Phenotypes associated with this allele

• Allele Symbol: Tg(Vil1-cre)997Gum
• Allele Name: transgene insertion 997, Deborah L Gumucio
• Allele ID: MGI:2448639
• Summary: 115 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
cn1	Atg16l1^tm1Kuv/Atg16l1^tm1Kuv Tg(Vil1-cre)997Gum/0	B6.Cg-Atg16l1^tm1Kuv Tg(Vil1-cre)997Gum	MGI:6296753
cn2	Atg16l1^tm1Kuv/Atg16l1^tm1Kuv Tg(Vil1-cre)997Gum/0 Xbp1^tm2Glm/Xbp1^tm2Glm	B6.Cg-Atg16l1^tm1Kuv Xbp1^tm2Glm Tg(Vil1-cre)997Gum	MGI:6296755
cn3	Cyld^tm1.1Mpa/Cyld^tm1.1Mpa Ikbkg^tm1.1Mpa/Y Tg(Vil1-cre)997Gum/0	B6.Cg-Cyld^tm1.1Mpa Ikbkg^tm1.1Mpa Tg(Vil1-cre)997Gum	MGI:5293402
cn4	Cyld^tm1.1Mpa/Cyld^tm1.1Mpa Ikbkg^tm1.1Mpa/Ikbkg^tm1.1Mpa Tg(Vil1-cre)997Gum/0	B6.Cg-Cyld^tm1.1Mpa Ikbkg^tm1.1Mpa Tg(Vil1-cre)997Gum	MGI:5293401
cn5	Cyld^tm1.1Mpa/Cyld^tm1.1Mpa Fadd^tm1Mpa/Fadd^tm1Mpa Tg(Vil1-cre)997Gum/0	B6.Cg-Fadd^tm1Mpa Cyld^tm1.1Mpa Tg(Vil1-cre)997Gum	MGI:5293400
cn6	Fadd^tm1Mpa/Fadd^tm1Mpa Myd88^tm1Aki/Myd88^tm1Aki Tg(Vil1-cre)997Gum/0	B6.Cg-Fadd^tm1Mpa Myd88^tm1Aki Tg(Vil1-cre)997Gum	MGI:5293405
cn7	Fadd^tm1Mpa/Fadd^tm1Mpa Ripk3^tm1Vmd/Ripk3^tm1Vmd Tg(Vil1-cre)997Gum/0	B6.Cg-Fadd^tm1Mpa Ripk3^tm1Vmd Tg(Vil1-cre)997Gum	MGI:5293399
cn8	Fadd^tm1Mpa/Fadd^tm1Mpa Tg(Vil1-cre)997Gum/0	B6.Cg-Fadd^tm1Mpa Tg(Vil1-cre)997Gum	MGI:5293398
cn9	Fadd^tm1Mpa/Fadd^tm1Mpa Tnf^tm1Gkl/Tnf^tm1Gkl Tg(Vil1-cre)997Gum/0	B6.Cg-Fadd^tm1Mpa Tnf^tm1Gkl Tg(Vil1-cre)997Gum	MGI:5293404
cn10	Ikbkg^tm1.1Mpa/Ikbkg^tm1.1Mpa Tg(Vil1-cre)997Gum/0	B6.Cg-Ikbkg^tm1.1Mpa Tg(Vil1-cre)997Gum	MGI:5293403
cn11	Ikbkg^tm1.1Mpa/Y Tg(Vil1-cre)997Gum/0	B6.Cg-Ikbkg^tm1.1Mpa Tg(Vil1-cre)997Gum	MGI:5293406
cn12	Naipc^tm1Kmma/Naipc^tm1Kmma Tg(Vil1-cre)997Gum/0	B6.Cg-Naipc^tm1Kmma Tg(Vil1-cre)997Gum	MGI:5896658
cn13	Slc3a2^tm1.1Merl/Slc3a2^tm1.1Merl Tg(Vil1-cre)997Gum/0	B6.Cg-Slc3a2^tm1.1Merl Tg(Vil1-cre)997Gum	MGI:5433666
cn14	Slc3a2^tm1.1Merl/Slc3a2^+ Tg(Vil1-cre)997Gum/0	B6.Cg-Slc3a2^tm1.1Merl Tg(Vil1-cre)997Gum	MGI:5433667
