to a novel environment compared to wild-type mice
• mice are less reluctant than wild-type mice to move into an open area
• reduced exploratory behavior in an open field test by 12 months although normal earlier
• exploratory behavior remains constant over several days whereas controls show higher initial exploratory behavior which drops off quickly
• at 14 to 17 months of age, mice perform better than Tg(GFAP-APOE_i4)#Hol Apoetm1Unc/Apoetm1Unc and wild-type mice in a rotating holeboard test
• increased water intake at 18 months
• increased food intake at 12 and 18 months but not earlier
• at 6 months as measured in an elevated plus maze
• mice spend more time than Tg(GFAP-APOE_i4)#Hol Apoetm1Unc/Apoetm1Unc in the center of an open field
• 41% increase in foot withdrawal latency from painful thermal stimuli
• 100% slower tail withdrawal latency
• after-discharge duration is significantly prolonged by the sixth trial
• delayed rekindling after 3-4 weeks

hematopoietic system
• mice maintained on a high fat diet and infected with Leishmania major generate more IL-4 and IL-5 producing CD4+ T cells compared to wild-type mice

nervous system
• after-discharge duration is significantly prolonged by the sixth trial
• delayed rekindling after 3-4 weeks
• restraint stress at 6 months results in disproportionately low ACTH levels as compared to plasma corticosterone levels
• very little Schwann cell cytoplasm
• blurring of lipid membrane border between axons and Schwann cells
• synaptophysin levels are somewhat more reduced than in controls after entorhinal cortex lesion
• cross-section of unmyelinated axons is irregular
• very little Schwann cell cytoplasm
• blurring of lipid membrane border between axons and Schwann cells
• reduced number of unmyelinated axons
• ratio of unmyelinated to myelinated axons is reduced

endocrine/exocrine glands
• increased lipid droplets seen at six months
• increased lipid droplets seen at six months
• fter 10 min of restraint stress plasma levels are elevated at six months but not at three months
• elevated adrenal levels at six months but not earlier
• restraint stress at 6 months results in disproportionately low ACTH levels as compared to plasma corticosterone levels

adipose tissue
• decreased interscapular brown fat at 18 but not at 6 months
• epididymal white fat reduced at both 6 and 18 months

cardiovascular system
• cellular composition of lesions is similar among Serpine1-deficient or transgenic, Apoe-deficient genotypes, or Apoe-deficient only mice; at early time points, a greater foam cell content is observed, with more prominent cholesterol clefts and necrotic areas evident with increasing age




Genotype
MGI:2384131
hm2
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Genetic
Background
B6.129P2-Apoetm1Unc/J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• 35% dead by 18 months

cardiovascular system
• in perhexiline-treated mice fed a high-fat diet
• endothelial nitric oxide synthase (eNOS) in mutant aortic wall is distinctly reduced (J:101576)
• Cx43 distribution at cell-cell junction shows significant disruption (J:142083)
• arterioles of the vascular pole show a "foamy" degeneration of smooth muscle cells
• homozygotes fed an atherosclerotic diet develop atherosclerotic alterations in the spiral modiolar artery (SMA)
• in contrast, no such changes are detected in the SMA of homozygotes fed a normal diet
• homozygotes exhibit a 13% increase in aortic pulse-wave velocity (PWV) relative to wild-type mice (428 14.5 cm/s vs 379 10.1 cm/s), indicating increased arterial stiffness and reduced vascular elasticity
• 23% of luminal surface in the aortic arch and thoracic aorta is covered by plaques at 4 months of age (J:60364)
• 61% covered by plaques at 13 months of age (J:60364)
• thickened intima, foam cell accumulation and thin collagen cap (J:60364)
• focal fragmentation of elastic laminae (J:60364)
• advanced atherosclerotic lesions; massive atheromas with abundant cholesterol crystals, neutral lipids, and diminished extracellular matrix in arotic roots and coronary arteries (J:73202)
• regular exercise does not reduce atherosclerotic lesion formation in homozygotes, as shown by a comparable % oil red-O staining of whole aortas from sedentary and exercised mutant mice (J:97385)
• at 24 weeks of age, homozygotes fed a normal diet (but not similarly-fed C57BL/6J control mice) show obvious atherosclerotic lesions in the aortic sinus and ascending aorta (J:101576)
• the number of atherosclerotic lesions in aortic sinus and ascending aorta is significantly increased in homozygotes fed an atherosclerotic diet vs a normal diet (J:101576)
• plaques in the luminal surface of the aorta are significantly larger in atherosclerotic diet homozygotes than in normal diet homozygotes (J:101576)
• intimal lesions are observed in atherosclerotic aortas in mutants (J:105736)
• at 13 months, homozygotes display atherosclerotic lesions extending from the carotid arteries, heart, and aorta down to the renal arteries and the iliac bifurcation (J:108154)
• lesions are most severe in the proximal aorta and at the bifurcation of carotid arteries; the proximal carotid arteries are relatively free of lesions (J:108154)
• major lesions are observed on lesser curvature of aortic arch in males and females with minor lesions found at branches of aortic arch (J:142083)
• lesions comprise around 14-16% of total aortic arch area in male and female mutants (J:142083)
• aortic lesions are observed in aortic sinus at level of aortic valve leaflets; lesions are about 27% of total aortal area (J:142083)
• on a high fat, high cholesterol diet, mutants exhibit moderate to severe aortic and carotid atherosclerosis (J:43846)
• severity of atherosclerosis is 2-fold and 99-fold higher in atherosclerotic diet homozygotes than in normal diet homozygotes and C57BL/6J control mice, respectively (J:101576)
• at times mesangiolysis is associated with ballooning dilatation ("microaneurysm") of adjacent glomerular capillaries
• at times mesangiolysis is associated with ballooning dilatation ("microaneurysm") of adjacent glomerular capillaries
• vascular stenosis is significantly increased in homozygotes fed an atherosclerotic diet vs a normal diet
• lumen stenosis of the spiral modiolar artery in the cochlea is exacerbated by an atherosclerotic diet relative to a normal diet
• at 13 months, homozygotes show a 23% increase in heart weight relative to wild-type mice (186 7.1 vs. 151 2.5 mg)
• at 13 months, homozygotes show a 59% increase in heart weight-to-body weight ratio relative to wild-type mice
• anesthetized homozygotes show significantly increased transaortic blood velocities relative to wild-type mice with peak aortic velocity at 133.4 7.8 cm/s vs 89.2 5.8 cm/s, and mean aortic velocity at 35.9 2.7 vs 22.0 1.6 cm/s, respectively
• in addition, anesthetized homozygotes show significantly increased transmitral blood velocities relative to wild-type mice with peak mitral velocities at 92 7.2 cm/s vs 47.2 5.3 cm/s, and mean mitral velocities at 20.6 1.7 vs 11.4 1.3 cm/s, respectively
• no significant differences in heart rate, peak aortic acceleration or ejection time are observed in the conscious or anesthetized state, when normalized to body weight
• however, homozygotes show alterations in aortic arch acceleration suggestive of increased peripheral wave reflections
• under anesthesia, homozygotes exhibit elevated flow velocities suggesting elevated cardiac output
• under anesthesia, homozygotes appear to exhibit significantly increased stroke volume
• under anesthesia, homozygotes appear to exhibit significantly reduced peripheral vascular resistance and compliance in the presence of normal blood pressures
• pulse wave velocity is insignificantly elevated at 4 months
• pulse wave velocity significantly elevated at 13 months
• impaired blood-brain barrier and blood-nerve barrier as indicated by extensive extravasation of serum proteins into sciatic nerve, spinal cord and cerebellum and occasional extravasation into cortex and subcortex
• immunostaining of ATIC (5-aminoimidazole-4-carboxamide ribonucleotide formyltransferase/IMP cyclohydrolase), ACTA2 (a smooth muscle marker) and EdU showed significantly increased expression of ATIC in proliferative vascular smooth muscle cells (VSMCs) of atherosclerotic plaques in mice fed a Western diet for 3 months
• in response to precontraction with phenylephrine and relaxation with acetylcholine, mice supplemented with adenosine dialdehyde (ADA; an inhibitor of S-adenosylhomocysteine hydrolase) or treated with a short hairpin RNA targeting Ahcy with or without indomethacin exhibit endothelial dysfunction compared with control mice
• however, relaxation in response to nitroprusside is normal
• homozygotes fed a normal or atherosclerotic diet show severely impaired endothelium-dependent relaxation to acetylcholine in aortic rings relative to age-matched C57BL/6J control mice
• aortae show macrophage and T cell extravasation within atherosclerotic lesions

muscle
• immunostaining of ATIC (5-aminoimidazole-4-carboxamide ribonucleotide formyltransferase/IMP cyclohydrolase), ACTA2 (a smooth muscle marker) and EdU showed significantly increased expression of ATIC in proliferative vascular smooth muscle cells (VSMCs) of atherosclerotic plaques in mice fed a Western diet for 3 months
• in response to precontraction with phenylephrine and relaxation with acetylcholine, mice supplemented with adenosine dialdehyde (ADA; an inhibitor of S-adenosylhomocysteine hydrolase) or treated with a short hairpin RNA targeting Ahcy with or without indomethacin exhibit endothelial dysfunction compared with control mice
• however, relaxation in response to nitroprusside is normal
• homozygotes fed a normal or atherosclerotic diet show severely impaired endothelium-dependent relaxation to acetylcholine in aortic rings relative to age-matched C57BL/6J control mice
• relaxation response to acetylcholine in blood vessels is significantly attenuated at 13 months of age
• maximal response to acetylcholine is considerably reduced

homeostasis/metabolism
• in perhexiline-treated mice fed a high-fat diet
• decrease in plasma total homocysteine levels
• decreased HDL/total cholesterol ratio
• decreased HDL/LDL ratio
• increasing with age; 4-fold increase in plasma total cholesterol levels in 10-12 week old mutants and 13-fold increase at 29 weeks (J:73202)
• exercise (15 or 60 min/day swim) causes no significant changes in total cholesterol levels among homozygotes or wild-type mice relative to sedentary, genotype-matched controls (J:97385)
• on a normal diet, homozygotes display significantly increased plasma total cholesterol (TC) levels relative to C57BL/6J control mice (J:101576)
• on an atherosclerotic diet, homozygotes show a further significant increase in plasma TC levels relative to homozygotes on a normal diet (J:101576)
• total serum cholesterol 70 fold higher than controls on a normal diet (J:104609)
• total serum cholesterol 20 fold higher than controls on high fat diet where controls show 4 fold increase over normal diet (J:104609)
• 5 fold increase in total cholesterol at 24 and 36 weeks (J:125978)
• significantly increased relative to wild-type controls at 24 weeks of age; levels in mutants after induction of chronic graft versus host disease (cGVH) to induce systemic lupus erythematosus (SLE) are equivalent to the Apoe-null mice (J:133606)
• in perhexiline-treated mice fed a high-fat diet
• on a normal diet, homozygotes display significantly increased plasma LDL cholesterol levels relative to C57BL/6J control mice (J:101576)
• on an atherosclerotic diet, homozygotes show a further significant increase in plasma LDL levels relative to homozygotes on a normal diet (J:101576)
• on a normal diet, homozygotes display significantly increased plasma VLDL cholesterol levels relative to C57BL/6J control mice (J:101576)
• on an atherosclerotic diet, homozygotes show a further significant increase in plasma VLDL cholesterol levels relative to homozygotes on a normal diet (J:101576)
• 2-fold increase in plasma triglyceride levels in 10-12 week old mutants (J:73202)
• on a normal diet, homozygotes display significantly increased plasma triglyceride levels relative to C57BL/6J control mice (J:101576)
• on an atherosclerotic diet, homozygotes show a further significant increase in plasma triglyceride levels relative to homozygotes on a normal diet (J:101576)
• homozygotes develop hyperlipidemia; however, HDL cholesterol levels, body weight and blood glucose remain unchanged relative to C57BL/6J control mice on a normal diet, with no further differences noted on an atheroscletoric diet
• lipid droplets filling glomerular capillary lumina at 36 weeks in about 50% of mice
• such thrombus-like structures commonly dsiplay a laminated appearance with adjacent foam cells in the mesangium
• reduced aortic concentration in response to precontraction with phenylephrine and relaxation with acetylcholine in mice supplemented with ADA or treated with a short hairpin RNA targeting Ahcy
• 1 of 11 aged mice on a normal diet develops cerebral xanthoma (J:43846)
• eruptive xanthomas on shoulder and back areas with lipids and extracellular matix as the predominant components (J:73202)
• activity of cholesterol synthesis enzyme HMG-CoA reductase is reduced up to 60% in aging mice compared to 30% in wild-type aging mice
• mice fed a Western diet for 3 months show significantly upregulated expression of ATIC -- a bifunctional enzyme of the last 2 steps in de novo purine synthesis (DNPS) -- in proliferative VSMCs of atherosclerotic plaques

growth/size/body
• at 13 months, homozygotes show a 23% increase in heart weight relative to wild-type mice (186 7.1 vs. 151 2.5 mg)
• at 13 months, homozygotes show a 59% increase in heart weight-to-body weight ratio relative to wild-type mice
• at 13 months, homozygotes show a 22% reduction in body weight relative to wild-type mice (34.5 0.9 vs. 44.5 1.1 g) (J:108154)
• nose to rump length less than controls at both 1 and 3 months
• body weight was less than controls at 3 months but identical at 8 months
• increased spleen weight while the thymus weight remains normal

hematopoietic system
• increased spleen weight while the thymus weight remains normal
• at 13 months, awake, unanesthetized homozygotes display slightly but significantly reduced hematocrits ( 11%) relative to wild-type mice at 41.7 1.1% vs 46.6 0.4%; in contrast, systolic blood pressures remain unaffected (140 7.6 mmHg vs 136 7.4 mmHg)
• decreased relative to controls
• with induction of SLE by cGVH, levels are slightly decreased compared to wild-type
• newly formed B cells are significantly increased compared to wild-type
• increased 2-fold compared to wild-type
• increased numbers of cytokine producing T cells
• clusters of CD4+ cells found in fatty streak lesions (J:47027)
• ratio of Th2 to Th1 cells is increased from 4.4 to 11.4 on a normal diet and up to 20.9 on a high cholesterol diet (J:47027)
• spleen cells display polyclonal B cell activation, with increased expression of MHC II, Fas, and CD86 and lower expression of CD21, CD22, and CD23
• mutants with cGVH-induced SLE show greatly increased levels compared to wild-type controls or untreated mutants
• IgM response to tetanus toxoid is significantly increased as compared to controls

cellular
• in perhexiline-treated mice fed a high-fat diet
• increased rate of bone formation
• regular exercise fails to reduce endogenous oxidant load and mitochondrial damage in hypercholesterolemic mutant mice (J:97385)
• in contrast, regular exercise results in reduced mitochondrial damage and oxidant load and increased SOD2 and adenine nucleotide translocator activities in normocholesterolemic control mice (J:97385)
• in mice supplemented with ADA or treated with a short hairpin RNA targeting Ahcy (J:298071)

hearing/vestibular/ear
• endothelial nitric oxide synthase (eNOS) in mutant cochlea is distinctly reduced
• on an atherosclerotic diet, homozygotes display a sclerosed and atrophic basilar membrane
• at 24 weeks, homozygotes fed a normal diet show almost complete loss of IHCs in the basal turn and some IHC loss in the middle turn
• IHC loss at the base turn is exacerbated by an atherosclerotic diet
• at 24 weeks, homozygotes fed a normal diet show almost complete loss of OHCs in the basal turn and some OHC loss in the middle turn
• OHC loss at the base turn is exacerbated by an atherosclerotic diet
• at 24 weeks, homozygotes fed a normal diet show significant degeneration of the organ of Corti in the basal turn while the middle turn is relatively normal
• degeneration of the organ of Corti is excerbated by an atherosclerotic diet, with complete loss noted in the basal turn in some animals
• on an atherosclerotic diet, homozygotes display a sclerosed and atrophic stria vascularis
• on an atherosclerotic diet, homozygotes display a sclerosed and atrophic tectorial membrane
• at 10 weeks, homozygotes fed a normal diet display higher ABR thresholds than C57BL/6J control mice at all test frequencies, with more hearing loss noted at 32 kHz; by 24 weeks, further hearing loss is detected at all test stimuli levels
• homozygotes fed an atherosclerotic diet show higher ABR thresholds than homozygotes fed a normal diet
• homozygotes fed a normal diet display hearing loss esp. at high frequencies as compared with C57BL/6J control mice
• a high positive correlation between ABR thresholds at 16 and 8 kHz, or click and atherosclerotic lesions, and atherosclerotic plaque area of the aorta, and plasma total choelsterol levels is observed in both normal diet and high-fat diet homozygotes

nervous system
• impaired blood-brain barrier and blood-nerve barrier as indicated by extensive extravasation of serum proteins into sciatic nerve, spinal cord and cerebellum and occasional extravasation into cortex and subcortex
• at 24 weeks, homozygotes fed a normal diet show almost complete loss of IHCs in the basal turn and some IHC loss in the middle turn
• IHC loss at the base turn is exacerbated by an atherosclerotic diet
• at 24 weeks, homozygotes fed a normal diet show almost complete loss of OHCs in the basal turn and some OHC loss in the middle turn
• OHC loss at the base turn is exacerbated by an atherosclerotic diet
• at 24 weeks, homozygotes fed a normal diet show a reduced number of spiral ganglion cells in the basal turn of the cochlea
• loss of ganglion cells is excerbated by an atherosclerotic diet

immune system
• increased spleen weight while the thymus weight remains normal
• decreased relative to controls
• with induction of SLE by cGVH, levels are slightly decreased compared to wild-type
• newly formed B cells are significantly increased compared to wild-type
• increased 2-fold compared to wild-type
• increased numbers of cytokine producing T cells
• clusters of CD4+ cells found in fatty streak lesions (J:47027)
• ratio of Th2 to Th1 cells is increased from 4.4 to 11.4 on a normal diet and up to 20.9 on a high cholesterol diet (J:47027)
• aortae show macrophage and T cell extravasation within atherosclerotic lesions
• spleen cells display polyclonal B cell activation, with increased expression of MHC II, Fas, and CD86 and lower expression of CD21, CD22, and CD23
• decreased antigen specific delayed hypersensitivity response
• mutants with cGVH-induced SLE show greatly increased levels compared to wild-type controls or untreated mutants
• IgM response to tetanus toxoid is significantly increased as compared to controls
• production is reduced when fed a high cholesterol diet
• after induction of cGVH-SLE, IgG and IgM anti-oxidized LDL and anti-cardiolipin antibodies are increased compared to wild-type or Apoe-null controls
• after induction of cGVH-SLE, mice display greatly increased levels of anti-chromatin antibodies compared to wild-type controls or non-cGVH mutants
• after induction of cGVH-SLE, mice display greatly increased levels compared to wild-type controls or non-cGVH-SLE mutants

behavior/neurological
• longer latency to find the platform in Morris maze tests
• slow to acquire a preference for the target quadrant and the magnitude of the preference is always less than controls
• elevated thigmotaxis in Morris maze tests

renal/urinary system
• arterioles of the vascular pole show a "foamy" degeneration of smooth muscle cells
• at times mesangiolysis is associated with ballooning dilatation ("microaneurysm") of adjacent glomerular capillaries
• increased glomerular tuft area
• glomerular cell numbers are increased
• at times mesangiolysis is associated with ballooning dilatation ("microaneurysm") of adjacent glomerular capillaries
• progressive increase in glomerular matrix, already evident at 24 weeks, associated with accumulation of laminin and collagen IV
• loss of mesangial matrix sometimes at 36 weeks but never at 24 weeks or in controls
• glomerular foam cells in the mesangium, capillary lumina and within the glomerular stalk close to the vascular pole
• lipid deposits in arteriolar walls in the vascular poles
• lipid droplets filling glomerular capillary lumina at 36 weeks in about 50% of mice

liver/biliary system
• no significant change in serum alanine transaminase with high fat diet as is seen in controls (marker for liver damage)
• hepatic uptake of LDL is increased two fold

vision/eye
• perinuclear vacuolation on a high cholesterol diet
• cell numbers reduced
• cell numbers reduced
• implicit times increased for a and b waves of dark adapted electroretinogram (J:70245)
• wave amplitudes attenuated for a and b waves of dark adapted electroretinogram (J:70245)

taste/olfaction
• preference for plain water over 0.1% iso-amyl alcohol moderate compared to the strong preference shown by controls
• slower than control to find buried food pellet although found pellets visually more rapidly
• latency to taste vanillin-cued quinine significantly increased only at day 5

skeleton
• higher bone mineral density in vertebral bodies
• increased bone volume to tissue volume ratio in the vertebra at both 3 and 8 months and in the tibia at 8 months of age
• increased trabecular bone volume in the vertebra at both 3 and 8 months and in the tibia at 8 months of age
• in vertebral bodies and tibia
• increased number of trabeculae in vertebral bodies
• increased rate of bone formation

respiratory system
• fewer but larger alveoli at 3 months of age
• less surface area to volume
• percent increase in hysteresivity with age greater than in controls
• lung volume similar to controls at 3 months but 2.5 fold greater at 8 months of age
• resistance to airflow greater than controls at 3 months but not at 8 months of age
• dynamic and static compliance greater than controls at 8 months of age

integument
• progressive skin lesions, mainly seen as eruptive xanthomas on shoulder and back areas with lipids and extracellular matix as the predominant components