cn15	Smyd5^tm1a(EUCOMM)Wtsi/Smyd5^tm1a(EUCOMM)Wtsi Tg(Vil1-cre)997Gum/0	B6.Cg-Smyd5^tm1a(EUCOMM)Wtsi Tg(Vil1-cre)997Gum	MGI:7716851
cn16	Tnfaip3^tm1.1Gvl/Tnfaip3^tm1.1Gvl Tg(Vil1-cre)997Gum/0	B6.Cg-Tnfaip3^tm1.1Gvl Tg(Vil1-cre)997Gum	MGI:4829679
cn17	Gt(ROSA)26Sor^tm1(CAG-CAMK2G*T287D,-EGFP)Whua/Gt(ROSA)26Sor^+ Tg(Vil1-cre)997Gum/0	involves: 129 * C57BL/6	MGI:6093452
cn18	Slc2a9^tm1Khm/Slc2a9^tm1Khm Tg(Vil1-cre)997Gum/0	involves: 129 * C57BL/6 * C57BL/6J	MGI:5760132
cn19	Apc^Min/Apc^+ Hsd11b2^tm1.1Mzz/Hsd11b2^tm1.1Mzz Tg(Vil1-cre)997Gum/0	involves: 129 * C57BL/6 * C57BL/6J	MGI:5547498
cn20	Slc31a1^tm2Djt/Slc31a1^tm2Djt Tg(Vil1-cre)997Gum/0	involves: 129 * C57BL/6 * FVB/N * SJL	MGI:3771153
cn21	Rela^tm1Asba/Rela^tm1Asba Tg(Vil1-cre)997Gum/0	involves: 129 * C57BL/6J * SJL	MGI:3799251
cn22	Dlg1^tm1Jhm/Dlg1^tm1Jhm Tg(Vil1-cre)997Gum/0	involves: 129 * C57BL/6 * SJL	MGI:4362042
cn23	St14^tm2Bug/St14^tm3Bug Tg(Vil1-cre)997Gum/0	involves: 129P2/OlaHsd * 129S6/SvEvTac * Black Swiss * C57BL/6 * SJL	MGI:4361214
cn24	Braf^tm1.1Brd/Braf^+ Cdkn2a^tm1.1Brn/Cdkn2a^tm1.1Brn Tg(Vil1-cre)997Gum/0	involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6 * SJL	MGI:5528298
cn25	Tnfrsf1a^tm3.1Gkl/Tnfrsf1a^tm3.1Gkl Tg(Vil1-cre)997Gum/0	involves: 129P2/OlaHsd * C57BL/6 * C57BL/6J * SJL	MGI:5573123
cn26	Tnfrsf1a^tm3.1Gkl/Tnfrsf1a^+ Tg(Vil1-cre)997Gum/0	involves: 129P2/OlaHsd * C57BL/6 * C57BL/6J * SJL	MGI:5573122
cn27	Atg16l1^tm1c(EUCOMM)Wtsi/Atg16l1^tm1c(EUCOMM)Wtsi Tcrd^tm1Mom/Tcrd^tm1Mom Tg(Vil1-cre)997Gum/0	involves: 129P2/OlaHsd * C57BL/6J * C57BL/6N * SJL	MGI:7564089
cn28	Il10^tm1Cgn/Il10^tm1Cgn Tg(Vil1-cre)997Gum/? Tlr5^tm1.1Gewr/Tlr5^tm1.1Gewr	involves: 129P2/OlaHsd * C57BL/6J * C57BL/6NTac * SJL	MGI:5751560
cn29	Yap1^tm1.1Dupa/Yap1^tm1.1Dupa Tg(Vil1-cre)997Gum/0	involves: 129P2/OlaHsd * C57BL/6J * SJL	MGI:4838643
cn30	Gadd45gip1^tm2Kong/Gadd45gip1^tm2Kong Tg(Vil1-cre)997Gum/0	involves: 129P2/OlaHsd * C57BL/6J * SJL	MGI:4420973
cn31	Sav1^tm1.1Dupa/Sav1^tm1.1Dupa Tg(Vil1-cre)997Gum/0	involves: 129P2/OlaHsd * C57BL/6J * SJL	MGI:4838642
cn32	Sav1^tm1.1Dupa/Sav1^tm1.1Dupa Yap1^tm1.1Dupa/Yap1^tm1.1Dupa Tg(Vil1-cre)997Gum/0	involves: 129P2/OlaHsd * C57BL/6J * SJL	MGI:4838644
cn33	Myd88^tm1Defr/Myd88^tm1Defr Tg(Vil1-cre)997Gum/0	involves: 129P2/OlaHsd * C57BL/6J * SJL	MGI:5297575
cn34	Ass1^tm1.1Ekoe/Ass1^tm1.1Ekoe Tg(Vil1-cre)997Gum/0	involves: 129P2/OlaHsd * C57BL/6 * SJL	MGI:5529839
cn35	Hfe^tm1Wsr/Hfe^tm1Wsr Tg(Vil1-cre)997Gum/?	involves: 129P2/OlaHsd * C57BL/6 * SJL	MGI:3821583
cn36	Myd88^tm1Aki/Myd88^tm1Aki Tnfaip3^tm1.1Gvl/Tnfaip3^tm1.1Gvl Tg(Vil1-cre)997Gum/0	involves: 129P2/OlaHsd * C57BL/6 * SJL	MGI:4829678
cn37	Gata6^tm2.1Sad/Gata6^tm2.1Sad Tg(Vil1-cre)997Gum/0	involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CD-1 * SJL	MGI:3662654
cn38	Lrp5^tm1Mawa/Lrp5^+ Tg(Vil1-cre)997Gum/0	involves: 129S1/Sv * 129X1/SvJ * C57BL/6J * SJL	MGI:5014229
cn39	Lrp5^tm2Mawa/Lrp5^+ Tg(Vil1-cre)997Gum/0	involves: 129S1/Sv * 129X1/SvJ * C57BL/6J * SJL	MGI:5014228
cn40	Lrp5^tm3.1Mawa/Lrp5^tm3.1Mawa Tg(Vil1-cre)997Gum/0	involves: 129S1/Sv * 129X1/SvJ * C57BL/6J * SJL	MGI:5014234
cn41	Edn2^tm1.1Nat/Edn2^tm1.1Nat Tg(Vil1-cre)997Gum/0	involves: 129S1/Sv * 129X1/SvJ * C57BL/6J * SJL	MGI:5519892
cn42	B3gnt6^tm1Lx/B3gnt6^tm1Lx C1galt1^tm1.1Rpmc/C1galt1^tm1.1Rpmc Tg(Vil1-cre)997Gum/0	involves: 129S1/Sv * C57BL/6J * SJL	MGI:5902495
cn43	Tnfaip3^tm1.1Gvl/Tnfaip3^tm1.1Gvl Tnfrsf1a^tm1Mak/Tnfrsf1a^tm1Mak Tg(Vil1-cre)997Gum/0	involves: 129S2/SvPas * C57BL/6 * SJL	MGI:4829677
cn44	Ern1^tm2.1Tiw/Ern1^tm2.1Tiw Xbp1^tm2Glm/Xbp1^tm2Glm Tg(Vil1-cre)997Gum/0	involves: 129S4/SvJae * 129S6/SvEvTac * C57BL/6 * SJL	MGI:5559520
cn45	Braf^tm1.1Brd/Braf^+ Tg(Vil1-cre)997Gum/0 Trp53^tm2Tyj/Trp53^tm2Tyj	involves: 129S4/SvJae * 129S7/SvEvBrd * C57BL/6 * SJL	MGI:5528297
cn46	Pten^tm1Hwu/Pten^tm1Hwu Tg(Vil1-cre)997Gum/0	involves: 129S4/SvJae * BALB/c * C57BL/6J * SJL	MGI:4941760