Genotype
MGI:3799495
hm3
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Genetic
Background
B6.Cg-Apoetm1Unc Faslpr
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• mice display greatly increased levels compared to wild-type controls or Apoe-null mice
• mice display greatly increased levels compared to wild-type controls or Apoe-null mice
• mice display greatly increased levels compared to wild-type controls or Apoe-null mice

homeostasis/metabolism
• significantly increased relative to wild-type controls or Fas-single mutants at 24 weeks of age; levels are higher than that of B6.129P2-Apoetm1Unc

cardiovascular system
• modest increase in total area of lipid deposits in aorta compared to Apoe-null mice

hematopoietic system
• mice display greatly increased levels compared to wild-type controls or Apoe-null mice




Genotype
MGI:3717197
hm4
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Genetic
Background
either: B6.129P2-Apoetm1Unc/J or (involves: 129P2/OlaHsd * C57BL/6J * ICR)
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
N
• no alterations in passive avoidance learning are observed; coordination levels measured in rotorod tests are similar to wild-type
• 6-month old female mice show subtle learning impairment in water maze task compared to transgenic mutants; 6-month old males show significantly decreased learning ability in the Morris water maze test
• mice have fewer rearing events and shorter rearing times than wild-type controls

nervous system
N
• upon 18 mg/kg kainic acid injection, significant loss of neocortical synaptophysin-positive presynaptic terminals and disruption of hippocampal axons are observed, similar to wild-type (J:55835)
• mice show significant loss of synaptophysin-positive presynaptic terminals and neuronal dendrites of the neocortex and hippocampus with age (7-9 months compared to 3-4 months), similar to wild-type (J:55835)
• mice exhibit age-dependent loss of synaptophysin-reactive terminals and microtubule-associated protein 2-positive neuronal dendrites in the neocortex and hippocampus, similar to wild-type (J:100975)




Genotype
MGI:3718006
hm5
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Genetic
Background
involves: 129P2/OlaHsd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
• in the elevated-plus maze, mice show increased anxiety with reduced time and distance moved in the open arms; mice have significantly lower number of open-arm entries than wild-type
• effect is age-dependent; phenotype is present in older mice, but not in young 2-4 month-old mice
• response is higher in mice at 6 months of age compared to wild-type

homeostasis/metabolism
• all males have higher plasma concentrations than wild-type after behavioral testing
• circulating VLDL/LDL cholesterol levels are increased compared to in Apobec1tm1Chan homozygotes and wild-type mice
• when fed a chow or Western-type diet for 2 weeks, mice exhibit increased serum cholesterol compared with Apobec1tm1Chan homozygotes and wild-type mice
• compared to in Tg(Eno2-APP751)10Cord Apoetm1Unc/Apoetm1Unc mice

nervous system
• compared to in Tg(Eno2-APP751)10Cord Apoetm1Unc/Apoetm1Unc mice
• mutants have lower levels of MAP 2-positive neuronal dendrites than wild-type; at 3 months, levels are similar in mutants and controls

cardiovascular system
• atherosclerotic lesions begin to form in the left common carotid by 2 weeks after partial ligation of the left common carotid
• atherosclerotic lesion development is well advanced by 4-6 weeks after partial ligation of the left common carotid
• bone marrow transplanted into Apoa1tm1Unc homozygotes confer susceptibility to atherosclerosis
• impaired vasodilation induced by sodium nitroprusside 7 days after partial ligation of the left common carotid

muscle
• impaired vasodilation induced by sodium nitroprusside 7 days after partial ligation of the left common carotid




Genotype
MGI:3764959
hm6
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Morphology of aortic lesions in Apoetm1Unc/Apoetm1Unc and Apoetm1Unc/Apoetm1Unc Ttpatm1Far/Ttpatm1Far mice

cardiovascular system
• most severe in the aortic arch region




Genotype
MGI:3714936
hm7
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• fatty streaks with foam cells are found in the proximal aorta of 3-8 month old mice fed normal chow (J:16573)
• the foam cells are often adjacent to valve attachment sites and can form multi-layers (J:16573)
• lesions get bigger with age and near total occlusion at the entrance of a coronary artery can be observed at 8 months of age (J:16573)
• 75% of mice develop lesions in the aortic arch with most females and some males having calcification within the lesions (J:40136)
• aortic cartilaginous metaplasia is noted in the most severely affected mice (J:40136)
• mice exhibit atherosclerotic lesions in the aorta and aortic root (J:41510)
• extent of atherosclerosis correlates with plasma cholesterol levels (J:41510)
• greater than in wild-type (J:80689)

homeostasis/metabolism
• mean HDL levels (33 mg/dl) are 45% of that found in controls
• mean total cholesterol levels are elevated about 5-fold over wild-type to 434 mg/dl (J:16573)
• total cholesterol levels are about 4-fold higher than controls with a mean of 379 mg/dl (J:40136)
• plasma cholesterol levels increase significantly with time (J:41510)
• relative to wild-type (J:80689)
• mice have elevated levels of LDL in the blood
• the majority of lipoprotein particles in the blood are in the VLDL size range (J:16573)
• very high levels of VLDL cholesterol (J:41510)
• circulating triglyceride levels are 123 mg/dl compared to 73 mg/dl in controls (J:16573)
• relative to wild-type (J:80689)
• relative to wild-type
• amount of PGE2 in aortas is 4X higher than in controls
• PGE2 level doubles on a high fat diet

nervous system
• elevated cholesterol in the exofacial leaflet of the synaptic plasma membrane but not so high as for Ldlr deficient mice
• cholesterol levels in the cytofacial leaflet are reduced
• astrocytes secrete less phospholipids or free cholesterol compared to wild-type astrocytes

immune system
• isolated small foci of mononuclear cells are present in lung after 6 weeks of high-fat feeding

respiratory system
• isolated small foci of mononuclear cells are present in lung after 6 weeks of high-fat feeding




Genotype
MGI:4358709
hm8
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * DBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• increase in APOB-48
• the HDL phospholipid fraction is enriched in 16:0 and 18:0 species and contains less 20:4 and 22:6 species compared to Ldlrtm1Her single mutants
• increase in the APOB lipoprotein cholesterol level compared to wild-type controls
• there is a 2.3 fold increase in the ratio of saturated + monounsaturated/polyunsaturated cholesterol ester fatty acid species compared to Ldlrtm1Her single mutants
• the ratio of saturated + monounsaturated/polyunsaturated cholesterol ester fatty acid species in the LDL fraction is significantly increased compared to Ldlrtm1Her single mutants
• about a 50% decrease in HDL compared to controls
• increased total cholesterol and esterfied cholesterol levels in the plasma




Genotype
MGI:3822450
hm9
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• lesions are observed in aortas of nontransgenic mice




Genotype
MGI:3836194
ht10
Allelic
Composition
Apoetm1Unc/Apoe+
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• circulating triglyceride levels are 39% higher than in wild-type controls




Genotype
MGI:3716843
ht11
Allelic
Composition
Apoeshl/Apoetm1Unc
Genetic
Background
involves: 129P2/OlaHsd * KOR
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoeshl mutation (1 available); any Apoe mutation (158 available)
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• in all mice




Genotype
MGI:7316557
cn12
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Nck1tm1Paw/Nck1tm1Paw
Nck2tm3Paw/Nck2tm3Paw
Tg(Cdh5-cre/ERT2)1Rha/0
Genetic
Background
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Nck1tm1Paw mutation (2 available); any Nck1 mutation (40 available)
Nck2tm3Paw mutation (0 available); any Nck2 mutation (29 available)
Tg(Cdh5-cre/ERT2)1Rha mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Assessment of atherosclerosis initiation and progression in tamoxifen-treated, high-fat diet fed Apoetm1Unc/Apoetm1Unc Tg(Cdh5-cre/ERT2)1Rha/0 Nck1tm1Paw/Nck1tm1Paw Nck2tm3Paw/Nck2tm3Paw mice.

cardiovascular system
• severity of lesions, atherosclerosis progression, and macrophage recruitment are reduced in male, but not female, following 16 weeks of a high-fat diet in tamoxifen-treated mice
• however, serum lipoprotein levels are normal

immune system
• severity of lesions, atherosclerosis progression, and macrophage recruitment are reduced in male, but not female, following 16 weeks of a high-fat diet in tamoxifen-treated mice




Genotype
MGI:7511828
cn13
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Atictm1c(EUCOMM)Hmgu/Atictm1c(EUCOMM)Hmgu
Gt(ROSA)26Sortm1(cre/ERT2)Tyj/Gt(ROSA)26Sor+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6J * C57BL/6N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Atictm1c(EUCOMM)Hmgu mutation (0 available); any Atic mutation (35 available)
Gt(ROSA)26Sortm1(cre/ERT2)Tyj mutation (3 available); any Gt(ROSA)26Sor mutation (993 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• both sexes of tamoxifen-treated mice fed a Western diet for 12 weeks show a significant decrease in atherosclerotic lesion size in whole aortas as well as smaller lesion areas and less lipid deposition in the aortic sinuses than control mice
• ACTA2 staining of aortic sinuses showed a significant reduction in the vascular smooth muscle cell (VSMC) content of atherosclerotic lesions in both sexes

homeostasis/metabolism
N
• both male and female mice treated with tamoxifen and subsequently fed a Western diet for 12 weeks show no significant differences in plasma glucose levels relative to controls
• male, but not female, mice treated with tamoxifen and subsequently fed a Western diet for 12 weeks show a modest reduction in plasma cholesterol levels relative to controls
• female, but not male, mice treated with tamoxifen and subsequently fed a Western diet for 12 weeks exhibit a significant increase in plasma triglyceride levels relative to controls




Genotype
MGI:7511826
cn14
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Atictm1c(EUCOMM)Hmgu/Atictm1c(EUCOMM)Hmgu
X/Tg(Myh11-icre/ERT2)1Soff
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJaeSor * C57BL/6J * C57BL/6N * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Atictm1c(EUCOMM)Hmgu mutation (0 available); any Atic mutation (35 available)
Tg(Myh11-icre/ERT2)1Soff mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• tamoxifen-treated mice fed a Western diet for 12 weeks show a significant decrease in atherosclerotic lesion size in whole aortas as well as smaller lesion areas and less lipid deposition in the aortic sinuses than similarly-fed control mice
• ACTA2 staining showed a significant reduction in the vascular smooth muscle cell (VSMC) content of atherosclerotic lesions in the aortic sinus

homeostasis/metabolism
N
• tamoxifen-treated mice fed a Western diet for 12 weeks show no significant differences in the level of plasma cholesterol, triglycerides, or glucose relative to controls




Genotype
MGI:5781094
cn15
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Ddit3tm1.1Irt/Ddit3tm1.1Irt
Taglntm2(cre)Yec/Tagln+
Genetic
Background
involves: 129P2/OlaHsd * 129S6/SvEvTac * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Ddit3tm1.1Irt mutation (1 available); any Ddit3 mutation (20 available)
Taglntm2(cre)Yec mutation (1 available); any Tagln mutation (28 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• aortic root shows a approximate 30% reduction in lesion area and necrotic area compared to Apoetm1Unc Ddit3tm1.1Irt double homozygotes, indicating decreased atherosclerotic plaque progression
• smooth muscle cell content is lower in aortic arch lesions compared to Ddit3tm1.1Irt Apoetm1Unc double homozygotes
• mice on a Western diet show a lower content of alpha-actin-positive vascular smooth muscle cells in the lesions compared to Ddit3tm1.1Irt Apoetm1Unc double homozygotes
• lesions show decreased vascular smooth muscle cell proliferation

homeostasis/metabolism
N
• after 12 weeks of Western diet feeding, mice exhibit similar body weight, blood glucose, total plasma cholesterol, HDL cholesterol, plasma triglycerides, and blood pressure as Apoetm1Unc Ddit3tm1.1Irt double homozygotes




Genotype
MGI:4818410
cn16
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Gja5tm1Mchn/Gja5tm1Mchn
Tg(TIE2-lacZ)182Sato/0
Genetic
Background
involves: 129P2/OlaHsd * BALB/c * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Gja5tm1Mchn mutation (1 available); any Gja5 mutation (19 available)
Tg(TIE2-lacZ)182Sato mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
N
• mice exhibit normal mean arterial pressure, heart rate, and endothelium-dependent vasomotor responses to KCl and norepinephrine
• whether fed a high-fat or standard diet, mice exhibit increased lipid staining in the thoracoabdominal aortas compared with Apoetm1Unc homozygotes
• whether fed a high-fat or standard diet, mice exhibit accelerated atherosclerosis compared with Apoetm1Unc homozygotes

immune system
• LPS-treated mice exhibit increased inflammatory cell recruitment, mostly neutrophils, into the alveolar spaces compared with similarly treated Apoetm1Unc homozygotes
• LPS-treated mice exhibit increased inflammatory cell recruitment, mostly neutrophils, into the alveolar spaces compared with similarly treated Apoetm1Unc homozygotes

respiratory system
• LPS-treated mice exhibit increased inflammatory cell recruitment, mostly neutrophils, into the alveolar spaces compared with similarly treated Apoetm1Unc homozygotes

hematopoietic system
• LPS-treated mice exhibit increased inflammatory cell recruitment, mostly neutrophils, into the alveolar spaces compared with similarly treated Apoetm1Unc homozygotes




Genotype
MGI:5912277
cn17
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Smarcd1tm1.1Jddl/Smarcd1tm1.1Jddl
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * DBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Smarcd1tm1.1Jddl mutation (1 available); any Smarcd1 mutation (30 available)
Speer6-ps1Tg(Alb-cre)21Mgn mutation (6 available); any Speer6-ps1 mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• area of atherosclerotic lesions is reduced by about 53% compared to mice homozygous null for Apoe alone

homeostasis/metabolism
• cholesterol levels are approximately 30% lower in Western diet fed mice compared to diet matched controls
• expression analysis indicates bile acid metabolism is reduced




Genotype
MGI:7516351
cn18
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Svep1tm1c(EUCOMM)Hmgu/Svep1tm1c(EUCOMM)Hmgu
Tg(Myh11-icre/ERT2)1Soff/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6N * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Svep1tm1c(EUCOMM)Hmgu mutation (0 available); any Svep1 mutation (169 available)
Tg(Myh11-icre/ERT2)1Soff mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• reduced atherosclerotic plaque burden in whole aorta and aortic arch and root after 8 and 16 weeks of HFD feeding
• reduced macrophage invasion of aortic atheromas and reduced necrotic core area after 8 and 16 weeks of HFD feeding
• increased atherosclerotic plaque collagen content after 16 weeks of HFD feeding

growth/size/body
N
• normal body weight after 8 and 16 weeks of HFD feeding

homeostasis/metabolism
N
• normal plasma total cholesterol, triglycerides and glucose levels after 8 weeks of HFD feeding
• normal plasma total cholesterol and glucose levels after 16 weeks of HFD feeding




Genotype
MGI:5552967
cn19
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Klf15tm2Jain/Klf15tm2Jain
Tg(Tagln-cre)1Jjl/0
Genetic
Background
involves: 129P2/OlaHsd * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Klf15tm2Jain mutation (0 available); any Klf15 mutation (19 available)
Tg(Tagln-cre)1Jjl mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Klf15tm2Jain/Klf15tm2Jain Tg(Tagln-cre)1Jjl/0 Apoetm1Unc/Apoetm1Unc aortas develop more atherosclerotic lesions after a high fat diet challenge

homeostasis/metabolism
N
• mice fed a high fat diet exhibit the same circulating levels of cholesterol and triglycerides as in Apoetm1Unc homozygotes

immune system
• increased macrophage in the aortic wall and atherosclerotic lesions of mice fed a high fat diet with Apoetm1Unc homozygotes
• increased macrophage in the aortic wall and atherosclerotic lesions of mice fed a high fat diet with Apoetm1Unc homozygotes

cardiovascular system
• in mice fed a high fat diet compared with Apoetm1Unc homozygotes
• decreased vascular smooth muscle cells in the aortic wall and atherosclerotic lesions of mice fed a high fat diet with Apoetm1Unc homozygotes
• increased macrophage in the aortic wall and atherosclerotic lesions of mice fed a high fat diet with Apoetm1Unc homozygotes

muscle
• decreased vascular smooth muscle cells in the aortic wall and atherosclerotic lesions of mice fed a high fat diet with Apoetm1Unc homozygotes

hematopoietic system
• increased macrophage in the aortic wall and atherosclerotic lesions of mice fed a high fat diet with Apoetm1Unc homozygotes




Genotype
MGI:4420802
cx20
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Cdkn1atm1Tyj/Cdkn1atm1Tyj
Genetic
Background
B6.129-Apoetm1Unc Cdkn1atm1Tyj
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Cdkn1atm1Tyj mutation (3 available); any Cdkn1a mutation (63 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• angiotensin II-treated mice exhibit less of an increase in mortality compared with similarly treated Apoetm1Unc homozygotes

cardiovascular system
• angiotensin II-treated mice exhibit a smaller increase in plaque area, plaque grade, aortic aneurysms, atheroma, and mortality but an increase in proliferation of vascular smooth muscle cells compared with similarly treated Apoetm1Unc homozygotes
• treatment with angiotensin II induces less vascular smooth muscle cell senescence and more proliferation compared to in similarly treated Apoetm1Unc homozygotes
• treatment with angiotensin II induces more vascular smooth muscle proliferation compared to in similarly treated Apoetm1Unc homozygotes

homeostasis/metabolism
• angiotensin II-treated mice exhibit a smaller increase in plaque area, plaque grade, aortic aneurysms, atheroma, and mortality but an increase in proliferation and decrease in senescence of vascular smooth muscle cells compared with similarly treated Apoetm1Unc homozygotes

cellular
• treatment with angiotensin II induces more vascular smooth muscle proliferation compared to in similarly treated Apoetm1Unc homozygotes
• treatment with angiotensin II induces less vascular smooth muscle cell senescence compared to in similarly treated Apoetm1Unc homozygotes

muscle
• treatment with angiotensin II induces less vascular smooth muscle cell senescence and more proliferation compared to in similarly treated Apoetm1Unc homozygotes
• treatment with angiotensin II induces more vascular smooth muscle proliferation compared to in similarly treated Apoetm1Unc homozygotes




Genotype
MGI:3527869
cx21
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Cx3cl1tm1Sgs/Cx3cl1tm1Sgs
Genetic
Background
B6.129-Apoetm1Unc Cx3cl1tm1Sgs
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Cx3cl1tm1Sgs mutation (0 available); any Cx3cl1 mutation (35 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• brachiocephalic artery lesion area is reduced by about 85% at 200 um and 400 um but not at 600 um from its branching site into the carotid and subclavian arteries in female double homozygotes compared to Apoe single homozygotes
• in male double homozygotes brachiocephalic artery lesion area is reduced by 82% at 200 um, 58% at 400 um, and 59% at 600 um
• aortic root lesion area is reduced by about 30% in double homozygous females at 12 weeks of age but not in males at 12 weeks or in either sex at 16 weeks
• lesions are less advanced than in Apoe single homozygotes and are composed almost entirely of foam cells

immune system
• atherosclerotic lesions are composed almost entirely of foam cells
• macrophage accumulation is reduced by 80% in the brachiocephalic artery at 200 um from its branching site into the carotid and subclavian arteries

hematopoietic system
• atherosclerotic lesions are composed almost entirely of foam cells
• macrophage accumulation is reduced by 80% in the brachiocephalic artery at 200 um from its branching site into the carotid and subclavian arteries

cellular
• atherosclerotic lesions are composed almost entirely of foam cells
• macrophage accumulation is reduced by 80% in the brachiocephalic artery at 200 um from its branching site into the carotid and subclavian arteries




Genotype
MGI:3618279
cx22
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Cx3cr1tm1Zm/Cx3cr1+
Genetic
Background
B6.129-Apoetm1Unc Cx3cr1tm1Zm
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Cx3cr1tm1Zm mutation (1 available); any Cx3cr1 mutation (45 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• lesion area in the thoracic aorta is decreased by about 50% compared to mice homozygous for the Apoe allele only




Genotype
MGI:3618277
cx23
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Cx3cr1tm1Zm/Cx3cr1tm1Zm
Genetic
Background
B6.129-Apoetm1Unc Cx3cr1tm1Zm
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Cx3cr1tm1Zm mutation (1 available); any Cx3cr1 mutation (45 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• lesion area in the aorta and aortic sinus is decreased by about 50% compared to mice homozygous for the Apoe allele only; however the accumulation of smooth muscle cells and collagen within the plaque is similar to wild-type
• a 50% reduction is seen in the aortic sinus area containing monocyte-macrophage markers




Genotype
MGI:4938323
cx24
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Ifngtm1Ts/Ifngtm1Ts
Genetic
Background
B6.129-Apoetm1Unc Ifngtm1Ts
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Ifngtm1Ts mutation (18 available); any Ifng mutation (49 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• about 50% of mice infused with angiotensin-II die within 2 to 10 days due to rupture of the abdominal aorta compared to 0 deaths of mutant mice wild-type for Ifng

cardiovascular system
• increase in the suprarenal aortic diameter in mice infused with 500 ng/kg/min angiotensin-II compared to mutant mice wild-type for Ifng
• about 50% of mice infused with 1000 ng/kg/min angiotensin-II die within 2 to 10 days due to rupture of the abdominal aorta compared to 0 deaths of mutant mice wild-type for Ifng
• increase in the incidence of abdominal aorta aneurysyms in in mice infused with 500 ng/kg/min angiotensin-II compared to mutant mice wild-type for Ifng

growth/size/body
• compared to mutant mice wild-type for Ifng




Genotype
MGI:3822293
cx25
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Pecam1Gt(OST16303)Lex/Pecam1Gt(OST16303)Lex
Genetic
Background
B6.129-Apoetm1Unc Pecam1Gt(OST16303)Lex
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Pecam1Gt(OST16303)Lex mutation (1 available); any Pecam1 mutation (227 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• Cx43 distribution at cell-cell junction shows less disruption than in single Apoe-deficient mice
• major lesions are observed on lesser curvature of aortic arch in males and females with minor lesions found at branches of aortic arch
• lesions comprise around 14-16% of total aortic arch area in male and female mutants
• aortic lesions are observed in aortic sinus at level of aortic valve leaflets; lesions are about 27% of total aortal area

homeostasis/metabolism
N
• cholesterol levels of double mutants on a Western or normal chow diet are not significantly different from diet-matched Apoe-null animals