cn47	Apc^Min/Apc^+ Pten^tm1Hwu/Pten^tm1Hwu Tg(Vil1-cre)997Gum/0	involves: 129S4/SvJae * BALB/c * C57BL/6J * SJL	MGI:4941759
cn48	Ffar2^tm2Soff/Ffar2^tm2Soff Ffar3^tm2.1Soff/Ffar3^tm2.1Soff Tg(Vil1-cre)997Gum/0	involves: 129S4/SvJae * C57BL/6 * C57BL/6J * SJL	MGI:5770568
cn49	Mirc31^tm1.1Aru/Mirc31^tm1.1Aru Tg(Vil1-cre)997Gum/0	involves: 129S4/SvJae * C57BL/6 * C57BL/6J * SJL	MGI:5560214
cn50	Mirc31^tm1.1Aru/Mirc31^tm1.1Aru Tg(Vil1-cre)997Gum/0 Tg(Vil1-Lin28b,-tdTomato)LoAru/0	involves: 129S4/SvJae * C57BL/6 * C57BL/6J * SJL	MGI:5560215
cn51	Apc^Min/Apc^+ Col1a1^tm1(CAG-Sirt1)Dsin/Col1a1^+ Tg(Vil1-cre)997Gum/0	involves: 129S4/SvJae * C57BL/6 * C57BL/6J * SJL	MGI:4430578
cn52	Rab11a^tm1.1Ngao/Rab11a^tm1.1Ngao Tg(Vil1-cre)997Gum/0	involves: 129S4/SvJae * C57BL/6J * SJL	MGI:5608787
cn53	Casr^tm1Wch/Casr^tm1Wch Tg(Vil1-cre)997Gum/0	involves: 129S4/SvJae * C57BL/6J * SJL	MGI:5306895
cn54	Apc^Min/Apc^+ Rab11a^tm1.1Ngao/Rab11a^tm1.1Ngao Tg(Vil1-cre)997Gum/0	involves: 129S4/SvJae * C57BL/6J * SJL/J	MGI:7642164
cn55	Cc2d1a^tm1.1Thkn/Cc2d1a^tm1.1Thkn Hes1^tm1.1Sat/Hes1^+ Tg(Vil1-cre)997Gum/0	involves: 129S4/SvJae * C57BL/6NTac * SJL	MGI:6459274
cn56	Apc^tm1Tno/Apc^tm1Tno Tg(Vil1-cre)997Gum/0	involves: 129S4/SvJae * C57BL/6 * SJL	MGI:3844315
cn57	Apc^tm1Tno/Apc^+ Tg(Vil1-cre)997Gum/0	involves: 129S4/SvJae * C57BL/6 * SJL	MGI:3844314
cn58	Cc2d1a^tm1.1Thkn/Cc2d1a^tm1.1Thkn Tg(Vil1-cre)997Gum/0	involves: 129S4/SvJae * C57BL/6 * SJL	MGI:6459275
cn59	Apc^Min/Apc^+ Erbb3^tm1.1Dwt/Erbb3^tm2.1Dwt Tg(Vil1-cre)997Gum/0	involves: 129S6/SvEvTac * C57BL/6 * C57BL/6J * SJL	MGI:4360363
cn60	Tg(Vil1-cre)997Gum/0 Tnfrsf11a^tm1.1Irw/Tnfrsf11a^tm1.1Irw	involves: 129S6/SvEvTac * C57BL/6 * C57BL/6NTac * SJL	MGI:5629980
cn61	Atg7^tm1Tchi/Atg7^tm1Tchi Xbp1^tm2Glm/Xbp1^tm2Glm Tg(Vil1-cre)997Gum/0	involves: 129S6/SvEvTac * C57BL/6 * CBA * SJL	MGI:5559519
cn62	Abca1^tm1Jp/Abca1^tm1Jp Speer6-ps1^Tg(Alb-cre)21Mgn/Speer6-ps1^+ Tg(Vil1-cre)997Gum/0	involves: 129S6/SvEvTac * C57BL/6 * DBA * SJL	MGI:4358977
cn63	Il25^tm1Cdon/Il25^tm1Cdon Tg(Vil1-cre)997Gum/0	involves: 129S6/SvEvTac * C57BL/6J * C57BL/6N * SJL	MGI:5767208
cn64	Slc52a3^tm1.1Said/Slc52a3^tm1.1Said Tg(Vil1-cre)997Gum/0	involves: 129S6/SvEvTac * C57BL/6J * C57BL/6N * SJL	MGI:6358742
cn65	Xbp1^tm2Glm/Xbp1^tm2Glm Tg(Vil1-cre)997Gum/0	involves: 129S6/SvEvTac * C57BL/6J * FVB/N * SJL	MGI:5441532
cn66	Xbp1^tm2Glm/Xbp1^+ Tg(Vil1-cre)997Gum/0	involves: 129S6/SvEvTac * C57BL/6J * FVB/N * SJL	MGI:5441533
cn67	Abca1^tm1Jp/Abca1^+ Tg(Vil1-cre)997Gum/0	involves: 129S6/SvEvTac * C57BL/6 * SJL	MGI:4358974
cn68	Abca1^tm1Jp/Abca1^tm1Jp Tg(Vil1-cre)997Gum/0	involves: 129S6/SvEvTac * C57BL/6 * SJL	MGI:4358973
cn69	Xbp1^tm2Glm/Xbp1^tm2Glm Tnfrsf1a^tm1Imx/Tnfrsf1a^tm1Imx Tg(Vil1-cre)997Gum/0	involves: 129S6/SvEvTac * C57BL/6 * SJL	MGI:5559521
cn70	Xbp1^tm2Glm/Xbp1^tm2Glm Tg(Vil1-cre)997Gum/0	involves: 129S6/SvEvTac * C57BL/6 * SJL	MGI:5559517
cn71	Erbb3^tm1.1Dwt/Erbb3^tm2.1Dwt Tg(Vil1-cre)997Gum/0	involves: 129S6/SvEvTac * C57BL/6 * SJL	MGI:4360362
cn72	Atg16l1^tm1Kuv/Atg16l1^tm1Kuv Xbp1^tm2Glm/Xbp1^tm2Glm Tg(Vil1-cre)997Gum/0	involves: 129S6/SvEvTac * C57BL/6 * SJL	MGI:5559514
cn73	Atoh1^tm2Hzo/Atoh1^tm3Hzo Tg(Vil1-cre)997Gum/0	involves: 129S7/SvEvBrd * C57BL/6J * SJL	MGI:3767180
cn74	Braf^tm1.1Brd/Braf^+ Tg(Vil1-cre)997Gum/0	involves: 129S7/SvEvBrd * C57BL/6 * SJL	MGI:5528296
cn75	Ano1^tm2Jrr/Ano1^tm2Jrr Tg(Vil1-cre)997Gum/0	involves: 129S7/SvEvBrd * C57BL/6 * SJL	MGI:6151440
cn76	Nr5a2^tm1Sakl/Nr5a2^tm1Sakl Tg(Vil1-cre)997Gum/0	involves: 129S/SvEv * 129S4/SvJaeSor * C57BL/6J * SJL	MGI:3797771
cn77	Soat2^tm1.1Llr/Soat2^tm1.1Llr Tg(Vil1-cre)997Gum/0	involves: 129S/SvEv * 129S4/SvJaeSor * C57BL/6J * SJL	MGI:5426956
cn78	Tnfrsf1a^tm2Gkl/Tnfrsf1a^+ Tg(Vil1-cre)997Gum/0	involves: 129S/SvEv * C57BL/6J * SJL	MGI:5573126
cn79	Atg5^tm1Myok/Atg5^tm1Myok Tg(Vil1-cre)997Gum/0	involves: 129S/SvEv * C57BL/6 * SJL	MGI:3818605