Genotype
MGI:4938324
cx26
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Cxcl10tm1Adl/Cxcl10tm1Adl
Genetic
Background
B6.129-Cxcl10tm1Adl Apoetm1Unc
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Cxcl10tm1Adl mutation (2 available); any Cxcl10 mutation (20 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• increased incidence of death due to ruptured abdominal aorta aneurysyms following angiotensin-II infusion compared to mutant mice wild-type for Cxcl10

cardiovascular system
• decrease in lesion size in the angiotensin-II induced model compared to mutant mice wild-type for Cxcl10
• display more severe morphological changes following angiotensin-II infusion compared to mutant mice wild-type for Cxcl10
• increase in the suprarenal aortic diameter and suprarenal/thoracic to infrarenal aortic area ratios in mice infused with angiotensin-II compared to mutant mice wild-type for Cxcl10
• large aortic aneurysms with spiral dissections are seen following angiotensin-II infusion
• decrease in CD4+ T cell accumulation in angiotensin-II induced aneurysms
• seen following angiotensin-II infusion
• increased incidence of death due to ruptured abdominal aorta aneurysyms following angiotensin-II infusion compared to mutant mice wild-type for Cxcl10
• large aortic aneurysms with spiral dissections are seen following angiotensin-II infusion
• increase in the incidence of grade III aneurysms following angiotensin-II infusion compared to mutant mice wild-type for Cxcl10
• seen following angiotensin-II infusion

immune system
• decrease in macrophage accumulation in the arterial wall in angiotensin-II treated mice
• decrease in CD4+ T cell accumulation in angiotensin-II induced aneurysms

hematopoietic system
• decrease in macrophage accumulation in the arterial wall in angiotensin-II treated mice
• decrease in CD4+ T cell accumulation in angiotensin-II induced aneurysms

cellular
• decrease in macrophage accumulation in the arterial wall in angiotensin-II treated mice




Genotype
MGI:5462232
cx27
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Thbdtm1.1(THBD)Sltz/Thbdtm1.1(THBD)Sltz
Genetic
Background
B6.129(FVB)-Thbdtm1.1(THBD)Sltz Apoetm1Unc
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Thbdtm1.1(THBD)Sltz mutation (0 available); any Thbd mutation (25 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
N
• mice fed a high fat diet exhibit the same increase in total cholesterol, atherosclerotic lesion area and time to occlusion of the carotid artery following photochemical injury as Apoetm1Unc homozygotes
• mice fed a high fat diet exhibit decreased amount of circulating activated protein C compared with Apoetm1Unc homozygotes




Genotype
MGI:5502603
cx28
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Hsd11b1tm1Lex/Hsd11b1tm1Lex
Genetic
Background
B6.129-Hsd11b1tm1Lex Apoetm1Unc
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Hsd11b1tm1Lex mutation (1 available); any Hsd11b1 mutation (28 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Decreased aortic root atherosclerosis susceptibility in Apoetm1Unc/Apoetm1Unc Hsd11b1tm1Lex/Hsd11b1tm1Lex mice

immune system
N
• mice fed a high fat diet and subjected to intraperitoneal thioglycollate challenge exhibit normal inflammatory cell migration
• foam cells from mice fed a high fat diet exhibit reduced cholesterol content compared with control cells
• in atherosclerotic lesions of mice fed a high fat diet
• peritoneal foam cells treated with oxidized LDL exhibit reduced secretion of G-CSF, KC, MCP-1 and TNFalpha compared with control cells
• in peritoneal foam cells treated with oxidized LDL

homeostasis/metabolism
• in mice fed a high fat diet as in Apoetm1Unc homozygotes
• decreased total, 7-ketocholesterol and 7beta-hydroxycholesterol levels in the aorta of mice fed a high fat diet compared with similarly treated Apoetm1Unc homozygotes
• foam cells from mice fed a high fat diet exhibit reduced cholesterol content compared with control cells

cardiovascular system
N
• mice fed a high fat diet exhibit normal blood pressure
• decreased total, 7-ketocholesterol and 7beta-hydroxycholesterol levels in the aorta of mice fed a high fat diet compared with similarly treated Apoetm1Unc homozygotes
• foam cells from mice fed a high fat diet exhibit reduced cholesterol content compared with control cells

behavior/neurological
N
• mice fed a high fat diet exhibit normal behavior

growth/size/body
N
• mice fed a high fat diet exhibit normal weight gain

hematopoietic system
• foam cells from mice fed a high fat diet exhibit reduced cholesterol content compared with control cells
• in atherosclerotic lesions of mice fed a high fat diet
• bone marrow-derived stem cells transferred into Apoetm1Unc recipient fed a high fat diet results in decreased atherosclerosis in whole thoracic aorta and descending aorta

cellular
• foam cells from mice fed a high fat diet exhibit reduced cholesterol content compared with control cells




Genotype
MGI:4939466
cx29
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Il1r1tm1Imx/Il1r1tm1Imx
Genetic
Background
B6.129-Il1r1tm1Imx Apoetm1Unc
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Il1r1tm1Imx mutation (4 available); any Il1r1 mutation (39 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• when fed a Western diet with high cholate, but not when fed standard chow or a Western diet
• mice receiving Apoetm1Unc bone marrow develop 1.9-fold smaller lesions compared with similarly treated Apoetm1Unc homozygotes
• when fed either a Western diet or a Western diet with high cholate compared with similarly treated Apoetm1Unc homozygotes
• when fed either a Western diet with high cholate, mice exhibit a greater active pressure-diameter response compared with similarly treated Apoetm1Unc homozygotes
• when fed either a Western diet with high cholate, mice exhibit greater constriction in response to sensitivity to L-NAME treatment compared with similarly treated Apoetm1Unc homozygotes
• when fed either a Western diet or a Western diet with high cholate, mice exhibit greater vasodilator sensitivity to acetyl choline compared with similarly treated Apoetm1Unc homozygotes

homeostasis/metabolism
• when fed either a Western diet compared with similarly treated Apoetm1Unc homozygotes

immune system
• when fed either a Western diet compared with similarly treated Apoetm1Unc homozygotes

muscle
• when fed either a Western diet with high cholate, mice exhibit greater constriction in response to sensitivity to L-NAME treatment compared with similarly treated Apoetm1Unc homozygotes
• when fed either a Western diet or a Western diet with high cholate, mice exhibit greater vasodilator sensitivity to acetyl choline compared with similarly treated Apoetm1Unc homozygotes




Genotype
MGI:4359427
cx30
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Nceh1tm1Ishi/Nceh1tm1Ishi
Genetic
Background
B6.129-Nceh1tm1Ishi Apoetm1Unc
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Nceh1tm1Ishi mutation (1 available); any Nceh1 mutation (35 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• free cholesterol levels are increased 1.5-fold and 1.3-fold for males and females, respectively, compared to in Apoetm1Unc homozygotes
• cholesterol esters are increased 2-fold and 1.3-fold in males and females, respectively, compared to in Apoetm1Unc homozygotes

cardiovascular system
• atherosclerotic lesions are increased compared to in Apoetm1Unc homozygotes (2.2-fold for males and 2.3-fold in females at 17 weeks, 1.7-fold in males and 2.4-fold for females at 21 weeks)




Genotype
MGI:4367467
cx31
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Nos3tm1Plh/Nos3tm1Plh
Genetic
Background
B6.129-Nos3tm1Plh Apoetm1Unc
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Nos3tm1Plh mutation (1 available); any Nos3 mutation (58 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• increase in lesion area relative to Apoe single mutants when fed a Western type diet
• unlike in Apoe single mutants no difference in lesion area is seen at 4 months of age in double mutants fed a Western type diet
• all mice show distal coronary arteriosclerosis associated with perivascular and endomyocardial fibrosis and endomyocardial scars consistent with nontransmural infarction
• 2 of 12 mice fed a Western type diet for 16 weeks developed acute Stanford type B aortic dissections that are not seen in Apoe single mutants
• thickening of the interventricular septum is seen in double mutants fed a Western type diet for 16 weeks
• thickening of the LV posterior wall is seen in double mutants fed a Western type diet for 16 weeks
• 2 of 10 mice fed a Western type diet for 16 weeks displayed massive dilation of the left ventricle
• all mice show distal coronary arteriosclerosis associated with perivascular and endomyocardial fibrosis and endomyocardial scars consistent with nontransmural infarction
• 3 of 12 mice fed a Western type diet for 16 weeks developed atherosclerotic suprarenal abdominal aortic aneurysms that are not seen in Apoe single mutants
• decrease in fractional shortening in double mutants fed a Western type diet for 16 weeks
• increased relative to wild-type controls and Apoe single mutants but similar to Nos3 single mutants

muscle
• decrease in fractional shortening in double mutants fed a Western type diet for 16 weeks




Genotype
MGI:4942389
cx32
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Cd44tm1Mak/Cd44+
Genetic
Background
B6.129P2-Cd44tm1Mak Apoetm1Unc
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Cd44tm1Mak mutation (1 available); any Cd44 mutation (72 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• reduced lesion area in the thoracic abdominal aorta
• normal plasma cholesterol levels




Genotype
MGI:4942387
cx33
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Cd44tm1Mak/Cd44tm1Mak
Genetic
Background
B6.129P2-Cd44tm1Mak Apoetm1Unc
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Cd44tm1Mak mutation (1 available); any Cd44 mutation (72 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• reduced lesion area in the aortic root and thoracic abdominal aorta in a gene dosage-dependent manner
• normal plasma cholesterol levels




Genotype
MGI:3794764
cx34
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Nos3tm1Unc/Nos3tm1Unc
Genetic
Background
B6.129P2-Nos3tm1Unc Apoetm1Unc
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Nos3tm1Unc mutation (6 available); any Nos3 mutation (58 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• microaneurysmal dilations in 20% of males
• sometimes involving coronary arteries
• plaques larger at 4 months than in Apoetm1Unc homozygotes, by 182% for males and 165% for females
• plaques in descending aorta in 90% of males as opposed to 20% of Apoetm1Unc males
• about 20mm higher than in Apoetm1Unc homozygotes

renal/urinary system
• 15% of glomeruli with large lipid deposits in foam cells filling the glomeruli
• glomerular injury progresses to dystrophic calcification and glomerular loss
• 15% lower than in Apoetm1Unc homozygotes

homeostasis/metabolism
• 66% higher than controls




Genotype
MGI:3811066
cx35
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Serpine1tm1Mlg/Serpine1tm1Mlg
Genetic
Background
B6.129-Serpine1tm1Mlg Apoetm1Unc
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Serpine1tm1Mlg mutation (3 available); any Serpine1 mutation (25 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• when fed a high fat Western diet for 6-30 weeks, mice develop atherosclerotic aortic lesions of the intimal and medial areas; incidence and severity are similar for Serpine1-deficient or transgenic Apoe-deficient genotypes
• lesions are somewhat larger than those observed on the Ldlr-deficient background
• cellular composition of lesions is similar among Serpine-deficient or transgenic, Apoe-deficient genotypes, or Apoe-deficient only mice; at early time points, a greater foam cell content is observed, with more prominent cholesterol clefts and necrotic areas evident with increasing age
• fibrin deposition is not significantly different among Serpine-deficient or transgenic, Apoe-deficient genotypes, or Apoe-deficient only mice

homeostasis/metabolism
• mice develop severe cholesterolemia when receiving a high fat diet from 6 to 30 weeks (elevated levels are detected at 6, 15, and 30 weeks)




Genotype
MGI:4833679
cx36
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Ccr2tm1Ifc/Ccr2tm1Ifc
Genetic
Background
B6.Cg-Apoetm1Unc Ccr2tm1Ifc
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Ccr2tm1Ifc mutation (1 available); any Ccr2 mutation (43 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• mice fed a high fat diet exhibit decreased lesion size and macrophage accumulation compared to in Apoetm1Unc homozygotes

hematopoietic system
• mice fed a high fat diet exhibit decreased circulating monocyte numbers compared to in Apoetm1Unc homozygotes

immune system
• mice fed a high fat diet exhibit decreased circulating monocyte numbers compared to in Apoetm1Unc homozygotes




Genotype
MGI:3784302
cx37
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Cdh18Tg(GFAP-APOE_i4)1Hol/0
Genetic
Background
B6.Cg-Apoetm1Unc Cdh18Tg(GFAP-APOE_i4)1Hol/J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Cdh18Tg(GFAP-APOE_i4)1Hol mutation (1 available); any Cdh18 mutation (56 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• the ratio of lipid to Apoe in HDL particles secreted from astrocytes is lower than in wild-type astrocytes but higher than in Apoetm1Unc homozygotes




Genotype
MGI:4833678
cx38
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Ccr2tm1Ifc/Ccr2tm1Ifc
Cx3cl1tm1Lira/Cx3cl1tm1Lira
Genetic
Background
B6.Cg-Apoetm1Unc Cx3cl1tm1Lira Ccr2tm1Ifc
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Ccr2tm1Ifc mutation (1 available); any Ccr2 mutation (43 available)
Cx3cl1tm1Lira mutation (0 available); any Cx3cl1 mutation (35 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• mice fed a high fat diet exhibit decreased lesion size and macrophage accumulation compared to in Apoetm1Unc homozygotes and Apoetm1Unc Ccr2tm1Ifc homozygotes

hematopoietic system
• mice fed a high fat diet exhibit decreased circulating monocyte numbers compared to in Apoetm1Unc homozygotes
• however, levels are the same as in Apoetm1Unc Ccr2tm1Ifc homozygotes

immune system
• mice fed a high fat diet exhibit decreased circulating monocyte numbers compared to in Apoetm1Unc homozygotes
• however, levels are the same as in Apoetm1Unc Ccr2tm1Ifc homozygotes




Genotype
MGI:3800213
cx39
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Faslpr/Faslpr
Genetic
Background
B6.Cg-Apoetm1Unc Faslpr
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Faslpr mutation (39 available); any Fas mutation (82 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
hematopoietic system
N
• at 5 months, there are no significant differences in most leukocyte subsets (NK-cells, monocytes/macrophages, and neutrophils) compared to controls
• significantly enlarged compared to Apoe-null, Fas-heterozygous mice or Apoe-wt, Fas-homozygous mice at 5 months
• numbers of circulating cells are significantly reduced
• numbers of circulating cells are significantly reduced comparted to Apoe-wt, Fas-homozygous mice at 5 months
• serum levels of IgG are significantly higher than in Apoe-null and Apoe-null, Fas-heterozygous mice at 6 weeks and at 5 months

growth/size/body
• significantly enlarged compared to Apoe-null, Fas-heterozygous mice or Apoe-wt, Fas-homozygous mice at 5 months

immune system
• significantly enlarged compared to Apoe-null, Fas-heterozygous mice or Apoe-wt, Fas-homozygous mice at 5 months
• numbers of circulating cells are significantly reduced
• numbers of circulating cells are significantly reduced comparted to Apoe-wt, Fas-homozygous mice at 5 months
• serum levels of IgG are significantly higher than in Apoe-null and Apoe-null, Fas-heterozygous mice at 6 weeks and at 5 months
• serum antibodies against oxidized phospholipid (OxPL) are decreased compared to Apoe-wt, Fas-homozygous and Apoe-null, Fas-wt controls
• levels of IgG anti-cardiolipin antibodies are increased at 5 months relative to controls
• levels of IgG anti-POVPC and anti-PGPC autoantibodies are significantly higher than in controls at 5 months; IgM anti-POVPC levels are increased also
• serum levels of IgG anti-dsDNA antibodies are significantly higher than in Apoe-null, Fas-wt controls and Apoe-null, Fas-heterozygous mice at 6 weeks and at 5 months
• renal damage is observed, with IgG and C3 deposits present in the mesangium and peripheral capillary loops

renal/urinary system
• at 5 months, renal sections show an increase in apoptotic cells
• increased apoptotic cells are seen in renal tubules at 5 months
• proteinuria is increased compared to Fas-homozygous controls; proteinuria is not evident at 1 month of age
• renal damage is observed, with IgG and C3 deposits present in the mesangium and peripheral capillary loops
• proliferation of glomerular cells and lobule formation are observed
• IgG and C3 deposits present in the mesangium and peripheral capillary loops
• glomerular tuft areas are enlarged compared to controls

cardiovascular system
• IgG deposition in thickened aortic intimas is seen at 5 months, but is not observed in controls; neglible complement C3 deposition is observed in double homozygotes
• increased lesion area at aortic valves in mice on a normal chow diet compared to Apoe-null, Fas-wt controls
• increase in apoptotic cells in vessel walls of heart (in vascular lesions) is observed at 5 months relative to controls

skeleton
• all limbs of female mutants have lower bone mineral densities (BMD) than male mutants at 5 months of age; ostopenia is similar to Apoe-wt, Fas-null mice at 5 months
• femoral BMD is lower in females than controls at 5 months and 9 months; vertebrae BMD shows a similar trend at 5 months and is lower at 9 months
• at 5 months, vertebrae BMD trends to lower values than controls; at 9 months, BMD is significantly lower
• femoral BMD in females is lower than in Apoe-null, Fas-wt controls at 5 months and at 9 months
• at 9 months, a progressive decrease in trabecular bones (BV/TV, connectivity density, trabecular number, trabecular thickness) is observed in females compared to female Apoe-null, Fas-wt controls

homeostasis/metabolism
• total serum cholesterol and unesterified cholesterol levels are lower than Apoe-null, Fas-wt controls
• proteinuria is increased compared to Fas-homozygous controls; proteinuria is not evident at 1 month of age

cellular
• at 5 months, renal sections show an increase in apoptotic cells
• increased apoptotic cells are seen in renal tubules at 5 months

endocrine/exocrine glands




Genotype
MGI:7713059
cx40
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Phactr1tm1.2Gdo/Phactr1tm1.2Gdo
Genetic
Background
B6.Cg-Apoetm1Unc Phactr1tm1.2Gdo
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Phactr1tm1.2Gdo mutation (0 available); any Phactr1 mutation (43 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
N
• systolic blood pressure is normal and mice do not exhibit altered vascular function; isometric tension studies in isolated aortas show that vasoconstriction response to phenylephrine is normal, response to L-NAME is not altered, and endothelial cell-dependent relaxation to acetylcholine is not impacted and no difference is seen in the endothelial cell-independent dilation to sodium nitroprusside
• mice show a small, but significant, increase in heart rate compared to single mutant Apoe homozygotes




Genotype
MGI:4358191
cx41
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Pik3cgtm1Dwu/Pik3cgtm1Dwu
Genetic
Background
B6.Cg-Apoetm1Unc Pik3cgtm1Dwu
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Pik3cgtm1Dwu mutation (1 available); any Pik3cg mutation (59 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• atherosclerotic lesions are reduced 52% at 35 weeks, 32% at 53 weeks, and 36% at 60 weeks compared to in Apoetm1Unc homozygotes

homeostasis/metabolism
• total and non-HDL cholesterol after 60 weeks compared to in Apoetm1Unc homozygotes




Genotype
MGI:3810982
cx42
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Tg(CMV-Serpine1)1Dgi/0
Genetic
Background
B6.Cg-Apoetm1Unc Tg(CMV-Serpine1)1Dgi
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Tg(CMV-Serpine1)1Dgi mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• when fed a high fat Western diet for 6-30 weeks, mice develop atherosclerotic aortic lesions of the intimal and medial areas; incidence and severity are similar for Serpine1-deficient or transgenic Apoe-deficient genotypes
• lesions are somewhat larger than those observed on the Ldlr-deficient background
• cellular composition of lesions is similar among all Serpine1-deficient or transgenic, Apoe-deficient genotypes, or Apoe-deficient only mice; at early time points, a greater foam cell content is observed, with more prominent cholesterol clefts and necrotic areas evident with increasing age

homeostasis/metabolism
• mice develop severe cholesterolemia when receiving a high fat diet from 6 to 30 weeks (elevated levels are detected at 6, 15, and 30 weeks)




Genotype
MGI:5699095
cx43
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Tg(EIF1AX-Aldh2*E487K)101Oht/Tg(EIF1AX-Aldh2*E487K)101Oht
Genetic
Background
B6.Cg-Apoetm1Unc Tg(EIF1AX-Aldh2*E487K)101Oht
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Tg(EIF1AX-Aldh2*E487K)101Oht mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
• 6 month old mutants are unable to learn the Morris water maze task and the time spent in the target quadrant during probe trials is shorter than in either single mutant




Genotype
MGI:3784381
cx44
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Tg(GFAP-APOE_i3)37Hol/0
Genetic
Background
B6.Cg-Apoetm1Unc Tg(GFAP-APOE_i3)37Hol
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Tg(GFAP-APOE_i3)37Hol mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
• mice consume food slower in a new environment than Tg(GFAP-APOE_i4)#Hol Apoetm1Unc/Apoetm1Unc and wild-type mice
• mice require more time to habituate to a novel environment compared to wild-type mice
• mice are less reluctant than wild-type mice to move into an open area
• at 14 to 17 months of age, mice perform better than Tg(GFAP-APOE_i4)#Hol Apoetm1Unc/Apoetm1Unc and wild-type mice in a rotating holeboard test
• mice exhibit increased protected risk assessment behaviors in an elevated plus maze compared to wild-type mice
• compared to wild-type mice
• mice exhibit increased numbers of fine movement (not related to ambulation) compared to wild-type mice
• mice spend less time than wild-type mice in the center of an open field