cn80	Itgb1^tm1Efu/Itgb1^tm1Efu Tg(Vil1-cre)997Gum/0	involves: 129X1/SvJ * C57BL/6J * SJL	MGI:3703443
cn81	Fpr2^tm1.1Jimw/Fpr2^tm1.1Jimw Tg(Vil1-cre)997Gum/0	involves: 129X1/SvJ * C57BL/6J * SJL	MGI:5504261
cn82	Nr1h4^tm1.1Gonz/Nr1h4^tm1.1Gonz Tg(Vil1-cre)997Gum/0	involves: 129X1/SvJ * C57BL/6 * SJL	MGI:3806161
cn83	Slc5a6^tm1.1Said/Slc5a6^tm1.1Said Tg(Vil1-cre)997Gum/?	involves: C57BL/6	MGI:5493511
cn84	Lmna^tm4Stw/Lmna^tm4Stw Tg(Vil1-cre)997Gum/0	involves: C57BL/6 * C57BL/6J	MGI:5774438
cn85	Apc^Min/Apc^+ Lmna^tm4Stw/Lmna^tm4Stw Tg(Vil1-cre)997Gum/0	involves: C57BL/6 * C57BL/6J	MGI:5774439
cn86	Atp2b1^tm1.1Raku/Atp2b1^tm1.1Raku Tg(Vil1-cre)997Gum/0	involves: C57BL/6 * C57BL/6J	MGI:5904968
cn87	Apc^Min/Apc^+ Elp3^tm1.1Tac/Elp3^tm1.1Tac Tg(Vil1-cre)997Gum/0	involves: C57BL/6 * C57BL/6J * C57BL/6NTac * SJL	MGI:5898003
cn88	Elp3^tm1.1Tac/Elp3^tm1.1Tac Tg(Vil1-cre)997Gum/0	involves: C57BL/6 * C57BL/6J * C57BL/6NTac * SJL	MGI:5898002
cn89	Tlr4^tm1Djh/Tlr4^tm1Djh Tg(Vil1-cre)997Gum/0	involves: C57BL/6 * C57BL/6J * FVB/N * SJL	MGI:5520917
cn90	Pkd2^tm1.1Gwu/Pkd2^tm1.1Gwu Tg(Vil1-cre)997Gum/0	involves: C57BL/6 * C57BL/6J * SJL	MGI:6251480
cn91	Spint1^tm2.1Hk/Spint1^tm2.1Hk Tg(Vil1-cre)997Gum/0	involves: C57BL/6 * C57BL/6J * SJL	MGI:5304853
cn92	Zfp148^tm1.1Jmer/Zfp148^tm1.1Jmer Tg(Vil1-cre)997Gum/0	involves: C57BL/6 * C57BL/6J * SJL	MGI:5502215
cn93	Mcc^tm1.1Maija/Mcc^tm1.1Maija Tg(Vil1-cre)997Gum/0	involves: C57BL/6 * C57BL/6J * SJL	MGI:6456093
cn94	Lpcat3^tm1c(EUCOMM)Wtsi/Lpcat3^tm1c(EUCOMM)Wtsi Tg(Vil1-cre)997Gum/0	involves: C57BL/6 * C57BL/6N * SJL	MGI:5822876
cn95	Map3k8^tm1.1Gkl/Map3k8^tm1.1Gkl Tg(Vil1-cre)997Gum/0	involves: C57BL/6 * FVB/N * SJL	MGI:5476714
cn96	Rdh7^tm1c(KOMP)Wtsi/Rdh7^tm1c(KOMP)Wtsi Tg(RARE-Hspa1b/lacZ)12Jrt/0 Tg(Vil1-cre)997Gum/0	involves: C57BL/6J * C57BL/6N * CD-1 * SJL	MGI:6362927
cn97	Atg16l1^tm1c(EUCOMM)Wtsi/Atg16l1^tm1c(EUCOMM)Wtsi Tg(Vil1-cre)997Gum/?	involves: C57BL/6J * C57BL/6N * SJL	MGI:5696541