Genotype
MGI:3784306
cx45
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Tg(GFAP-APOE_i4)22Hol/0
Genetic
Background
B6.Cg-Apoetm1Unc Tg(GFAP-APOE_i4)22Hol
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Tg(GFAP-APOE_i4)22Hol mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• in vitro, neuron outgrowth is slower than in Tg(GFAP-APOE_i3)37Hol Apoetm1Unc/Apoetm1Unc neurons
• in vitro, neurite length is shorter than in Tg(GFAP-APOE_i3)37Hol Apoetm1Unc/Apoetm1Unc neurons

cellular
• in vitro, neuron outgrowth is slower than in Tg(GFAP-APOE_i3)37Hol Apoetm1Unc/Apoetm1Unc neurons
• in vitro, neurite length is shorter than in Tg(GFAP-APOE_i3)37Hol Apoetm1Unc/Apoetm1Unc neurons




Genotype
MGI:3784380
cx46
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Tg(GFAP-APOE_i4)#Hol/0
Genetic
Background
B6.Cg-Apoetm1Unc Tg(GFAP-APOE_i4)#Hol
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Tg(GFAP-APOE_i4)#Hol mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
• mice require more time to habituate to a novel environment compared to wild-type mice
• at 14 to 17 months of age, mice did not perform as well as Apoetm1Unc homozygotes and Tg(GFAP-APOE_i3)37Hol Apoetm1Unc/Apoetm1Unc mice in a rotating holeboard test
• however, mice perform as well as wild-type mice in a rotating holeboard test
• mice exhibit an impairment in working memory in a radial arm maze test compared to wild-type mice
• compared to wild-type mice
• mice exhibit increased numbers of fine movement (not related to ambulation) compared to wild-type mice
• mice spend less time than wild-type mice and Apoetm1Unc homozygotes in the center of an open field




Genotype
MGI:5500052
cx47
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Arhgef26tm1.1Kbur/Arhgef26tm1.1Kbur
Genetic
Background
B6.Cg-Arhgef26tm1.1Kbur Apoetm1Unc
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Arhgef26tm1.1Kbur mutation (0 available); any Arhgef26 mutation (51 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• in the aortic arch descending thoracic aorta of mice fed a western diet compared with Apoetm1Unc homozygotes
• however, mice fed standard chow do not exhibit a significant difference




Genotype
MGI:4947400
cx48
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Crptm1Hjf/Crptm1Hjf
Genetic
Background
B6.Cg-Crptm1Hjf Apoetm1Unc
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Crptm1Hjf mutation (1 available); any Crp mutation (18 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• in female mice fed a low-fat, semi-synthetic diet at 16 weeks of age
• in female mice fed a low-fat, semi-synthetic diet at 16 weeks of age
• in female mice fed a low-fat, semi-synthetic diet at 12 weeks of age

cardiovascular system
• at 12 weeks of age, female mice fed a low-fat, semi-synthetic diet exhibit an increase in susceptibility to atherosclerosis in the aortic root compared with Apoetm1Unc homozygotes
• at 16 weeks of age, male mice fed a low-fat, semi-synthetic diet exhibit an increase in susceptibility to atherosclerosis in the aortic root compared with Apoetm1Unc homozygotes




Genotype
MGI:3815438
cx49
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Fabp4tm1Brsp/Fabp4tm1Brsp
Fabp5tm1Hota/Fabp5tm1Hota
Genetic
Background
B6.Cg-Fabp4tm1Brsp Fabp5tm1Hota Apoetm1Unc
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Fabp4tm1Brsp mutation (0 available); any Fabp4 mutation (44 available)
Fabp5tm1Hota mutation (0 available); any Fabp5 mutation (16 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
N
• mice fed a high fat diet exhibit a 100% survival rate at 1 year compared to a 33% survival for Apoetm1Unc homozygotes

homeostasis/metabolism
• fasting serum glucose levels are reduced 48% in female mice compared to Apoetm1Unc homozygotes
• however, serum glucose levels in male mice is the same as in controls
• fasting serum cholesterol levels are 18% lower in male mice and 29% lower in female mice compared to in Apoetm1Unc homozygotes
• however, serum cholesterol levels in female mice are the same as in controls
• fasting serum triglyceride levels are 32% lower in male mice and 42% lower in female mice compared to in Apoetm1Unc homozygotes
• however, serum triglyceride levels in female mice are the same as in controls
• compared to Apoetm1Unc homozygotes
• compared to Apoetm1Unc homozygotes

cardiovascular system
• male mice exhibit a 53% reduction in mean atherosclerotic lesion and a 45% reduction in mean lesion are of the en face aorta compared to Apoetm1Unc homozygotes
• female mice exhibit a 37% reduction in mean atherosclerotic lesion and a 37% reduction in mean lesion are of the en face aorta compared to Apoetm1Unc homozygotes
• when fed a high fat diet, male mice exhibit a 26% reduction in atherosclerosis of the proximal aorta with a 78% reduction in the en face aorta lesion compared to in Apoetm1Unc homozygotes

growth/size/body
• body weight of male mice is 10% lower than in Apoetm1Unc homozygotes
• however, female mice weigh the same as controls




Genotype
MGI:5514345
cx50
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Faslgld/Faslgld
Genetic
Background
B6.Cg-Faslgld Apoetm1Unc
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Faslgld mutation (7 available); any Fasl mutation (37 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• mutants on a Western diet for 12 weeks exhibit atherosclerotic lesions in the aorta (J:91058)
• aortae show higher levels of macrophage and T cell extravasation within lesions and higher levels of apoptotic cells within lesions than in single Apoe homozygotes (J:91058)
• treatment with mycophenolate mofetil decreases the severity of atherosclerosis seen in mice fed a Western diet (J:200141)
• lesion area of mutants fed a Western diet is greater than in single Apoe homozygotes, with a 3-fold increase in plaque area
• mutants on a normal diet exhibit larger atherosclerotic lesion area than single Apoe homozygotes
• aortae show macrophage and T cell extravasation within atherosclerotic lesions, showing a greater increase in macrophages and T cells than in single Apoe homozygotes

cellular
• mutants exhibit a 40% higher frequency of apoptotic material in the lymph nodes than single Fasl homozygotes
• higher levels of apoptotic cells are seen within atherosclerotic lesions than in single Apoe homozygotes
• clearance of apoptotic material by macrophages is reduced even further compared to single Fasl homozygotes when fed a Western diet

hematopoietic system
• clearance of apoptotic material by macrophages is reduced even further compared to single Fasl homozygotes when fed a Western diet
• on a Western and normal diet
• spleen weight is increased to almost double that seen in single Fasl homozygotes on a Western diet and 5-fold that seen in wild-type or single Apoe homozygotes (J:91058)
• treatment with mycophenolate mofetil, an immunosuppressive agent, reduces spleen weight (J:200141)
• total number of all T cell subsets is increased in the lymph nodes, however no differences in the percentages of CD4+, CD8+ or double negative T cells are seen
• IgG levels are elevated on both the normal and Western diet

homeostasis/metabolism
• decrease in high density lipoprotein levels compared to wild-type mice
• mutants become hypercholesterolemic on a Western diet but to a lesser extent than single Apoe homozygotes (J:91058)
• increase in low density lipoprotein (LDL) levels compared to wild-type mice
• increase in very low density lipoprotein (VLDL) levels compared to wild-type mice, however levels are lower than in single Apoe homozygotes
• mild increase in plasma triglyceride levels when fed a Western or normal diet

immune system
• aortae show macrophage and T cell extravasation within atherosclerotic lesions, showing a greater increase in macrophages and T cells than in single Apoe homozygotes
• clearance of apoptotic material by macrophages is reduced even further compared to single Fasl homozygotes when fed a Western diet
• on a Western and normal diet
• spleen weight is increased to almost double that seen in single Fasl homozygotes on a Western diet and 5-fold that seen in wild-type or single Apoe homozygotes (J:91058)
• treatment with mycophenolate mofetil, an immunosuppressive agent, reduces spleen weight (J:200141)
• total number of all T cell subsets is increased in the lymph nodes, however no differences in the percentages of CD4+, CD8+ or double negative T cells are seen
• IgG levels are elevated on both the normal and Western diet
• mutants exhibit a 40% higher frequency of apoptotic material in the lymph nodes than single Fasl homozygotes
• increase in lymph node size and weight both on the Western and normal diets; this increase is larger than in single Fasl homozygotes (J:91058)
• serum levels of anti-cardiolipin antibody are about 4-fold higher than in single Fasl homozygotes on both the normal and Western diets
• anti-nuclear antibody (ANA) titers are elevated compared to single Fasl homozygotes on a normal diet and further elevated by Western diet (J:91058)
• treatment with mycophenolate mofetil decreases the anti-nuclear antibody titer (J:200141)
• infiltration of inflammatory cells and modest crest formation

renal/urinary system
• infiltration of inflammatory cells and modest crest formation
• kidneys have larger, more cellular glomeruli (J:91058)
• treatment with mycophenolate mofetil decreases glomerular tuft size and cell count (J:200141)

growth/size/body
• on a Western and normal diet
• spleen weight is increased to almost double that seen in single Fasl homozygotes on a Western diet and 5-fold that seen in wild-type or single Apoe homozygotes (J:91058)
• treatment with mycophenolate mofetil, an immunosuppressive agent, reduces spleen weight (J:200141)




Genotype
MGI:3784303
cx51
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Tg(GFAP-APOE_i3)37Hol/0
Genetic
Background
B6.Cg-Tg(GFAP-APOE_i3)37Hol Apoetm1Unc/J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Tg(GFAP-APOE_i3)37Hol mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• in vitro, neuron outgrowth is faster than in Apoetm1Unc/Apoetm1Unc Tg(GFAP-APOE_i4)22Hol neurons
• in vitro, neurite length is longer than in Apoetm1Unc/Apoetm1Unc Tg(GFAP-APOE_i4)22Hol neurons
• however, neurite outgrowth rate is equivalent to in Apoetm1Unc/Apoetm1Unc Tg(GFAP-APOE_i4)22Hol neurons when neurons are treated with RAP or anti-LRP IgG
• the ratio of lipid to Apoe in HDL particles secreted from astrocytes is lower than in wild-type astrocytes but higher than in Apoetm1Unc homozygotes

cellular
• in vitro, neuron outgrowth is faster than in Apoetm1Unc/Apoetm1Unc Tg(GFAP-APOE_i4)22Hol neurons
• in vitro, neurite length is longer than in Apoetm1Unc/Apoetm1Unc Tg(GFAP-APOE_i4)22Hol neurons
• however, neurite outgrowth rate is equivalent to in Apoetm1Unc/Apoetm1Unc Tg(GFAP-APOE_i4)22Hol neurons when neurons are treated with RAP or anti-LRP IgG




Genotype
MGI:5699561
cx52
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Glg1Gt(RST092)Byg/Glg1+
Genetic
Background
B6J.129P2-Apoetm1Unc Glg1Gt(RST092)Byg
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Glg1Gt(RST092)Byg mutation (0 available); any Glg1 mutation (65 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
N
• mice exhibit no significant differences in right and left ventricular chamber thickness or in myocardial collagen deposition relative to Apoetm1Unc homozygotes
• after 9 weeks on a Western diet, mice exhibit atherosclerotic lesions with increased collagen deposition and fewer macrophages per mm2 of lesion relative to lesions from Apoetm1Unc homozygotes, as shown by collagen-specific (Sirius Red) and macrophage-specific (CD68) staining of aortic valves
• altered lesion composition suggests increased plaque stability; however, no differences in lesion area and thickness or in accumulation of smooth muscle cells are observed relative to Apoetm1Unc homozygotes

immune system
• after 9 weeks on a Western diet, mice exhibit a significantly reduced macrophage content in atherosclerotic lesions relative to Apoetm1Unc homozygotes
• mice exhibit a significantly reduced macrophage content and CD68 expression in liver tissue relative to Apoetm1Unc homozygotes

hematopoietic system
• after 9 weeks on a Western diet, mice exhibit a significantly reduced macrophage content in atherosclerotic lesions relative to Apoetm1Unc homozygotes
• mice exhibit a significantly reduced macrophage content and CD68 expression in liver tissue relative to Apoetm1Unc homozygotes

homeostasis/metabolism
• after 9 weeks on a Western diet, mice exhibit significantly increased collagen deposition in atherosclerotic lesions relative to Apoetm1Unc homozygotes

cellular
• after 9 weeks on a Western diet, mice exhibit a significantly reduced macrophage content in atherosclerotic lesions relative to Apoetm1Unc homozygotes




Genotype
MGI:2177115
cx53
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Msr1tm1Csk/Msr1tm1Csk
Genetic
Background
either: (involves: 129P2/OlaHsd * 129X1/SvJ * C57BL/6J * ICR) or (involves: 129P2/OlaHsd * 129X1/SvJ * 129/Sv * ICR)
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Msr1tm1Csk mutation (5 available); any Msr1 mutation (12 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• atherosclerotic plaques, but smaller than those seen in Apoetm1Unc mutant mice

homeostasis/metabolism
• increased plasma cholesterol concentrations
• plasma cholesterol concentrations greater than Apoetm1Unc mutant mice




Genotype
MGI:3790694
cx54
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Hptm1Alev/Hptm1Alev
Genetic
Background
involves: 129
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Hptm1Alev mutation (0 available); any Hp mutation (13 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• iron deposition in atherosclerotic lesions is almost two times greater than what is observed in mice that are homozygotes for just the Apoetm1Unc allele
• there is also increased amounts of oxidized lipids and proteins occurring in the plaques

immune system
• 50% more macrophages are found in atherosclerotic lesions than in mice that are homozygous for just the Apoetm1Unc allele

cellular
• 50% more macrophages are found in atherosclerotic lesions than in mice that are homozygous for just the Apoetm1Unc allele

hematopoietic system
• 50% more macrophages are found in atherosclerotic lesions than in mice that are homozygous for just the Apoetm1Unc allele




Genotype
MGI:4821395
cx55
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Egr1tm1Jmi/Egr1tm1Jmi
Genetic
Background
involves: 129 * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Egr1tm1Jmi mutation (1 available); any Egr1 mutation (21 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• 2.5 fold decrease in lesions at 14 weeks of age compared to Apoetm1Unc/tmiUnc
• 7 fold difference in lesion numbers at 24 weeks of age




Genotype
MGI:4354296
cx56
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Lpltm1Sem/Lpltm1Sem
Genetic
Background
involves: 129P2/OlaHsd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Lpltm1Sem mutation (0 available); any Lpl mutation (45 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• following carotid injury with ferric chloride, neointimal area is greater than in similarly treated Apoetm1Unc homozygotes
• however, the medial area of the healing blood vessel is normal
• following carotid injury with ferric chloride, the intima to media ratio is increased compared to in similarly treated Apoetm1Unc homozygotes
• following carotid injury with ferric chloride, neointimal hyperplasia induces more pronounced luminal stenosis than in similarly treated Apoetm1Unc homozygotes
• following carotid injury with ferric chloride, mice develop severe occlusive thrombi with complete degradation of the medial elastic fibers unlike in similarly treated Apoetm1Unc homozygotes
• unlike Apoetm1Unc homozygotes, mice fail to exhibit an increase in plasma triglyceride and cholesterol levels following carotid artery injury with ferric chloride and high cholesterol diet
• unlike Apoetm1Unc homozygotes, mice fail to exhibit an increase in plasma cholesterol levels following carotid artery injury with ferric chloride and high cholesterol diet
• pre-injury and at 12 weeks following aortic injury with ferric chloride, mice exhibit increased plasma cholesterol and non-HDL cholesterol levels compared with Apoetm1Unc homozygotes
• pre-injury and at 12 weeks following aortic injury with ferric chloride, mice exhibit increased plasma triglyceride levels compared with Apoetm1Unc homozygotes
• at 12 weeks following aortic injury with ferric chloride, mice exhibit severe combined hyperlipidemia compared with Apoetm1Unc homozygotes
• following carotid injury with ferric chloride, mice develop severe occlusive thrombi with complete degradation of the medial elastic fibers unlike in similarly treated Apoetm1Unc homozygotes

cardiovascular system
• following carotid injury with ferric chloride, neointimal area is greater than in similarly treated Apoetm1Unc homozygotes
• however, the medial area of the healing blood vessel is normal
• following carotid injury with ferric chloride, the intima to media ratio is increased compared to in similarly treated Apoetm1Unc homozygotes
• following carotid injury with ferric chloride, neointimal hyperplasia induces more pronounced luminal stenosis than in similarly treated Apoetm1Unc homozygotes
• following carotid injury with ferric chloride, mice develop severe occlusive thrombi with complete degradation of the medial elastic fibers unlike in similarly treated Apoetm1Unc homozygotes

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
familial combined hyperlipidemia DOID:13809 OMIM:144250
J:151434




Genotype
MGI:3721542
cx57
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Tg(APPV717F)109Ili/Tg(APPV717F)109Ili
Genetic
Background
involves: 129P2/OlaHsd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Tg(APPV717F)109Ili mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• by 12 months of age, mice have amyloid beta (Abeta) deposits in the hippocampus and cortex
• deposits are diffuse in appearance; deposition is prominent in dentate hilus, but little or none in molecular layer of dentate gyrus
• at 12 months, mice have high levels of insoluble Abeta42
• at 3 months, cerebrospinal fluid levels of Abeta40 are elevated
• at 3 months, cerebrospinal fluid levels of Abeta42 are elevated

homeostasis/metabolism
• by 12 months of age, mice have amyloid beta (Abeta) deposits in the hippocampus and cortex
• deposits are diffuse in appearance; deposition is prominent in dentate hilus, but little or none in molecular layer of dentate gyrus
• at 12 months, mice have high levels of insoluble Abeta42
• at 3 months, cerebrospinal fluid levels of Abeta40 are elevated
• at 3 months, cerebrospinal fluid levels of Abeta42 are elevated

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
Alzheimer's disease DOID:10652 J:107702




Genotype
MGI:4888254
cx58
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Cd36tm1Mfe/Cd36tm1Mfe
Genetic
Background
involves: 129P2/OlaHsd * 129S1/Sv * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Cd36tm1Mfe mutation (1 available); any Cd36 mutation (34 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• females with reduced triacyl glycerol on a high fat diet
• females with higher cholesterol levels on a normal fat diet
• more subcutaneous xanthomas than found when Apoetm1Unc is alone

cardiovascular system
• 76% reduction in atherosclerotic lesions in the aorta when on a high fat diet as compared to Apoetm1Unc
• area covered by lesions is 5% as compared to 30% in Apoetm1Unc homozygous males
• lesions 45% smaller in size in males and mostly restricted to the aortic arch rather than throughout the aortic tree
• female lesions closer in size to Apoetm1Unc controls
• smaller lesions on a low fat diet as well and also for females
• lesions composed of more densely packed lipid laden foam cells

growth/size/body
• gain significantly more weight on a high fat diet than Apoetm1Unc controls
• on a normal diet only males are significantly heavier than controls

immune system
• considerably less modified LDL is bound and cellular uptake is reduced
• native LDL binding is normal

cellular

hematopoietic system
• considerably less modified LDL is bound and cellular uptake is reduced
• native LDL binding is normal




Genotype
MGI:3721541
cx59
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Clutm1Jakh/Clutm1Jakh
Tg(APPV717F)109Ili/Tg(APPV717F)109Ili
Genetic
Background
involves: 129P2/OlaHsd * 129S2/SvPas
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Clutm1Jakh mutation (1 available); any Clu mutation (32 available)
Tg(APPV717F)109Ili mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• at 6 months of age, most mice have substantial amyloid beta (Abeta) deposits
• by 12 months of age, mice have more amyloid beta (Abeta) deposits in the hippocampus and cortex than other genotypes
• Abeta deposits are more numerous and fill all parts of hippocampus and some of the cortex by 12 months; abundant compact and diffuse plaques are observed
• mice have greater levels of thioflavine-S-positive (fibrillar) Abeta deposits than other genotypes, similar to transgenic homozygotes with normal Apoe and Clu
• at 3 months, cerebrospinal fluid levels of Abeta40 are elevated; Abeta40 increase is greater than in transgenic, single Apoe-null mice
• at 3 months, cerebrospinal fluid levels of Abeta42 are elevated

homeostasis/metabolism
• mice have significant amyloid burden, greater than shown by other genotypes
• at 12 months, mice have highest tissue levels of soluble Abeta40 and Abeta42, with high levels of insoluble Abeta42
• at 3 months, mice have higher levels of carbonate soluble Abeta40 and Abeta42 compared to other genotypes
• at 6 months of age, most mice have substantial amyloid beta (Abeta) deposits
• by 12 months of age, mice have more amyloid beta (Abeta) deposits in the hippocampus and cortex than other genotypes
• Abeta deposits are more numerous and fill all parts of hippocampus and some of the cortex by 12 months; abundant compact and diffuse plaques are observed
• mice have greater levels of thioflavine-S-positive (fibrillar) Abeta deposits than other genotypes, similar to transgenic homozygotes with normal Apoe and Clu
• at 3 months, cerebrospinal fluid levels of Abeta40 are elevated; Abeta40 increase is greater than in transgenic, single Apoe-null mice
• at 3 months, cerebrospinal fluid levels of Abeta42 are elevated

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
Alzheimer's disease DOID:10652 J:107702




Genotype
MGI:4438110
cx60
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Ncf1tm1Shl/Ncf1tm1Shl
Genetic
Background
involves: 129P2/OlaHsd * 129S2/SvPas
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Ncf1tm1Shl mutation (2 available); any Ncf1 mutation (38 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• development of atherosclerosis is considerably reduced 2 weeks after ligation of the left common carotid as compared to Apoetm1Unc
• atherosclerosis continues to be reduced 3 weeks after ligation of the left common carotid as compared to Apoetm1Unc but no longer significantly
• aneurysms reduced to 17% of animals rather than 40% as seen in Apoetm1Unc mice
• aneurisms reduced to 17% of animals rather than 90% as seen in Apoetm1Unc mice
• diameter and weight of aneurisms considerably reduced relative to Apoetm1Unc mice but still enlarged relative to controls
• angiotensin-II induced affect on blood pressure is blunted

immune system
• leukocyte infiltration into the adventitia of the aorta is attenuated




Genotype
MGI:5558016
cx61
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Scarb1tm1Kri/Scarb1tm1Kri
Genetic
Background
involves: 129P2/OlaHsd * 129S2/SvPas * BALB/c * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Scarb1tm1Kri mutation (2 available); any Scarb1 mutation (53 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Apoetm1Unc/Apoetm1Unc Scarb1tm1Kri/Scarb1tm1Kri mice develop occlusive, atherosclerotic coronary artery disease

mortality/aging
• median survival time of approximately 6 weeks

cardiovascular system
• in the coronary arteries
• coronary artery occlusion
• at 31 days of age small myocardial infarctions are seen and by 43 days of age extensive myocardial infarctions are present
• develop occlusive, atherosclerotic coronary artery disease after 21 days of age
• increase in the heart to body weight ratio in mice over 21 days of age

growth/size/body
• increase in the heart to body weight ratio in mice over 21 days of age




Genotype
MGI:4439279
cx62
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Itgb3tm1Hyn/Itgb3tm1Hyn
Genetic
Background
involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Itgb3tm1Hyn mutation (6 available); any Itgb3 mutation (45 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• at 16 weeks of age after 10 weeks on a western style diet only 52% of mice compared to 100% survival for diet matched Ldlr single mutants
• no increase in mortality is seen in mice kept on a standard chow diet
• at 12 weeks of age after 6 weeks on a western style diet, survival is reduced to 38% for mice compared to 96% for diet matched Apoe single mutants
• similar to that in Itgb3 single mutants
• only 62% survival to weaning for compared to 96% survival in mice null for Apoe alone

immune system
• isolated small foci of mononuclear cells are present in lung after 6 weeks of high-fat feeding
• in mice fed a high fat diet pneumonitis is the cause of death

respiratory system
• isolated small foci of mononuclear cells are present in lung after 6 weeks of high-fat feeding
• in mice fed a high fat diet pneumonitis is the cause of death

hematopoietic system
• western diet fed mice are anemic compared to diet matched mice null for Apoe alone

growth/size/body
• after 6 weeks on a western diet mice weighed less than diet matched Apoe single mutants

homeostasis/metabolism
• after 6 weeks on a western diet mice weighed less than diet matched Apoe single mutants

cardiovascular system
• on a western diet, lesions are 2.6 fold greater at the arch, 3.3 fold greater at the thoracic aorta, and 5.6-fold greater at the abdominal aorta compared to diet matched Apoe single mutants
• on chow diet at approximately 11 months of age, lesions are 2.4 fold greater at the arch, 3 fold greater at the thoracic aorta than in diet matched Apoe single mutants.