cn98	Api5^em1Cad/Api5^+ Atg16l1^tm1c(EUCOMM)Wtsi/Atg16l1^tm1c(EUCOMM)Wtsi Tg(Vil1-cre)997Gum/0	involves: C57BL/6J * C57BL/6N * SJL	MGI:7564126
cn99	Api5^em1Cad/Api5^em1Cad Atg16l1^tm1c(EUCOMM)Wtsi/Atg16l1^tm1c(EUCOMM)Wtsi Tg(Vil1-cre)997Gum/0	involves: C57BL/6J * C57BL/6N * SJL	MGI:7564119
cn100	Tg(Vil1-cre)997Gum/? Tlr4^lps-del/Tlr4^lps-del Tlr5^tm1.1Gewr/Tlr5^tm1.1Gewr	involves: C57BL/6J * C57BL/6NTac * C57BL/10ScN * SJL	MGI:5751557
cn101	Tg(Vil1-cre)997Gum/? Tlr5^tm1.1Gewr/Tlr5^tm1.1Gewr	involves: C57BL/6J * C57BL/6NTac * SJL/J	MGI:5751550
cn102	Ano10^tm1Jrr/Ano10^tm1Jrr Tg(Vil1-cre)997Gum/0	involves: C57BL/6J * SJL	MGI:6151439
cn103	Il15ra^tm1Ama/Il15ra^tm2.1Ama Tg(Vil1-cre)997Gum/0	involves: C57BL/6J * SJL	MGI:4417845
cn104	Ltbr^tm1Avt/Ltbr^tm1Avt Tg(Vil1-cre)997Gum/0	involves: C57BL/6J * SJL	MGI:4453319
cn105	Frmd8^em2Smoc/Frmd8^em2Smoc Tg(Vil1-cre)997Gum/0	involves: C57BL/6J * SJL	MGI:7549294
cn106	Apc^Min/Apc^+ Igf2bp1^tm1Vssp/Igf2bp1^tm1Vssp Tg(Vil1-cre)997Gum/0	involves: C57BL/6J * SJL	MGI:5523866
cn107	Cdc42^tm1Brak/Cdc42^+ Rab8a^tm1.1Aha/Rab8a^+ Tg(Vil1-cre)997Gum/0	involves: C57BL/6J * SJL	MGI:5427871
cn108	Cdc42^tm1Brak/Cdc42^tm1Brak Tg(Vil1-cre)997Gum/0	involves: C57BL/6J * SJL	MGI:5427868
cn109	Nox1^tm1.1Anrt/Nox1^tm1.1Anrt Tg(Vil1-cre)997Gum/0	involves: C57BL/6J * SJL	MGI:5486337
cn110	Sec24c^tm1c(EUCOMM)Wtsi/Sec24c^tm1c(EUCOMM)Wtsi Tg(Vil1-cre)997Gum/0	involves: C57BL/6 * SJL	MGI:5896385
cn111	Rab8a^tm1.1Aha/Rab8a^tm1.1Aha Tg(Vil1-cre)997Gum/?	involves: C57BL/6 * SJL	MGI:3720321
cn112	Arfrp1^tm2Asch/Arfrp1^tm2Asch Tg(Vil1-cre)997Gum/?	involves: C57BL/6 * SJL	MGI:3821726
cn113	Rab8a^tm1.1Aha/Rab8a^tm1.2Aha Tg(Vil1-cre)997Gum/?	involves: C57BL/6 * SJL	MGI:3720322
cn114	Atg16l1^tm1Kuv/Atg16l1^tm1Kuv Tg(Vil1-cre)997Gum/0	involves: C57BL/6 * SJL	MGI:5559513
cn115	Abcg5^tm1.1Hobb/Abcg5^tm1.1Hobb Abcg8^tm1.1Hobb/Abcg8^tm1.1Hobb Tg(Vil1-cre)997Gum/?	involves: C57BL/6 * SJL	MGI:5607632