Genotype
MGI:3652962
cx63
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Fut4tm1Jbl/Fut4tm1Jbl
Fut7tm1Jbl/Fut7tm1Jbl
Genetic
Background
involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Fut4tm1Jbl mutation (1 available); any Fut4 mutation (7 available)
Fut7tm1Jbl mutation (1 available); any Fut7 mutation (15 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• decreased lesion size at 6 months of age




Genotype
MGI:3799448
cx64
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Scarb1tm1Kri/Scarb1tm1Kri
Genetic
Background
involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Scarb1tm1Kri mutation (2 available); any Scarb1 mutation (53 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
hematopoietic system
• abnormally large but with normal cellular hemoglobin levels
• non uniform cell populations
• target-like appearance
• intracellular inclusions
• mitochondria present
• often spiculated
• reticulocytes appear in the circulation
• a systemic process interferes with reticulocyte maturation




Genotype
MGI:3850552
cx65
Allelic
Composition
Apobec1tm1Chan/Apobec1tm1Chan
Apoetm1Unc/Apoetm1Unc
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apobec1tm1Chan mutation (0 available); any Apobec1 mutation (28 available)
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• circulating VLDL/LDL cholesterol levels are decreased compared to in Apoetm1Unc homozygotes
• circulating VLDL/LDL cholesterol levels are increased compared to in Apobec1tm1Chan homozygotes and wild-type mice
• when fed a chow, mice exhibit decreased total serum cholesterol compared with Apoetm1Unc homozygotes
• when fed a chow or a Western-type diet for 2 or 4 weeks, mice exhibit decreased total serum cholesterol compared with Apobec1tm1Chan homozygotes and wild-type mice
• when fed a chow diet or a Western-type diet for 2 or 4 weeks, serum triglyceride is higher than in wild-type mice
• when fed a Western-type diet for 2 or 4 weeks, mice exhibit increased serum triglyceride compared with Apobec1tm1Chan or Apoetm1Unc homozygotes
• when fed a Western-type diet for 10 weeks, mice exhibit increased serum triglyceride compared with Apoetm1Unc homozygotes




Genotype
MGI:5317889
cx66
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Ccr1tm1Gao/Ccr1tm1Gao
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Ccr1tm1Gao mutation (9 available); any Ccr1 mutation (40 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• increased plaque size on a high fat diet

immune system
• increased number of secreting cells




Genotype
MGI:4831159
cx67
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Ccr2tm1Ifc/Ccr2+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Ccr2tm1Ifc mutation (1 available); any Ccr2 mutation (43 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• atherosclerotic lesions in mice fed a high fat diet for 5 weeks are smaller than in similarly treated Apoetm1Unc homozygotes
• however, no difference was observed at later time points




Genotype
MGI:4831158
cx68
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Ccr2tm1Ifc/Ccr2tm1Ifc
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Ccr2tm1Ifc mutation (1 available); any Ccr2 mutation (43 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• in mice fed a high fat diet for 5, 9, and 13 weeks, atherosclerotic lesions are smaller than in similarly treated Apoetm1Unc homozygotes
• however, serum cholesterol levels are the same as in Apoetm1Unc homozygotes

immune system
• fewer macrophages in mice fed a high fat diet are present in the aorta compared to in similarly treated Apoetm1Unc homozygotes

cellular
• fewer macrophages in mice fed a high fat diet are present in the aorta compared to in similarly treated Apoetm1Unc homozygotes

hematopoietic system
• fewer macrophages in mice fed a high fat diet are present in the aorta compared to in similarly treated Apoetm1Unc homozygotes




Genotype
MGI:3652791
cx69
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Timp1tm1Pds/Y
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Timp1tm1Pds mutation (1 available); any Timp1 mutation (15 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• males fed an atherogenic, high-fat diet for 10 or 22 weeks develop a higher number of ruptures in the aortic media, in which all elastic laminae are digested and infiltrated with macrophages and form pseudo-microaneurysms, than single homozygous Apoetm1Unc mutant males




Genotype
MGI:3653653
cx70
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Ttpatm1Far/Ttpatm1Far
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Ttpatm1Far mutation (1 available); any Ttpa mutation (23 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Morphology of aortic lesions in Apoetm1Unc/Apoetm1Unc and Apoetm1Unc/Apoetm1Unc Ttpatm1Far/Ttpatm1Far mice

homeostasis/metabolism
• at 30 weeks of age, chow-fed double homozygous mutant females show no significant differences in total plasma cholesterol levels, HDL cholesterol levels or plasma ascorbate and urate levels relative to single Apoetm1Unc homozygotes
• however, double mutant females display a ~2-fold increase in total F2-isoprostane levels in the proximal and distal aorta, indicating that increased lipid peroxidation contributes to lesion development

cardiovascular system
• at 30 weeks of age, chow-fed double homozygous mutant females exhibit a ~36% increase in total aortic lesion area relative to single Apoetm1Unc homozygotes
• specifically, double mutant females have 42% and 53% larger aortic lesions in the aortic arch and thorax region, respectively, relative to single Apoetm1Unc homozygotes; no differences in lesion size in the abdominal aorta are observed
• double mutant aortic root lesions exhibit more complex features, including a large necrotic core, numerous needle-shaped lucencies indicative of cholesterol crystals, and fibrous capping from smooth muscle cells




Genotype
MGI:3653676
cx71
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Ttpatm1Far/Ttpa+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Ttpatm1Far mutation (1 available); any Ttpa mutation (23 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• chow-fed mice heterozygous for Ttpatm1Far and homozygous for Apoetm1Unc show a 24% reduction of plasma alpha-tocopherol levels relative to single Apoetm1Unc homozygotes

cardiovascular system
• at 30 weeks of age, chow-fed female mice heterozygous for Ttpatm1Far and homozygous for Apoetm1Unc have 13% larger atherosclerotic lesions in the aortic arch region relative to single Apoetm1Unc homozygotes




Genotype
MGI:5427502
cx72
Allelic
Composition
Apoetm1Unc/Apoetm3(APOE_i4)Yhg
Zbtb20Tg(PDGFB-APPSwInd)20Lms/0
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Apoetm3(APOE_i4)Yhg mutation (0 available); any Apoe mutation (158 available)
Zbtb20Tg(PDGFB-APPSwInd)20Lms mutation (1 available); any Zbtb20 mutation (58 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• aged mice exhibit reduced amyloid plaques compared to Apoetm3(APOE_i4)Yhg/Apoetm3(APOE_i4)Yhg Tg(PDGFB-APPSwInd)20Lms mice

homeostasis/metabolism
• aged mice exhibit reduced amyloid plaques compared to Apoetm3(APOE_i4)Yhg/Apoetm3(APOE_i4)Yhg Tg(PDGFB-APPSwInd)20Lms mice




Genotype
MGI:5427501
cx73
Allelic
Composition
Apoetm1Unc/Apoetm2(APOE_i3)Yhg
Zbtb20Tg(PDGFB-APPSwInd)20Lms/0
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Apoetm2(APOE_i3)Yhg mutation (0 available); any Apoe mutation (158 available)
Zbtb20Tg(PDGFB-APPSwInd)20Lms mutation (1 available); any Zbtb20 mutation (58 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• aged mice exhibit reduced amyloid plaques compared to Apoetm2(APOE_i3)Yhg/Apoetm2(APOE_i3)Yhg Tg(PDGFB-APPSwInd)20Lms mice

homeostasis/metabolism
• aged mice exhibit reduced amyloid plaques compared to Apoetm2(APOE_i3)Yhg/Apoetm2(APOE_i3)Yhg Tg(PDGFB-APPSwInd)20Lms mice




Genotype
MGI:3761832
cx74
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Soat1tm1Far/Soat1tm1Far
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Soat1tm1Far mutation (3 available); any Soat1 mutation (42 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Apoetm1Unc/Apoetm1Unc Soat1tm1Far/Soat1tm1Far mice display severe xanthomatosis

homeostasis/metabolism
• free cholesterol content of the skin is 6- to 7-fold higher than in single Apoe mutant controls at 4 months of age
• by 120 days of age, mean serum cholesterol levels are lower in double mutants than in single Apoe homozygotes fed a chow diet; disparity in cholesterol levels is more marked and occurs at an earlier age in mutants fed a Western diet
• reduced VLDL and IDL cholesterol compared to single Apoe homozygotes
• mutants fed a Western diet exhibit a massive cholesterol xanthoma by 3-4 months of age
• free cholesterol crystal deposits are seen in brains of mutants fed a Western diet for 3 months, mostly near the choroid plexus

cardiovascular system
• mutants fed a Western diet develop atherosclerotic lesions, however lesions are smaller than in single Apoe homozygotes
• aortic lesion composition differs from that in Apoe homozygotes, with lower neutral lipid content and fewer cholesterol crystals and a paucity of macrophages in the most advanced lesions

immune system
• cholesterol deposition in the skin is accompanied by a severe, pleomorphic inflammatory cell infiltrate with features of acute and chronic inflammation, including large numbers of neutrophils, multinucleated giant cells with occasional intracellular cholesterol clefts, and frequent mononuclear cells, lymphocytes, and plasma cells

nervous system
• free cholesterol crystal deposits are seen in brains of mutants fed a Western diet for 3 months, mostly near the choroid plexus

integument
• cholesterol deposition in the skin is accompanied by a severe, pleomorphic inflammatory cell infiltrate with features of acute and chronic inflammation, including large numbers of neutrophils, multinucleated giant cells with occasional intracellular cholesterol clefts, and frequent mononuclear cells, lymphocytes, and plasma cells
• by 2-3 months of age, fur appears dull and mutants show pruritus
• diffuse hair loss occurs by 5-6 months of age and leads to severe lesions
• free cholesterol content of the skin is 6- to 7-fold higher than in controls at 4 months of age
• mutants fed a Western diet exhibit more severe skin changes and at an earlier age (6 weeks) than wild-type or mutants fed a chow diet
• the dermis exhibits diffuse needle-shaped lucencies indicative of cholesterol crystals; crystals appear predominantly extracellularly and are seen in or below the reticular dermis
• deeper layers of the dermis show marked proliferation of fibroblasts and extensive collagen deposition
• hyperkeratosis at the skin surface
• develop severe skin lesions within months when fed a chow diet
• by 2-3 months of age, show pruritus
• by 5-6 months of age, excoriation occurs and leads to severe lesions




Genotype
MGI:3762636
cx75
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Soat2tm1Far/Soat2tm1Far
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Soat2tm1Far mutation (1 available); any Soat2 mutation (40 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• near absence of atherosclerotic lesions after 27 weeks on a CHOW diet
• near absence of atherosclerotic lesions after 9 weeks on a Western diet

homeostasis/metabolism
• 58% increase in serum HDL cholesterol levels compared to Apoetm1Unc/Apoetm1Unc control mice
• 60% reduction in total serum cholesterol compared to Apoetm1Unc/Apoetm1Unc control mice, primarily due to a reduction in plasma cholesterol esters
• plasma free cholesterol is reduced by 18% compared to Apoetm1Unc/Apoetm1Unc control mice
• 90% increase in total serum triglycerides compared to Apoetm1Unc/Apoetm1Unc control mice
• increase in the activity of the major enzyme responsible for synthesizing cholesterol esters in the plasma, lecithin/cholesterol acyltransferase




Genotype
MGI:3849583
cx76
Allelic
Composition
Angptl3tm1Lex/Angptl3tm1Lex
Apoetm1Unc/Apoetm1Unc
Genetic
Background
involves: 129P2/OlaHsd * 129S5/SvEvBrd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Angptl3tm1Lex mutation (2 available); any Angptl3 mutation (36 available)
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• serum cholesterol levels are 49% lower than in Apoe null homozygote controls
• serum triglyceride levels are 86% lower than in Apoe null homozygote controls




Genotype
MGI:6455724
cx77
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Cyp4f13Gt(OST14770)Lex/Cyp4f13Gt(OST14770)Lex
Genetic
Background
involves: 129P2/OlaHsd * 129S5/SvEvBrd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Cyp4f13Gt(OST14770)Lex mutation (1 available); any Cyp4f13 mutation (26 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• in bone marrow-derived macrophages to HDL acceptors
• however, efflux to ApoA1 is normal
• reduced total cholesterol and cholesterol esters in bone marrow-derived macrophages after AcLDL loading
• however, free cholesterol levels are normal

cardiovascular system
• smaller lesions with increased necrotic area in female and male mice fed a high-fat diet

hematopoietic system
• bone marrow-derived macrophages fail to exhibit an increase in migration in response to LTB4 unlike wild-type cells

cellular
• bone marrow-derived macrophages fail to exhibit an increase in migration in response to LTB4 unlike wild-type cells
• in bone marrow-derived macrophages to HDL acceptors
• however, efflux to ApoA1 is normal

immune system
• bone marrow-derived macrophages fail to exhibit an increase in migration in response to LTB4 unlike wild-type cells




Genotype
MGI:6455725
cx78
Allelic
Composition
Apoetm1Unc/Apoe+
Cyp4f13Gt(OST14770)Lex/Cyp4f13Gt(OST14770)Lex
Genetic
Background
involves: 129P2/OlaHsd * 129S5/SvEvBrd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Cyp4f13Gt(OST14770)Lex mutation (1 available); any Cyp4f13 mutation (26 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• smaller lesions in female and male mice fed a high-fat diet




Genotype
MGI:4367614
cx79
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Mmp9tm1Tvu/Mmp9tm1Tvu
Genetic
Background
involves: 129P2/OlaHsd * 129S6/SvEvTac
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Mmp9tm1Tvu mutation (2 available); any Mmp9 mutation (50 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• following temporary ligation, mice develop intimal atherosclerotic plaques with reduced volume, length, smooth muscle cells, and intraplaque foam cells and macrophages compared with similarly treated Apoetm1Unc homozygotes
• following temporary ligation, fewer smooth muscle cells are found in atherosclerotic plaques compared to in similarly treated Apoetm1Unc homozygotes

immune system
• following temporary ligation, fewer foam cells and macrophages are found in atherosclerotic plaques compared to in similarly treated Apoetm1Unc homozygotes

muscle
• following temporary ligation, fewer smooth muscle cells are found in atherosclerotic plaques compared to in similarly treated Apoetm1Unc homozygotes

hematopoietic system
• following temporary ligation, fewer foam cells and macrophages are found in atherosclerotic plaques compared to in similarly treated Apoetm1Unc homozygotes




Genotype
MGI:4361697
cx80
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Spp1tm1Blh/Spp1+
Genetic
Background
involves: 129P2/OlaHsd * 129S6/SvEvTac * Black Swiss * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Spp1tm1Blh mutation (2 available); any Spp1 mutation (43 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• Angiotensin II-induced atherosclerotic lesions exhibit reduced lesion area compared to in similarly treated Apoetm1Unc homozygotes




Genotype
MGI:4361696
cx81
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Spp1tm1Blh/Spp1tm1Blh
Genetic
Background
involves: 129P2/OlaHsd * 129S6/SvEvTac * Black Swiss * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Spp1tm1Blh mutation (2 available); any Spp1 mutation (43 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• Angiotensin II-induced atherosclerotic lesions exhibit reduced medial inflammation, lesion area, cellularity, macrophage viability, and foam cells compared to in similarly treated Apoetm1Unc homozygotes
• however, untreated aged male mice exhibit normal atherosclerotic lesion development
• Angiotensin II-treated mice exhibit reduced abdominal aortic aneurysm incidence and diameter compared with similarly treated Apoetm1Unc homozygotes

immune system
• macrophage viability in Angiotensin II-treated mice is lower than in similarly treated Apoetm1Unc homozygotes

hematopoietic system
• macrophage viability in Angiotensin II-treated mice is lower than in similarly treated Apoetm1Unc homozygotes




Genotype
MGI:5428435
cx82
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Cyp19a1tm1Esi/Cyp19a1tm1Esi
Genetic
Background
involves: 129P2/OlaHsd * 129S6/SvEvTac * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Cyp19a1tm1Esi mutation (1 available); any Cyp19a1 mutation (39 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
growth/size/body
• increased body weight at 3, 6, and 12 months of age
• increase in liver weight at 3 and 6 months of age

cardiovascular system
• 3 month old mutants exhibit small aortic root lesions that are extensive at 6 months of age
• double mutants tend to have slightly larger lesion sizes than single Apoe mutants
• mutants develop large atherosclerotic lesions in the aortic root by 12 months of age; lesions are advanced in development and show a clear fibrous component
• however there is little evidence of atherosclerotic plaque formation within the thoracic aorta with only small lesion development seen in the thoracic aorta at 12 months of age
• mutants have moderately increased mean arterial blood pressure at 3 months of age
• mutants develop hypertension by 6 months of age which is sustained in older animals

adipose tissue
• mutants exhibit an increase in adipocyte size with a larger mean diameter compared to wild-type adipocytes, however no difference in the number of individual adipocytes
• increase in gonadal adipose

homeostasis/metabolism
• 3 month old mutants show a small elevation in baseline blood glucose concentration after an overnight fast
• mutants of all ages show reduced plasma insulin levels
• random-fed non-fasting mutants show an increase in serum cholesterol levels
• plasma levels of C-reactive protrein (CRP) are increased in 12 month old mutants
• plasma levels of IL-6 are increased in 12 month old mutants
• plasma levels of TNF-alpha are increased in 12 month old mutants
• mutants administered a bolus of glucose show elevated plasma glucose
• 3 month old mutants show a blunted plasma glucose response in response to exogenous insulin administration; this blunted response becomes more pronounced with age

immune system
• plasma levels of C-reactive protrein (CRP) are increased in 12 month old mutants
• plasma levels of IL-6 are increased in 12 month old mutants
• plasma levels of TNF-alpha are increased in 12 month old mutants

liver/biliary system
• from 6 months of age, livers begin to show yellow coloration
• increase in liver weight at 3 and 6 months of age
• 3 month old mutants start to show small lipid droplets forming within livers which become more pronounced at 6 and 12 months of age

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
abdominal obesity-metabolic syndrome DOID:0060611 OMIM:PS605552
J:184647




Genotype
MGI:3785086
cx83
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Lipgtm1Tq/Lipgtm1Tq
Genetic
Background
involves: 129P2/OlaHsd * 129S6/SvEvTac * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Lipgtm1Tq mutation (1 available); any Lipg mutation (29 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• when fed a high fat diet, male mice exhibit a 2-fold increase in serum cholesterol compared to in either single homozygote on either a normal or high fat diet
• compared to in Apoetm1Unc homozygotes
• compared to in wild-type mice
• compared to in wild-type mice
• in male mice on a high fat diet

cardiovascular system
• formation of atherosclerotic plaques is attenuated compared to in Apoetm1Unc homozygotes
• when fed a normal diet, atherosclerotic lesions are 67% smaller in females and 71% smaller in males compared to in Apoetm1Unc homozygotes
• when fed a high fat diet, atherosclerotic lesion formation is attenuated in male mice and lesion size is decreased 24% compared to in Apoetm1Unc homozygotes
• atherosclerotic lesions contain fewer macrophage infiltration than in Apoetm1Unc homozygotes
• monocyte/macrophage binding to atherosclerotic lesions in vitro is reduced compared to in Apoetm1Unc homozygotes




Genotype
MGI:5451045
cx84
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Dp(17Nfkbil1-Or2h1)1Cogr/0
Genetic
Background
involves: 129P2/OlaHsd * 129S6/SvEvTac * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Dp(17Nfkbil1-Or2h1)1Cogr mutation (1 available); any Dp(17Nfkbil1-Or2h1)1Cogr mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Decreased susceptibility to atherosclerosis in Apoetm1Unc/Apoetm1Unc Dp(17Nfkbil1-Or2h1)1Cogr/0 mice

cardiovascular system
• mice fed a high fat diet develop smaller plaques than in Apoetm1Unc homozygotes

homeostasis/metabolism
N
• mice fed a high fat diet exhibit the same cholesterol and glucose serum levels and glucose tolerance as Apoetm1Unc homozygotes




Genotype
MGI:4367224
cx85
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Ldlrtm1Her/Ldlrtm1Her
Genetic
Background
involves: 129P2/OlaHsd * 129S7/SvEvBrd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Ldlrtm1Her mutation (19 available); any Ldlr mutation (81 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• plasma cholesterol on a high fat diet reaches 4120 mg/dl
• triglyceride levels are unaffected by diet




Genotype
MGI:5819053
cx86
Allelic
Composition
Apobtm2Sgy/Apobtm2Sgy
Apoetm1Unc/Apoetm1Unc
Lepob/Lepob
Genetic
Background
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apobtm2Sgy mutation (4 available); any Apob mutation (224 available)
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Lepob mutation (5 available); any Lep mutation (21 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• at 12 weeks of age, atherosclerotic lesions are seen mainly in the aortic region of the whole aorta
• leptin treatment, but not food restriction, results in lower atherosclerotic lesion size
• elevated blood pressure
• treatment with enalapril corrects the elevated blood pressure

growth/size/body
• increase in body weight, with mice weighing about 63 grams at 15-16 weeks of age

homeostasis/metabolism
• mice are hyperglycemic and glycemic control fluctuates with age
• mice show improved in blood glucose with food restriction but not with leptin treatment
• increase in blood insulin levels
• neither food restriction or leptin treatment has an effect on insulin level
• mice have higher VLDL levels than LDL, with lower HDL levels compared to wild-type mice which have HDL as the dominant lipoprotein species and very low levels of LDL and VLDL
• mice have lower HDL levels
• cholesterol levels are elevated almost 10-fold compared to wild-type mice
• both leptin treatment and food restriction result in 52.6% and nonsignificant 18.5% reduction, respectively, of cholesterol levels
• mice have higher VLDL levels than LDL levels
• plasma triglyceride levels are 4-fold higher at 15-16 weeks of age than in wild-type mice
• neither food restriction or leptin treatment has an effect on plasma triglyceride levels
• glucose intolerance is evident at 7-8 weeks of age and sustained until 15-16 weeks

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
abdominal obesity-metabolic syndrome 1 DOID:14221 OMIM:605552
J:133453




Genotype
MGI:3582202
cx87
Allelic
Composition
Soat1tm1Ishi/Soat1tm1Ishi
Apoetm1Unc/Apoetm1Unc
Genetic
Background
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Soat1tm1Ishi mutation (0 available); any Soat1 mutation (42 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Cutaneous xanthomatosis and alopecia in Soat1tm1Ishi/Soat1tm1Ishi Apoetm1Unc/Apoetm1Unc and Soat1tm1Ishi/Soat1tm1Ishi Ldlrtm1Her/Ldlrtm1Her mice

vision/eye

homeostasis/metabolism
• adrenocortical lipid depletion
• increased serum cholesterol levels
• hypercholesterolemia when fed a high fat diet
• cutaneous xanthomatosis

integument
• macrophage infiltration of dermis
• rough skin

endocrine/exocrine glands




Genotype
MGI:3710350
cx88
Allelic
Composition
Apobec1tm1Ishi/Apobec1tm1Ishi
Apoetm1Unc/Apoetm1Unc
Genetic
Background
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apobec1tm1Ishi mutation (0 available); any Apobec1 mutation (28 available)
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• plasma cholesterol levels are lower (436.5+/-59.2mg/dl) than in Apoetm1Unc homozygotes (621.5+/-126.7mg/dl)
• plasma levels of triglycerides are greater (238.0+/-113.3%) than in the Apoetm1Unc homozygote (98.1+/-91.1%)




Genotype
MGI:4361863
cx89
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Spp1tm1Rit/Spp1tm1Rit
Genetic
Background
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Spp1tm1Rit mutation (6 available); any Spp1 mutation (43 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• atherosclerotic lesions in female mice are 34% smaller than in Apoetm1Unc homozygotes
• male mice exhibit increased vascular calcification of aortic root sections compared to in Apoetm1Unc homozygotes

homeostasis/metabolism
• total circulating cholesterol and non-HDL-cholesterol levels are increased 1.5-fold in male mice compared to in Apoetm1Unc homozygotes
• plasma triglyceride levels are increased 4-fold in male mice compared to in Apoetm1Unc homozygotes




Genotype
MGI:4361864
cx90
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Spp1tm1Rit/Spp1+
Genetic
Background
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Spp1tm1Rit mutation (6 available); any Spp1 mutation (43 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• atherosclerotic lesions in female mice are 43% smaller than in Apoetm1Unc homozygotes with reduced aortic wall inflammation

homeostasis/metabolism
• total circulating cholesterol and non-HDL-cholesterol levels are increased in male mice compared to in Apoetm1Unc homozygotes
• in male mice compared to in Apoetm1Unc homozygotes




Genotype
MGI:4837860
cx91
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Nos2tm1Mrl/Nos2tm1Mrl
Genetic
Background
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Nos2tm1Mrl mutation (5 available); any Nos2 mutation (67 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
N
• no effect on plasma cholesterol, triglycderide, or nitrate levels when compared to Apoetm1Unc controls on any diet tested
• total cholesterol in the aorta is reduced 40% in males and 50% in females
• free cholesterol in the aorta is reduced 40% in males and 50% in females
• cholesterol ester in the aorta is reduced 57% in males and 72% in females

growth/size/body
• females are slightly heavier than controls
• no weight effect in males

cardiovascular system
• lesions are smaller and flatter
• male lesions are 50% smaller
• female lesions are 30% smaller




Genotype
MGI:5882610
cx92
Allelic
Composition
Apobtm1Sgy/Apobtm1Sgy
Apoetm1Unc/Apoetm1Unc
Genetic
Background
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apobtm1Sgy mutation (2 available); any Apob mutation (224 available)
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• mice exhibit more atherosclerotic lesions in aortas than single Apoetm1Unc homozygotes
• mice exhibit atherosclerotic lesions in the aortic root to a similar extent as in single Apoetm1Unc homozygotes
• most lesions are located in the aortic arch, although some lesions extend into the thoracic and abdominal aortas
• extent of atherosclerosis correlates with plasma cholesterol levels

growth/size/body
• mice are heavier than single Apoetm1Unc homozygotes at 200 days of age

homeostasis/metabolism
• total cholesterol levels are higher than in single Apoetm1Unc homozygotes at 7 weeks, 3 and 6 months, and 200 days
• plasma cholesterol levels increase significantly with time
• very high levels of VLDL cholesterol
• triglyceride levels are higher than in single Apoetm1Unc homozygotes




Genotype
MGI:5882611
cx93
Allelic
Composition
Apobtm2Sgy/Apobtm2Sgy
Apoetm1Unc/Apoetm1Unc
Genetic
Background
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apobtm2Sgy mutation (4 available); any Apob mutation (224 available)
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• mice exhibit fewer atherosclerotic lesions in aortas and smaller lesions in the aortic root than single Apoetm1Unc homozygotes
• extent of atherosclerosis correlates with plasma cholesterol levels

growth/size/body
• mice are slightly, but significantly lighter than single Apoetm1Unc homozygotes at 200 days of age

homeostasis/metabolism
• triglyceride levels are higher than in single Apoetm1Unc homozygotes
• the VLDL is more enriched in triglyceride than the VLDL from double Apobtm1Sgy Apoetm1Unc homozygotes
• mean size of VLDL is larger than that of the VLDL from single Apoetm1Unc homozygotes or double Apobtm1Sgy Apoetm1Unc homozygotes
• the IDL and LDL particles are larger than that from single Apoetm1Unc homozygotes or double Apobtm1Sgy Apoetm1Unc homozygotes
• HDL cholesterol levels at 200 days of age are slightly, but significantly, higher than in single Apoetm1Unc homozygotes or double Apobtm1Sgy Apoetm1Unc homozygotes
• very high levels of VLDL cholesterol
• total cholesterol levels are lower at 7 weeks, 3 and 6 months, and 200 days of age compared to single Apoetm1Unc homozygotes or double Apobtm1Sgy Apoetm1Unc homozygotes
• plasma cholesterol levels decrease with time




Genotype
MGI:3789482
cx94
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Ldlrtm1Her/Ldlrtm1Her
Genetic
Background
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Ldlrtm1Her mutation (19 available); any Ldlr mutation (81 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• two out of 8 hypoxic hearts show thrombosis as well as atherosclerotic plaques
• elevated STU segment as a result of induced hypoxia
• noticeable at 16% oxygen concentration
• ECG is corrected by 10 minutes after restoration of normal oxygen
• hypoxia response unaffected by treatment with a thrombin inhibitor
• mice treated with a thrombin inhibitor display lower Troponin-T levels and fewer fibrinogen + cells than untreated mice 48 hours after hypoxia
• in mice treated with a thrombin inhibitor 48 hours after hypoxia
• infarctions are irregular in shape and subendocardial or intramural

homeostasis/metabolism
• mice treated with a thrombin inhibitor display lower Troponin-T levels and fewer fibrinogen + cells than untreated mice 48 hours after hypoxia
• in mice treated with a thrombin inhibitor 48 hours after hypoxia
• infarctions are irregular in shape and subendocardial or intramural
• mice treated with a thrombin inhibitor display lower Troponin-T levels and fewer fibrinogen + cells than untreated mice 48 hours after hypoxia

nervous system
• elevated cholesterol in the exofacial leaflet of the synaptic plasma membrane but not so high as for Ldlr deficient mice with normal Apoe alleles
• cholesterol levels in the cytofacial leaflet are reduced
• cholesterol/phospholipid ratio in the synaptic plasma membrane is elevated but not so much as for Ldlr deficient mice with normal Apoe alleles




Genotype
MGI:3789200
cx95
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Rag2tm1Fwa/Rag2+
Genetic
Background
involves: 129P2/OlaHsd * 129S/SvEv
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Rag2tm1Fwa mutation (45 available); any Rag2 mutation (119 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
growth/size/body
• body weight of mice treated with estradiol is reduced relative to that of untreated controls

reproductive system
• in response to estradiol treatment

homeostasis/metabolism
• reduced total cholesterol in response to estradiol treatment
• in response to estradiol treatment

cardiovascular system
• decreased fatty streak lesions in the aortic root in response to estradiol treatment




Genotype
MGI:3789198
cx96
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Rag2tm1Fwa/Rag2tm1Fwa
Genetic
Background
involves: 129P2/OlaHsd * 129S/SvEv
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Rag2tm1Fwa mutation (45 available); any Rag2 mutation (119 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
growth/size/body
• body weight of mice treated with estradiol is reduced relative to that of untreated controls

reproductive system
• in response to estradiol treatment

homeostasis/metabolism
• reduced total cholesterol in response to estradiol treatment
• in response to estradiol treatment

cardiovascular system
• increased fatty streak lesions in the aortic root in response to estradiol treatment




Genotype
MGI:3789134
cx97
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Il1rntm1Dih/Il1rntm1Dih
Genetic
Background
involves: 129P2/OlaHsd * 129S/SvEv * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Il1rntm1Dih mutation (1 available); any Il1rn mutation (24 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• increased death rate on a high cholesterol diet

homeostasis/metabolism
• significantly reduced plasma cholesterol levels relative to Apoetm1Unc homozygous controls on a normal diet

growth/size/body
• relative to singly homozyous Apoetm1Unc

immune system
• massive infiltration of macrophage in the aortic arch

cardiovascular system
N
• no intimal thickening occurs on a high cholesterol diet
• elastic lamina in the media of the aortic root is destroyed
• elastic lamina in the media of the coronary arteries is destroyed

cellular
• massive infiltration of macrophage in the aortic arch

hematopoietic system
• massive infiltration of macrophage in the aortic arch




Genotype
MGI:5776478
cx98
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Sprr3tm1.1Ppy/Sprr3tm1.1Ppy
Genetic
Background
involves: 129P2/OlaHsd * 129S/SvEv * C57BL/6J * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Sprr3tm1.1Ppy mutation (1 available); any Sprr3 mutation (16 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
N
• endothelial cell survival and proliferation are normal
• 3-fold increase in lesion area in mice fed either normal chow or a high-fat diet compared to in Apoetm1Unc homozygotes
• increased susceptibility is not attributable to bone-marrow derived cells as determined by transplant experiments
• reduced lesion vascular smooth muscle cell (VSMC) content due to apoptosis whether fed standard chow or a high-fat diet compared with control mice
• however, disease-free arteries exhibit normal VSMC content
• reduced lesion vascular smooth muscle cell (VSMC) content due to apoptosis whether fed standard chow or a high-fat diet compared with control mice
• vascular smooth muscle cells exhibit increased cellular sensitivity to hydrogen peroxide compared with control cells
• however, disease-free arteries exhibit normal VSMC apoptosis rates

cellular
• in vascular smooth muscle cells

muscle
• reduced lesion vascular smooth muscle cell (VSMC) content due to apoptosis whether fed standard chow or a high-fat diet compared with control mice
• however, disease-free arteries exhibit normal VSMC content
• reduced lesion vascular smooth muscle cell (VSMC) content due to apoptosis whether fed standard chow or a high-fat diet compared with control mice
• vascular smooth muscle cells exhibit increased cellular sensitivity to hydrogen peroxide compared with control cells
• however, disease-free arteries exhibit normal VSMC apoptosis rates




Genotype
MGI:5552968
cx99
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Klf15tm1Jain/Klf15tm1Jain
Genetic
Background
involves: 129P2/OlaHsd * 129X1/SvJ
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Klf15tm1Jain mutation (0 available); any Klf15 mutation (19 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• in mice fed a high fat diet compared with Apoetm1Unc homozygotes

homeostasis/metabolism
• in mice fed a high fat diet compared with Apoetm1Unc homozygotes
• in mice fed a high fat diet compared with Apoetm1Unc homozygotes

cardiovascular system
• greater plaque size in mice fed a high fat diet or standard chow compared with Apoetm1Unc homozygotes




Genotype
MGI:2654938
cx100
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Pon1tm1Lus/Pon1tm1Lus
Genetic
Background
involves: 129P2/OlaHsd * 129X1/SvJ * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Pon1tm1Lus mutation (1 available); any Pon1 mutation (25 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• 42% increase in atherosclerotic lesion area on a chow diet compared to single Apoe homozygotes at 4 months of age

cellular
• increased oxidative stress in serum and peritoneal and arterial macrophages
• 71% increase increase in peroxides content in arterial macrophages and 80% increase in peritoneal macrophages, decrease in glutathione content, and 19% decrease in the capacity of peritoneal macrophages to oxidize LDL




Genotype
MGI:3785902
cx101
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Npc1m1N/Npc1m1N
Genetic
Background
involves: 129P2/OlaHsd * BALB/c
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Npc1m1N mutation (3 available); any Npc1 mutation (74 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism




Genotype
MGI:5796685
cx102
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Cbstm1Unc/Cbstm1Unc
Tg(Mt1-CBS)25Waku/0
Genetic
Background
involves: 129P2/OlaHsd * C3H * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Cbstm1Unc mutation (3 available); any Cbs mutation (43 available)
Tg(Mt1-CBS)25Waku mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• zinc-induced mice fed a high-fat diet exhibit increased atherosclerotic lesions compared to controls
• zinc-induced mice fed a high-fat diet exhibit enhanced Ly-6C monocyte/macrophage accumulation in atherosclerotic lesions

growth/size/body
• zinc-induced mice fed a high fat diet develop severe hyperhomocysteinemia associated with a 15.6% reduction in body weight

hematopoietic system
• increase in monocyte population in blood, spleen, and bone marrow of 15 months old zinc-induced mice fed a regular diet
• zinc-induced mice fed a regular diet with severe hyperhomocysteinemia exhibit elevated CD11b+Ly-6Chi and CD11b+Ly-6Cmid inflammatory monocyte subsets

homeostasis/metabolism
• plasma homocysteine levels are increased in zinc-induced mutants fed a regular or a high-fat diet
• plasma methionine levels are increased in zinc-induced mutants fed a regular diet
• however, methionine levels are normal in zinc-induced mutants fed a high-fat diet
• high-fat diet fed zinc-induced mice show increased plasma levels of the proinflammatory cytokine TNF-alpha and the chemotactic factor MCP-1

immune system
• increase in monocyte population in blood, spleen, and bone marrow of 15 months old zinc-induced mice fed a regular diet
• zinc-induced mice fed a regular diet with severe hyperhomocysteinemia exhibit elevated CD11b+Ly-6Chi and CD11b+Ly-6Cmid inflammatory monocyte subsets
• high-fat diet fed zinc-induced mice show increased plasma levels of the proinflammatory cytokine TNF-alpha and the chemotactic factor MCP-1

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
homocystinuria DOID:9263 OMIM:236200
OMIM:236250
J:168131




Genotype
MGI:3836254
cx103
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Csf1op/Csf1op
Genetic
Background
involves: 129P2/OlaHsd * C3HeB/Fe * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Csf1op mutation (1 available); any Csf1 mutation (48 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• mice are almost entirely free of fatty lesions in the aortic root compared to the 75% of atherosclerotic lesions in mice homozygote null for just the Apoe gene

homeostasis/metabolism
• total cholesterol levels are extremely high with a mean of 1056 mg/dl compared to 112 mg/dl for controls or 379 mg/dl mice for Apoe null mice




Genotype
MGI:3766466
cx104
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Ath29C57BL/6J/?
Genetic
Background
involves: 129P2/OlaHsd * C3H/HeJ * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Ath29C57BL/6J mutation (0 available); any Ath29 mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• increased aortic lesion size in CHOW-fed female animals




Genotype
MGI:5473362
cx105
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Ptgdrtm1Dgen/Ptgdrtm1Dgen
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Ptgdrtm1Dgen mutation (0 available); any Ptgdr mutation (29 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• in 1 of 2 studies of mice fed a high fat diet
• modest in the aorta at 16 and 24, but not 32, weeks in mice fed a high fat diet
• in some mice fed a high fat diet




Genotype
MGI:5317846
cx106
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Ccr5tm1Blck/Ccr5tm1Blck
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Ccr5tm1Blck mutation (7 available); any Ccr5 mutation (31 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• reduced plaque areas after 10-12 weeks on a high fat or high cholesterol diet
• both in the aortic root and the thoracoabdominal artery
• also at 22 weeks when fed a normal diet

immune system
• in atherosclerotic plaques reduced 24% compared to Apoetm1Unc
• monocyte/macrophage in atherosclerotic plaques reduced 77% compared to Apoetm1Unc
• reduced proliferative responses of splenocytes and of lymph node cells by 25% compared to Apoetm1Unc
• significantly decreased secretion by splenocytes
• increased content in atherosclerotic plaques
• increased secretion by both splenocytes and by lymph node cells

hematopoietic system
• in atherosclerotic plaques reduced 24% compared to Apoetm1Unc
• monocyte/macrophage in atherosclerotic plaques reduced 77% compared to Apoetm1Unc
• reduced proliferative responses of splenocytes and of lymph node cells by 25% compared to Apoetm1Unc




Genotype
MGI:5317842
cx107
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Ccr5tm1Kuz/Ccr5tm1Kuz
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Ccr5tm1Kuz mutation (2 available); any Ccr5 mutation (31 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• reduced plaque areas after 10-12 weeks on a high fat or high cholesterol diet
• both in the aortic root and the thoracoabdominal artery
• also at 22 weeks when fed a normal diet
• increased smooth muscle content in atherosclerotic plaques

immune system
• in atherosclerotic plaques reduced 24% compared to Apoetm1Unc
• monocyte/macrophage in atherosclerotic plaques reduced 77% compared to Apoetm1Unc
• reduced proliferative responses of splenocytes and of lymph node cells by 25% compared to Apoetm1Unc
• significantly decreased secretion by splenocytes
• increased content in atherosclerotic plaques
• increased secretion by both splenocytes and by lymph node cells

muscle
• increased smooth muscle content in atherosclerotic plaques

hematopoietic system
• in atherosclerotic plaques reduced 24% compared to Apoetm1Unc
• monocyte/macrophage in atherosclerotic plaques reduced 77% compared to Apoetm1Unc
• reduced proliferative responses of splenocytes and of lymph node cells by 25% compared to Apoetm1Unc




Genotype
MGI:7516347
cx108
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Svep1em1Nost/Svep1em1Nost
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Svep1em1Nost mutation (0 available); any Svep1 mutation (169 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
N
• normal development of atherosclerotic plaque after 8 and 16 weeks of HFD feeding

growth/size/body
N
• normal body weight after 8 and 16 weeks of HFD feeding

homeostasis/metabolism
N
• normal serum total cholesterol, triglycerides and glucose levels after 8 and 16 weeks of HFD feeding




Genotype
MGI:3588777
cx109
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Tlr4tm1Aki/Tlr4tm1Aki
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Tlr4tm1Aki mutation (7 available); any Tlr4 mutation (91 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• 24% reduction in atherosclerotic lesions relative to mice homozygous only for Apoetm1Unc
• reduced lipid content of aortic sinus plaques
• reduced infiltration of plaques by macrophage




Genotype
MGI:3784391
cx110
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Tg(Eno2-APP*751)10Cord/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Tg(Eno2-APP*751)10Cord mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• compared to in Apoetm1Unc homozygotes, Tg(Eno2-APP*751)10Cord Tg(GFAP-APOE_i4)1Hol Apoetm1Unc/Apoetm1Unc mice and Tg(Eno2-APP*751)10Cord Tg(GFAP-APOE*4)1Hol Apoetm1Unc/Apoetm1Unc

nervous system
• compared to in Apoetm1Unc homozygotes, Tg(Eno2-APP*751)10Cord Tg(GFAP-APOE_i4)1Hol Apoetm1Unc/Apoetm1Unc mice and Tg(Eno2-APP*751)10Cord Tg(GFAP-APOE*4)1Hol Apoetm1Unc/Apoetm1Unc
• mice exhibit more severe microgliosis following middle cerebral artery occlusion compared to Tg(Eno2-APP*751)10Cord Tg(GFAP-APOE_i4)1Hol Apoetm1Unc/Apoetm1Unc mice and Tg(Eno2-APP*751)10Cord Tg(GFAP-APOE*4)1Hol Apoetm1Unc/Apoetm1Unc mice




Genotype
MGI:3784385
cx111
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Tg(APPV717F)109Ili/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Tg(APPV717F)109Ili mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• 40% of mice exhibit plaque depositions at 12 months of age with one mouse remaining plaque free at 21 months (J:127846)
• 23% of mice at 15 months, 33% at 18 months and 55% at 21 months exhibit fibrillar plaques in the outer molecular layer of the dentate gyrus (J:127846)
• mice exhibit plaques in the stratum oriens and radiatum of the hippocampus and hilus of the dentate gyrus (J:127846)
• 3 of 4 mice exhibit plaques by 12 months of age (J:133058)

homeostasis/metabolism
• 40% of mice exhibit plaque depositions at 12 months of age with one mouse remaining plaque free at 21 months (J:127846)
• 23% of mice at 15 months, 33% at 18 months and 55% at 21 months exhibit fibrillar plaques in the outer molecular layer of the dentate gyrus (J:127846)
• mice exhibit plaques in the stratum oriens and radiatum of the hippocampus and hilus of the dentate gyrus (J:127846)
• 3 of 4 mice exhibit plaques by 12 months of age (J:133058)




Genotype
MGI:4460235
cx112
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Il10tm1Cgn/Il10tm1Cgn
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Il10tm1Cgn mutation (15 available); any Il10 mutation (45 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• lesion development substantially increased at 16 weeks relative to Apoetm1Unc alone
• lesion size about 10 fold greater at 48 weeks than at 16 weeks but similar to controls

homeostasis/metabolism
• shift in cholesterol from VLDL to LDL
• shift in cholesterol from VLDL to LDL
• elevated at both 16 and 48 weeks
• increased thrombin formation
• enhanced thrombotic response to injected thrombin
• intracoronary platelet thrombi are significantly more frequent

immune system
• elevated at both 16 and 48 weeks




Genotype
MGI:3784384
cx113
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Tg(APPV717F)109Ili/0
Tg(GFAP-APOE_i3)37Hol/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Tg(APPV717F)109Ili mutation (0 available)
Tg(GFAP-APOE_i3)37Hol mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• by 15 to 18 months, 31% of mice exhibit plaques in the hippocampus (J:127846)
• the amount of amyloid deposited is less than in Tg(APPV717F)109Ili Tg(GFAP-APOE_i4)#Hol Apoetm1Unc/Apoetm1Unc and much less than in Tg(APPV717F)109Ili Apoetm1Unc/Apoetm1Unc mice (J:127846)
• plaques are observed in the the outer molecular layer of the dentate gyrus and the stratum oriens and radiatum of the hippocampus (J:127846)
• mice exhibit fibrillar plaques in the outer molecular layer of the dentate gurys (J:127846)
• 20% of mice exposed to traumatic brain injury (TBI) at 9 to 10 months of age exhibit amyloid plaques by 12 to 13 months of age while mice not exposed to TBI do not exhibit plaques until 15 months of age (J:133058)
• mice exhibit decreased plaque formation and severity following TBI compared to in similarly treated Tg(APPV717F)109Ili Tg(GFAP-APOE_i4)#Hol Apoetm1Unc/Apoetm1Unc mice (J:133058)

homeostasis/metabolism
• by 15 to 18 months, 31% of mice exhibit plaques in the hippocampus (J:127846)
• the amount of amyloid deposited is less than in Tg(APPV717F)109Ili Tg(GFAP-APOE_i4)#Hol Apoetm1Unc/Apoetm1Unc and much less than in Tg(APPV717F)109Ili Apoetm1Unc/Apoetm1Unc mice (J:127846)
• plaques are observed in the the outer molecular layer of the dentate gyrus and the stratum oriens and radiatum of the hippocampus (J:127846)
• mice exhibit fibrillar plaques in the outer molecular layer of the dentate gurys (J:127846)
• 20% of mice exposed to traumatic brain injury (TBI) at 9 to 10 months of age exhibit amyloid plaques by 12 to 13 months of age while mice not exposed to TBI do not exhibit plaques until 15 months of age (J:133058)
• mice exhibit decreased plaque formation and severity following TBI compared to in similarly treated Tg(APPV717F)109Ili Tg(GFAP-APOE_i4)#Hol Apoetm1Unc/Apoetm1Unc mice (J:133058)




Genotype
MGI:3801012
cx114
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Tg(Prnp-Abca1)EHol/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Tg(Prnp-Abca1)EHol mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• frequent deposits are observed in hilus of dentate gyrus
• almost no thioflavin-S positive fibrillar Abeta plaques are observed in cortex and hippocampus
• mice show 2- to 3-fold less Abeta in the brain relative to Tg(APPV717F)109Ili, Apoe-wild-type controls

homeostasis/metabolism
• frequent deposits are observed in hilus of dentate gyrus
• almost no thioflavin-S positive fibrillar Abeta plaques are observed in cortex and hippocampus
• mice show 2- to 3-fold less Abeta in the brain relative to Tg(APPV717F)109Ili, Apoe-wild-type controls




Genotype
MGI:3784390
cx115
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Tg(Eno2-APP*751)10Cord/0
Tg(GFAP-APOE_i3)37Hol/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Tg(Eno2-APP*751)10Cord mutation (0 available)
Tg(GFAP-APOE_i3)37Hol mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• compared to in Tg(Eno2-APP*751)10Cord Apoetm1Unc/Apoetm1Unc mice

nervous system
• compared to in Tg(Eno2-APP*751)10Cord Apoetm1Unc/Apoetm1Unc mice
• mice exhibit less severe microgliosis following medial cerebral artery occlusion compared to Tg(Eno2-APP*751)10Cord Apoetm1Unc/Apoetm1Unc mice




Genotype
MGI:3784389
cx116
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Tg(Eno2-APP*751)10Cord/0
Cdh18Tg(GFAP-APOE_i4)1Hol/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Cdh18Tg(GFAP-APOE_i4)1Hol mutation (1 available); any Cdh18 mutation (56 available)
Tg(Eno2-APP*751)10Cord mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• compared to in Tg(Eno2-APP*751)10Cord Apoetm1Unc/Apoetm1Unc mice

nervous system
• compared to in Tg(Eno2-APP*751)10Cord Apoetm1Unc/Apoetm1Unc mice
• mice exhibit less severe microgliosis following medial cerebral artery occlusion compared to Tg(Eno2-APP*751)10Cord Apoetm1Unc/Apoetm1Unc mice




Genotype
MGI:3784387
cx117
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Tg(APPV717F)109Ili/0
Tg(GFAP-APOE_i2)14Hol/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Tg(APPV717F)109Ili mutation (0 available)
Tg(GFAP-APOE_i2)14Hol mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• 66% of mice exhibit plaques after 18 months
• mice exhibit plaques in the stratum oriens and radiatum of the hippocampus and hilus of the dentate gyrus but no the molecular layer of the dentate gyrus
• however, no fibrillar plaques are detected

homeostasis/metabolism
• 66% of mice exhibit plaques after 18 months
• mice exhibit plaques in the stratum oriens and radiatum of the hippocampus and hilus of the dentate gyrus but no the molecular layer of the dentate gyrus
• however, no fibrillar plaques are detected




Genotype
MGI:3784383
cx118
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Tg(APPV717F)109Ili/0
Tg(GFAP-APOE_i4)#Hol/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Tg(APPV717F)109Ili mutation (0 available)
Tg(GFAP-APOE_i4)#Hol mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• by 15 to 18 months, 60% of mice exhibit plaques in the hippocampus (J:127846)
• the amount of amyloid deposited is more than in Tg(APPV717F)109Ili Tg(GFAP-APOE_i3)37Hol Apoetm1Unc/Apoetm1Unc mice but much less than in Tg(APPV717F)109Ili Apoetm1Unc/Apoetm1Unc mice (J:127846)
• plaques are observed in the outer molecular layer of the dentate gyrus and the stratum oriens and radiatum of the hippocampus (J:127846)
• mice exhibit fibrillar plaques in the outer molecular layer of the dentate gyrus (J:127846)
• 55.6% of mice exposed to traumatic brain injury (TBI) at 9 to 10 months of age exhibit amyloid plaques by 12 to 13 months of age while mice not exposed to TBI do not exhibit plaques until 15 months of age (J:133058)
• mice exhibit increased plaque formation and severity following TBI compared to in similarly treated Tg(APPV717F)109Ili Tg(GFAP-APOE_i3)37Hol Apoetm1Unc/Apoetm1Unc mice (J:133058)
• 44% of mice exhibit thioflavine-S+ amyloid staining (fibrillar amyloid) in the molecular layer unlike in Tg(APPV717F)109Ili Tg(GFAP-APOE_i3)37Hol Apoetm1Unc/Apoetm1Unc and Tg(APPV717F)109Ili Apoetm1Unc/Apoetm1Unc mice (J:133058)

homeostasis/metabolism
• by 15 to 18 months, 60% of mice exhibit plaques in the hippocampus (J:127846)
• the amount of amyloid deposited is more than in Tg(APPV717F)109Ili Tg(GFAP-APOE_i3)37Hol Apoetm1Unc/Apoetm1Unc mice but much less than in Tg(APPV717F)109Ili Apoetm1Unc/Apoetm1Unc mice (J:127846)
• plaques are observed in the outer molecular layer of the dentate gyrus and the stratum oriens and radiatum of the hippocampus (J:127846)
• mice exhibit fibrillar plaques in the outer molecular layer of the dentate gyrus (J:127846)
• 55.6% of mice exposed to traumatic brain injury (TBI) at 9 to 10 months of age exhibit amyloid plaques by 12 to 13 months of age while mice not exposed to TBI do not exhibit plaques until 15 months of age (J:133058)
• mice exhibit increased plaque formation and severity following TBI compared to in similarly treated Tg(APPV717F)109Ili Tg(GFAP-APOE_i3)37Hol Apoetm1Unc/Apoetm1Unc mice (J:133058)
• 44% of mice exhibit thioflavine-S+ amyloid staining (fibrillar amyloid) in the molecular layer unlike in Tg(APPV717F)109Ili Tg(GFAP-APOE_i3)37Hol Apoetm1Unc/Apoetm1Unc and Tg(APPV717F)109Ili Apoetm1Unc/Apoetm1Unc mice (J:133058)




Genotype
MGI:3713848
cx119
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Serpind1tm1Moto/Serpind1+
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Serpind1tm1Moto mutation (0 available); any Serpind1 mutation (21 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• atherosclerotic plaque area in the aortic root is significantly increased compared to Apoe-deficient, Serpind1-sufficient mice; lipid deposition and PAR-1-positive cells in the plaques are more prominently observed in aortic root of mutants

cellular
• superoxide production in the aortic root is greater than in controls

homeostasis/metabolism
• excretion levels of 8-hydorxy-2'-deoxyguanosine, a marker of oxidative stress-induced DNA damage, are higher in double mutants than in controls

renal/urinary system
• excretion levels of 8-hydorxy-2'-deoxyguanosine, a marker of oxidative stress-induced DNA damage, are higher in double mutants than in controls




Genotype
MGI:4358706
cx120
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Lcattm1Hgc/Lcattm1Hgc
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * DBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Lcattm1Hgc mutation (0 available); any Lcat mutation (25 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
N
• unlike Lcat single mutants, the free cholesterol/esterfied cholesterol ratio is not significantly different from controls
• increase in APOB-48
• about a 2 fold increase in all plasma lipid constituents compared to mice homozygous null for Lcat and Ldlr
• compared to Apoe single mutants the percentage of long chain PUFA in the total APOB lipoprotein cholesterol ester fraction is decreased
• compared to Apoe single mutants cholesteryl stearate and oleate levels are increased 46% and 22%, respectively
• there is a 1.6 fold increase in the ratio of saturated + monounsaturated/polyunsaturated cholesterol ester fatty acid species compared to Apoe single mutants




Genotype
MGI:3789132
cx121
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Tg(CAG-IL1RN)2Cga/?
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * DBA/1 * FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Tg(CAG-IL1RN)2Cga mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• atherosclerotic lesions in the aortic root are reduced by 40% relative to Apoetm1Unc single homozygotes
• 67% reduction in the descending aorta
• reduced susceptibility in the aortic arch

immune system
• reduced levels of serum Amyloid A

homeostasis/metabolism
• reduced levels of serum Amyloid A




Genotype
MGI:3789130
cx122
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Tg(CAG-IL1RN)1Cga/?
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * DBA/1 * FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Tg(CAG-IL1RN)1Cga mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• atherosclerotic lesions in the aortic root are reduced by 47% relative to Apoetm1Unc single homozygotes
• 53% reduction in the descending aorta
• reduced susceptibility in the aortic arch

immune system
• undetectable levels of serum Amyloid A

homeostasis/metabolism
• undetectable levels of serum Amyloid A




Genotype
MGI:5451015
cx123
Allelic
Composition
Abca1tm1Jdm/Abca1tm1Jdm
Abcg1tm1Dgen/Abcg1tm1Dgen
Apoetm1Unc/Apoetm1Unc
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * DBA * DBA/1LacJ
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Abca1tm1Jdm mutation (1 available); any Abca1 mutation (90 available)
Abcg1tm1Dgen mutation (0 available); any Abcg1 mutation (46 available)
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
hematopoietic system
• mice fed a high fat diet exhibit increased hematopoietic stem and multipotential progenitor cell (HSPC) mobilization compared with wild-type mice
• however, treatment with recombinant HDL suppresses this increase




Genotype
MGI:2653578
cx124
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Tg(NOS3)2Crom/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Tg(NOS3)2Crom mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• decrease in atherosclerosis compared to single Apoe homozygotes
• mutants fed a Western diet show a decrease in systemic blood pressure, although heart rate is normal

homeostasis/metabolism
• ~15-16% decrease in plasma cholesterol on a normal chow diet or Western diet compared to single Apoe homozygotes




Genotype
MGI:2653579
cx125
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Tg(NOS3)3Crom/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Tg(NOS3)3Crom mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• decrease in atherosclerosis compared to single Apoe homozygotes
• mutants fed a Western Diet show a decrease in systemic blood pressure although heart rate is normal

homeostasis/metabolism
• ~15-16% decrease in plasma cholesterol on a normal chow diet or Western diet compared to single Apoe homozygotes




Genotype
MGI:3722317
cx126
Allelic
Composition
Apoetm1Unc/Apoe+
Tg(APPV717I)1130Kha/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Tg(APPV717I)1130Kha mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• absence of Apoe does not modify or improve mouse survival relative to Tg(APPV717I)1130Kha mice expressing Apoe; significant mortality before 150 days of age is observed




Genotype
MGI:3822447
cx127
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Tg(Cyp21a1-Apoe)614Fet/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Tg(Cyp21a1-Apoe)614Fet mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• total plasma cholesterol levels (TPC) are 132 +/- 12 mg/dl compared to normal range of control mice (70-100 mg/dl); levels of transgenic Apoe-null mice are almost normalized to levels of control littermates heterozygous for the mouse Apoe allele
• mice have >3% (about 2.2 ug/ml) of wild-type plasma Apoe levels

cardiovascular system
• mice show almost complete suppression of cholesteryl ester deposition (CE lesions) compared to nontransgenic Apoe-null littermates




Genotype
MGI:3822449
cx128
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Tg(Cyp21a1-Apoe)619Fet/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Tg(Cyp21a1-Apoe)619Fet mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• mice have very reduced levels of Apoe (0-2 ug/ml) compared to wild-type plasma Apoe levels
• plasma lipoprotein profiles are indistinguishable from Apoe-null nontransgenic littermates; LDL and VLDL distributions are similar to Apoe-deficient mice
• total plasma cholesterol levels (TPC) are about 580 mg/dl (mean TPC approx 302 mg/dl) compared to control mice (70-100 mg/dl); mice are hypercholesterolemic, similar to non-transgenic Apoe-deficient mice

cardiovascular system
• almost no lesion staining is observed in mice between 7.5 months to >2.5 years of age, despite persistent hypercholesterolemia, but lesions are observed throughout aortas of nontransgenic Apoe-null littermates
• aorta cholesteryl ester (CE) depositions are reduced by 86% compared to nontransgenic Apoe-null littermates




Genotype
MGI:3722316
cx129
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Tg(APPV717I)1130Kha/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Tg(APPV717I)1130Kha mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• absence of Apoe does not modify or improve mouse survival relative to Tg(APPV717I)1130Kha mice expressing Apoe; significant mortality before 150 days of age is observed




Genotype
MGI:4420430
cx130
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Nfe2l2tm1Mym/Nfe2l2tm1Mym
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Nfe2l2tm1Mym mutation (5 available); any Nfe2l2 mutation (90 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• mice fed a high fat diet exhibit decreased atherosclerotic plaques compared with Apoetm1Unc homozygotes
• mice fed a high fat diet exhibit improved aortic stiffness compared with Apoetm1Unc homozygotes

homeostasis/metabolism
• when fed a high fat diet compared with Apoetm1Unc homozygotes
• when fed a high fat diet compared with Apoetm1Unc homozygotes

cellular
• mice fed a high fat diet exhibit increased oxidative stress compared with Apoetm1Unc homozygotes

immune system
• macrophages of mice fed a high fat diet exhibit decreased modified low density lipoprotein uptake compared to in Apoetm1Unc homozygotes

hematopoietic system
• macrophages of mice fed a high fat diet exhibit decreased modified low density lipoprotein uptake compared to in Apoetm1Unc homozygotes




Genotype
MGI:7628726
cx131
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Thbs4tm1Olsa/Thbs4tm1Olsa
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Thbs4tm1Olsa mutation (0 available); any Thbs4 mutation (68 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
hematopoietic system
• in atherosclerotic lesions when fed western diet
• increased CD38+ pro-inflammatory macrophages in atherosclerotic lesions when fed western diet

homeostasis/metabolism
N
• normal plasma LDL/VLDL and HDL levels when fed either western diet or regular chow
• increased free and total cholesterol levels when fed western diet
• normal when fed regular chow
• increased plasma CXCL1 and CCL2 levels when fed western diet

immune system
• in atherosclerotic lesions when fed western diet
• increased CD38+ pro-inflammatory macrophages in atherosclerotic lesions when fed western diet
• increased plasma CXCL1 and CCL2 levels when fed western diet




Genotype
MGI:6477559
cx132
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Hhipl1tm1a(KOMP)Wtsi/Hhipl1tm1a(KOMP)Wtsi
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6J * C57BL/6N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Hhipl1tm1a(KOMP)Wtsi mutation (3 available); any Hhipl1 mutation (32 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• after 12 weeks on a high-fat Western diet, male double homozygotes show a 53% reduction in % aortic lesion area by en face analysis and a 33% reduction in mean plaque area in aortic roots relative to single Apoetm1Unc homozygotes
• under a Western diet, aortic root lesions of double homozygotes show a 47% reduction in SMA-positive staining indicating reduced smooth muscle cell content as well as a reduction in lipid content but no differences in macrophage or collagen content within plaques
• no differences in body weight, plasma lipid levels or blood pressure are observed relative to single Apoetm1Unc homozygotes




Genotype
MGI:2653531
cx133
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Tg(APOC1)1Bres/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6J * CBA/J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Tg(APOC1)1Bres mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• mice have more atherosclerosis compared to Apoe-deficient mice

homeostasis/metabolism
• level is ~double compared to Apoe-deficient mice
• intermediate-density lipoprotein (IDL) + LDL cholesterol level is increased relative to Apoe-null mice
• levels are increased almost 10-fold in males and ~3-fold in females
• VLDL triglyceride fraction is enriched significantly compared to Apoe-deficient mice
• more severe than Apoe-deficient littermates in fasting and non-fasting states
• mice show increased hepatic lipase activity relative to Apoe-deficient mice
• mice show increased lipoprotein lipase activity than wild-type and Apoe-null mice




Genotype
MGI:3717195
cx134
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Tg(Eno2-APOE_i4)1Rabr/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6J * ICR
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Tg(Eno2-APOE_i4)1Rabr mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
N
• coordination levels measured in rotorod tests are similar to wild-type, as is passive avoidance learning
• 6-month old females show similar performance in spatial learning (Morris water maze)
• 6-month old males show significantly higher latency to locate platform compared to females

nervous system
N
• upon 18 mg/kg kainic acid injection, significant loss of neocortical synaptophysin-positive presynaptic terminals and disruption of hippocampal axons are observed, similar to wild-type
• mice show significant loss of synaptophysin-positive presynaptic terminals and neuronal dendrites of the neocortex and hippocampus with age (7-9 months compared to 3-4 months) (J:55835)
• mice display similar degeneration to that observed in Apoe-deficient mice (J:100975)




Genotype
MGI:3717196
cx135
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Tg(Eno2-APOE_i3)1Rabr/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6J * ICR
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Tg(Eno2-APOE_i3)1Rabr mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
N
• no alterations in passive avoidance learning are observed
• 6-month old female mice show significant impairment in learning in the Morris water maze paradigm; mice display no improvement over four consecutive trials
• mice perform better than other genotypes and controls in the rotorod test, displaying a significantly increased latency to fall from the rod

nervous system
• after injection of 18 mg/kg kainic acid, mice show no disruption of hippocampal axons, whereas wild-type show significant loss of synaptophysin-positive neocortical presynaptic terminals (J:55835)
• mice do not show the same age dependent loss of neocortical and hippocampal presynaptic terminals and neuronal dendrites as Apoe-null and Apoe-null, Apoe3-trangenic mice (J:55835)
• age-related neuronal pathologies observed in Apoe-deficient mice are prevented by transgene expression (J:100975)




Genotype
MGI:5297861
cx136
Allelic
Composition
Ay/a
Apoetm1Unc/Apoetm1Unc
Ccr2tm1Mae/Ccr2tm1Mae
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6J * KK/TaJcl
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
a mutation (229 available); any a mutation (463 available)
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Ay mutation (12 available); any a mutation (463 available)
Ccr2tm1Mae mutation (3 available); any Ccr2 mutation (43 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
N
• mutants are protected against the metabolic syndrome, atherosclerosis, and diabetic nephropathy that develops in Ay/a Apoetm1Unc double mutants




Genotype
MGI:5297860
cx137
Allelic
Composition
Ay/a
Apoetm1Unc/Apoetm1Unc
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6J * KK/TaJcl
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
a mutation (229 available); any a mutation (463 available)
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Ay mutation (12 available); any a mutation (463 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• mutants develop larger atherosclerotic plaques than a/a Apoetm1Unc/Apoetm1Unc mice
• plaques contain a higher proportion of macrophage infiltration

growth/size/body
• mutants exhibit increased weight gain, despite similar food intake as controls

hematopoietic system
• increase in the proportion of inflammatory monocytes in the blood, liver, muscle, and kidney, but not epididymal fat pads

homeostasis/metabolism

immune system
• increase in the proportion of inflammatory monocytes in the blood, liver, muscle, and kidney, but not epididymal fat pads
• increase in systemic inflammation

renal/urinary system
• mutants develop features of diabetic nephropathy
• mutants exhibit mesangial expansion as indicated by glycogen deposition in the glomeruli
• 20-30% of mutants exhibit nodular sclerosis in the kidney

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
abdominal obesity-metabolic syndrome DOID:0060611 OMIM:PS605552
J:177084




Genotype
MGI:7516350
cx138
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Svep1tm1a(EUCOMM)Hmgu/Svep1+
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Svep1tm1a(EUCOMM)Hmgu mutation (1 available); any Svep1 mutation (169 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• reduced atherosclerotic plaque burden in whole aorta and aortic arch and root after 8 weeks of HFD feeding
• reduced macrophage invasion of aortic root neointima after 8 weeks of HFD feeding

growth/size/body
N
• normal body weight after 8 weeks of HFD feeding

homeostasis/metabolism
N
• normal plasma total cholesterol, triglycerides and glucose levels after 8 weeks of HFD feeding




Genotype
MGI:3690213
cx139
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Tg(MSR1-Plau)1Ddi/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Tg(MSR1-Plau)1Ddi mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• die suddenly beginning at around 11 weeks of age when fed an atherogenic diet, compared to no increase in mortality in Apoe homozyous controls
• mutants that die suddenly show myocardial infarcts, stenoses, and total occlusions of proximal coronary arteries

cardiovascular system
• in a longer atherogenic diet study, develop severe occlusive proximal coronary artery disease and extensive myocardial infarcts
• after 10 weeks on an atherogenic diet, exhibit increased atherosclerosis compared to controls (Apoe homozygotes) as indicated by increased intimal area in aortic root sections and sudanophilic area on pinned aortas
• after 10 weeks on an atherogenic diet, exhibit dilated aortic roots and increased medial destruction compared to controls
• develop occlusive coronary artery disease (J:101486)
• in a longer atherogenic diet study, develop severe occlusive proximal coronary artery disease (J:102208)
• exhibit significantly more collagenous scar formation in hearts at 15-weeks of age than single Apoe homozygotes
• hearts are larger than in single Apoe homozygotes at 15, but not 3, weeks of age
• hearts show more inflammatory cells, mostly macrophages, than single Apoe homozygotes
• accumulation of macrophages in hearts occurs as early as 5 weeks of age, before the onset of cardiac fibrosis or occlusive coronary artery disease

immune system
• hearts show more inflammatory cells, mostly macrophages, than single Apoe homozygotes
• accumulation of macrophages in hearts occurs as early as 5 weeks of age, before the onset of cardiac fibrosis or occlusive coronary artery disease

growth/size/body
• hearts are larger than in single Apoe homozygotes at 15, but not 3, weeks of age




Genotype
MGI:3775795
cx140
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Leprdb/Leprdb
Genetic
Background
involves: 129P2/OlaHsd * C57BLKS/J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Leprdb mutation (17 available); any Lepr mutation (122 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
vision/eye
• higher levels of "advanced glycation end products" in the extracellular matrix
• Ager mRNA levels elevated in the retina
• increase of capillary lesions
• significantly higher number of acellular capillaries
• increased capillary outpouching indicative of early microaneurysms

cardiovascular system
• increase of capillary lesions
• significantly higher number of acellular capillaries
• increased capillary outpouching indicative of early microaneurysms




Genotype
MGI:3718008
cx141
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Tg(Eno2-APOE_i4)1Rabr/0
Genetic
Background
involves: 129P2/OlaHsd * ICR
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Tg(Eno2-APOE_i4)1Rabr mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
• in the elevated-plus maze, mice show increased anxiety with reduced time and distance moved in the open arms; mice have significantly lower number of open-arm entries than wild-type
• response is higher in mice at 6 months of age compared to wild-type or Tg(Eno2-APOE*3)1Rabr/Apoetm1Unc mice but lower than Apoetm1Unc single mutants

nervous system
• mutants have lower levels of MAP 2-positive neuronal dendrites than wild-type; at 3 months, levels are similar in mutants and controls




Genotype
MGI:3718007
cx142
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Tg(Eno2-APOE_i3)1Rabr/0
Genetic
Background
involves: 129P2/OlaHsd * ICR
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Tg(Eno2-APOE_i3)1Rabr mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
N
• mice show comparable levels of anxiety compared to wild-type in the elevated-plus maze and comparable acoustic startle reflex to wild-type mice




Genotype
MGI:3852641
cx143
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Tnfrsf11btm1Eac/Tnfrsf11btm1Eac
Genetic
Background
involves: 129S4/SvJaeSor * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Tnfrsf11btm1Eac mutation (1 available); any Tnfrsf11b mutation (31 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• increased extractable calcium in the aorta at 40 and 60 weeks
• 38% show calcification of the medial layer of the brachiocephalic artery
• calcification of the intimal layer of the brachiocephalic artery by 40-60 weeks
• increased area of lesions in the brachiocephalic artery at 40 and 60 weeks but not at 20 weeks
• increased number of lesions with laminated elastic fibers
• larger areas of collagen and proteoglycan deposition
• 40% addition reduction in lesion cellularity as compared to mice only homozygous for Apoetm1Unc




Genotype
MGI:3576623
cx144
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Pla2g15tm1Ytan/Pla2g15tm1Ytan
Genetic
Background
involves: 129S/SvEv * B6.129P2-Apoetm1Unc/J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Pla2g15tm1Ytan mutation (0 available); any Pla2g15 mutation (30 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• the area of atherosclerotic lesions was significantly increased in the aortas compared to those in homozygous Apoe mutant mice on a normal diet, however cholesterol and triglycerol levels were no different than seen in Apoe mutants
• when fed an atherogenic diet, the extent of atherogenesis was no different from homozygous Apoe mutant mice despite exceptionally high cholesterol levels

homeostasis/metabolism
• exceptionally high plasma cholesterol levels when fed an atherogenic diet

immune system
• peritoneal macrophages were more sensitive to apoptosis induced by exposure to oxidized low-density lipoprotein

hematopoietic system
• peritoneal macrophages were more sensitive to apoptosis induced by exposure to oxidized low-density lipoprotein




Genotype
MGI:3621887
cx145
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Cst3tm1Karl/Cst3tm1Karl
Genetic
Background
involves: 129S/SvEv * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Cst3tm1Karl mutation (0 available); any Cst3 mutation (14 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• aortic tissue extracts from double knockouts show higher levels of cathepsins S and L and the long form of cathepsin B than ApoE null controls
• aortic smooth muscle cells exhibit an augmented ability to degrade elastin in vitro

cardiovascular system
• double knockout mice display thinning of the tunica media in the aortic arch compared to ApoE knockouts
• double knockouts show more framentation of elastic laminae than in either the ApoE or Cst3 single knockout mouse
• double knockout mice display thinning of the tunica media in the aortic arch compared to ApoE knockouts
• atherosclerotic lesions from aortas of double knockouts had increased smooth muscle cell content (9.3% vs. 4.2% positive lesion area) and collagen (14.4% vs. 4.6%) compared to ApoE knockout mice; fibrous caps develop significantly more in double mutants than controls
• in vitro double knockout smooth muscle cells proliferate more rapidly than control cells which might contribute to the increase in SMC and collagen content in aortic lesions

muscle
• in vitro double knockout smooth muscle cells proliferate more rapidly than control cells which might contribute to the increase in SMC and collagen content in aortic lesions




Genotype
MGI:4418046
cx146
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Cav1tm1Mls/Cav1tm1Mls
Genetic
Background
involves: 129/Sv * 129P2/OlaHsd * C57BL/6J * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Cav1tm1Mls mutation (2 available); any Cav1 mutation (31 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• 70% reduction in atherosclerotic lesion area, indicating protection against the development of aortic atheromas

homeostasis/metabolism
• 1.3 to 1.5-fold increase in non-HDL plasma cholesterol levels when fed a normal or high-fat diet
• on a normal or high-fat diet
• on a normal or high-fat diet
• approximate 2.3-fold increase in plasma triglyceride when fed a normal or high-fat diet




Genotype
MGI:3789127
cx147
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Lgals3tm1Poi/Lgals3tm1Poi
Genetic
Background
involves: 129/Sv * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Lgals3tm1Poi mutation (4 available); any Lgals3 mutation (29 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• at 25 to 31 weeks of age, mice exhibit a lower number inflammatory infiltrate and mast cells in adventitia than Apoetm1Unc homozygotes
• at 36 to 44 months of age, mice exhibit fewer atherosclerotic lesions and atheromatous plaques compared to in Apoetm1Unc homozygotes and do not exhibit an age-related increase in lesion number, athlerosclerotic microaneurysms or periaortic vascular channels that are evident in Apoetm1Unc homozygotes

homeostasis/metabolism
• compared to in Lgals3tm1Poi homozygotes




Genotype
MGI:3794639
cx148
Allelic
Composition
Albq4A/J/Albq4A/J
Apoetm1Unc/Apoetm1Unc
Genetic
Background
involves: A/J * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Albq4A/J mutation (0 available); any Albq4 mutation (0 available)
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• susceptibility to albuminuria in males

renal/urinary system
• susceptibility to albuminuria in males




Genotype
MGI:3794640
cx149
Allelic
Composition
Albq4A/J/Albq4C57BL/6J
Apoetm1Unc/Apoetm1Unc
Genetic
Background
involves: A/J * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Albq4A/J mutation (0 available); any Albq4 mutation (0 available)
Albq4C57BL/6J mutation (0 available); any Albq4 mutation (0 available)
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• susceptibility to albuminuria in males

renal/urinary system
• susceptibility to albuminuria in males




Genotype
MGI:3707035
cx150
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Gofm2C57BL/6J/?
Genetic
Background
involves: C3H/HeJ * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Gofm2C57BL/6J mutation (0 available); any Gofm2 mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
adipose tissue
• increased gonadal fat mass in females




Genotype
MGI:3707034
cx151
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Gofm1C57BL/6J/?
Genetic
Background
involves: C3H/HeJ * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Gofm1C57BL/6J mutation (0 available); any Gofm1 mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
adipose tissue
• increased gonadal fat mass in females




Genotype
MGI:3819480
cx152
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Tnfsf4Ath1-C57BL/6J/Tnfsf4Ath1-C57BL/6J
Genetic
Background
involves: C3H/HeJ * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Tnfsf4Ath1-C57BL/6J mutation (0 available); any Tnfsf4 mutation (33 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• increased aortic lesion area in female animals fed a high fat diet




Genotype
MGI:3819478
cx153
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Athsq3C3H/HeJ/Athsq3C3H/HeJ
Genetic
Background
involves: C3H/HeJ * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Athsq3C3H/HeJ mutation (0 available); any Athsq3 mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• decreased aortic lesion area in male animals fed a high fat diet




Genotype
MGI:3819477
cx154
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Ath33C3H/HeJ/Ath33C3H/HeJ
Genetic
Background
involves: C3H/HeJ * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Ath33C3H/HeJ mutation (0 available); any Ath33 mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• increased aortic lesion area in animals fed a high fat diet




Genotype
MGI:3819476
cx155
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Ath32C57BL/6J/Ath32C57BL/6J
Genetic
Background
involves: C3H/HeJ * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Ath32C57BL/6J mutation (0 available); any Ath32 mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• increased aortic lesion area in animals fed a high fat diet




Genotype
MGI:3819481
cx156
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Ath29C57BL/6J/Ath29C57BL/6J
Genetic
Background
involves: C3H/HeJ * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Ath29C57BL/6J mutation (0 available); any Ath29 mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• increased aortic lesion area in animals fed a high fat diet




Genotype
MGI:3769560
cx157
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Nhdlq12C3H/HeJ/Nhdlq12C57BL/6J
Genetic
Background
involves: C3H/HeJ * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Nhdlq12C3H/HeJ mutation (0 available); any Nhdlq12 mutation (0 available)
Nhdlq12C57BL/6J mutation (0 available); any Nhdlq12 mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism




Genotype
MGI:3769557
cx158
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Nhdlq11C3H/HeJ/Nhdlq11C3H/HeJ
Genetic
Background
involves: C3H/HeJ * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Nhdlq11C3H/HeJ mutation (0 available); any Nhdlq11 mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype



Genotype
MGI:3769556
cx159
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Nhdlq11C3H/HeJ/Nhdlq11C57BL/6J
Genetic
Background
involves: C3H/HeJ * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Nhdlq11C3H/HeJ mutation (0 available); any Nhdlq11 mutation (0 available)
Nhdlq11C57BL/6J mutation (0 available); any Nhdlq11 mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype



Genotype
MGI:3769550
cx160
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Trigq4C3H/HeJ/Trigq4C57BL/6J
Genetic
Background
involves: C3H/HeJ * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Trigq4C3H/HeJ mutation (0 available); any Trigq4 mutation (0 available)
Trigq4C57BL/6J mutation (0 available); any Trigq4 mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism




Genotype
MGI:3769549
cx161
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Trigq4C3H/HeJ/Trigq4C3H/HeJ
Genetic
Background
involves: C3H/HeJ * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Trigq4C3H/HeJ mutation (0 available); any Trigq4 mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism




Genotype
MGI:3769548
cx162
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Hdlq91C3H/HeJ/?
Genetic
Background
involves: C3H/HeJ * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Hdlq91C3H/HeJ mutation (0 available); any Hdlq91 mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism




Genotype
MGI:3769564
cx163
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Pnhdlc1C57BL/6J/Pnhdlc1C57BL/6J
Genetic
Background
involves: C3H/HeJ * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Pnhdlc1C57BL/6J mutation (0 available); any Pnhdlc1 mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism




Genotype
MGI:3769566
cx164
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Pnhdlc6C3H/HeJ/?
Genetic
Background
involves: C3H/HeJ * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Pnhdlc6C3H/HeJ mutation (0 available); any Pnhdlc6 mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism




Genotype
MGI:3769547
cx165
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Hdlq19C57BL/6J/Hdlq19C57BL/6J
Genetic
Background
involves: C3H/HeJ * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Hdlq19C57BL/6J mutation (0 available); any Hdlq19 mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism




Genotype
MGI:3769546
cx166
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Hdlq86C3H/HeJ/?
Genetic
Background
involves: C3H/HeJ * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Hdlq86C3H/HeJ mutation (0 available); any Hdlq86 mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype



Genotype
MGI:3769545
cx167
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Hdlq86C3H/HeJ/Hdlq86C3H/HeJ
Genetic
Background
involves: C3H/HeJ * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Hdlq86C3H/HeJ mutation (0 available); any Hdlq86 mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype



Genotype
MGI:3769543
cx168
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Hdl5C57BL/6J/Hdl5C57BL/6J
Genetic
Background
involves: C3H/HeJ * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Hdl5C57BL/6J mutation (0 available); any Hdl5 mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism




Genotype
MGI:3769568
cx169
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Trigq3C3H/HeJ/Trigq3C3H/HeJ
Genetic
Background
involves: C3H/HeJ * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Trigq3C3H/HeJ mutation (0 available); any Trigq3 mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism




Genotype
MGI:3769542
cx170
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Cath1C3H/HeJ/Cath1C57BL/6J
Genetic
Background
involves: C3H/HeJ * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Cath1C3H/HeJ mutation (0 available); any Cath1 mutation (0 available)
Cath1C57BL/6J mutation (0 available); any Cath1 mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• increased carotid artery lesion size




Genotype
MGI:3769541
cx171
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Cath1C57BL/6J/Cath1C57BL/6J
Genetic
Background
involves: C3H/HeJ * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Cath1C57BL/6J mutation (0 available); any Cath1 mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• increased carotid artery lesion size




Genotype
MGI:3769569
cx172
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Trigq3C3H/HeJ/?
Genetic
Background
involves: C3H/HeJ * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Trigq3C3H/HeJ mutation (0 available); any Trigq3 mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism




Genotype
MGI:3819474
cx173
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Ath30C57BL/6J/Ath30C57BL/6J
Genetic
Background
involves: C3H/HeJ * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Ath30C57BL/6J mutation (0 available); any Ath30 mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• increased aortic lesion area in female animals fed a high fat diet




Genotype
MGI:3819475
cx174
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Ath31C57BL/6J/Ath31C57BL/6J
Genetic
Background
involves: C3H/HeJ * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Ath31C57BL/6J mutation (0 available); any Ath31 mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• increased aortic lesion area in female animals fed a high fat diet




Genotype
MGI:5613592
cx175
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Athsq3C57BL/6J/Athsq3C57BL/6J
Genetic
Background
involves: C3H/HeJ * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Athsq3C57BL/6J mutation (0 available); any Athsq3 mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• increased aortic lesion area in animals fed a high fat diet




Genotype
MGI:3707039
cx176
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Gofm4C3H/HeJ/?
Genetic
Background
involves: C3H/HeJ * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Gofm4C3H/HeJ mutation (0 available); any Gofm4 mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
adipose tissue
• increased gonadal fat mass in females




Genotype
MGI:3769561
cx177
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Nhdlq12C57BL/6J/Nhdlq12C57BL/6J
Genetic
Background
involves: C3H/HeJ * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Nhdlq12C57BL/6J mutation (0 available); any Nhdlq12 mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism




Genotype
MGI:3707037
cx178
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Gofm3C57BL/6J/?
Genetic
Background
involves: C3H/HeJ * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Gofm3C57BL/6J mutation (0 available); any Gofm3 mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
adipose tissue
• increased gonadal fat mass




Genotype
MGI:3707036
cx179
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Gofm2C3H/HeJ/?
Genetic
Background
involves: C3H/HeJ * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Gofm2C3H/HeJ mutation (0 available); any Gofm2 mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
adipose tissue
• increased gonadal fat mass in males




Genotype
MGI:3799494
cx180
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Faslpr/Faslpr
Genetic
Background
MRL.Cg-Apoetm1Unc Faslpr
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (33 available); any Apoe mutation (158 available)
Faslpr mutation (39 available); any Fas mutation (82 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• mice display greatly increased levels compared to wild-type controls or Apoe-null mice
• IgG and IgM anti-oxidized LDL and anti-cardiolipin antibodies are increased compared to controls
• mice display greatly increased levels compared to wild-type controls or Apoe-null mice
• mice display greatly increased levels compared to wild-type controls or Apoe-null mice

homeostasis/metabolism
• significantly increased relative to wild-type controls at 24 weeks of age or Fas-single mutants

cardiovascular system
• modest increase in total area of lipid deposits in aorta compared to Apoe-null mice

hematopoietic system
• mice display greatly increased levels compared to wild-type controls or Apoe-null mice





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last database update
12/10/2024
MGI 6.24
The Jackson Laboratory