Genotype
MGI:6296753

cn1

• Allelic Composition: Atg16l1^tm1Kuv/Atg16l1^tm1Kuv; Tg(Vil1-cre)997Gum/0
• Genetic Background: B6.Cg-Atg16l1^tm1Kuv Tg(Vil1-cre)997Gum

• ♀: phenotype observed in females
• ♂: phenotype observed in males
• N: normal phenotype

digestive/alimentary system

increased enterocyte apoptosis ( J:269933 )

• in the ileum of DSS-treated mice exacerbated by IL22 treatment

• however, co-treatment with anti-IFNAR antibodies reduces the crypt region cell death under hard DSS treatment plus IL22

• organoid cell death induced by IFNbeta is amplified

increased susceptibility to induced colitis ( J:269933 )

• under a harsh DSS treatment regime, mice exhibit increased inflammatory regardless of anti-IFNAR treatment compared with control mice

• however, severity of colonic inflammation is not exacerbated by IL22 treatment

small intestinal inflammation ( J:269933 )

• under mild or harsh DSS treatment regimes, mice exhibit increased ileal inflammation exacerbated by IL22 treatment compared with control mice

• however, co-treatment with anti-IFNAR antibodies reduces the severity of small intestinal inflammation under hard DSS treatment plus IL22

growth/size/body

decreased body weight ( J:269933 )

• in mice treated with IL22 and DSS

immune system

increased susceptibility to induced colitis ( J:269933 )

• under a harsh DSS treatment regime, mice exhibit increased inflammatory regardless of anti-IFNAR treatment compared with control mice

• however, severity of colonic inflammation is not exacerbated by IL22 treatment

small intestinal inflammation ( J:269933 )

• under mild or harsh DSS treatment regimes, mice exhibit increased ileal inflammation exacerbated by IL22 treatment compared with control mice

• however, co-treatment with anti-IFNAR antibodies reduces the severity of small intestinal inflammation under hard DSS treatment plus IL22

cellular

increased enterocyte apoptosis ( J:269933 )

• in the ileum of DSS-treated mice exacerbated by IL22 treatment

• however, co-treatment with anti-IFNAR antibodies reduces the crypt region cell death under hard DSS treatment plus IL22

• organoid cell death induced by IFNbeta is amplified

Genotype
MGI:6296755

cn2

• Allelic Composition: Atg16l1^tm1Kuv/Atg16l1^tm1Kuv; Tg(Vil1-cre)997Gum/0; Xbp1^tm2Glm/Xbp1^tm2Glm
• Genetic Background: B6.Cg-Atg16l1^tm1Kuv Xbp1^tm2Glm Tg(Vil1-cre)997Gum

digestive/alimentary system

increased enterocyte apoptosis ( J:269933 )

• in the ileum of mice exacerbated by IL22 treatment

small intestinal inflammation ( J:269933 )

• in the ileum of mice exacerbated by IL22 treatment

immune system

small intestinal inflammation ( J:269933 )

• in the ileum of mice exacerbated by IL22 treatment

cellular

increased enterocyte apoptosis ( J:269933 )

• in the ileum of mice exacerbated by IL22 treatment

Genotype
MGI:5293402

cn3

• Allelic Composition: Cyld^tm1.1Mpa/Cyld^tm1.1Mpa; Ikbkg^tm1.1Mpa/Y; Tg(Vil1-cre)997Gum/0
• Genetic Background: B6.Cg-Cyld^tm1.1Mpa Ikbkg^tm1.1Mpa Tg(Vil1-cre)997Gum

digestive/alimentary system

crypts of Lieberkuhn abscesses ( J:175865 )

♂

colitis ( J:175865 )

♂ • as in Ikbkg^tm1.1Mpa/Ikbkg^tm1.1Mpa Tg(Vil-cre)997Gum

endocrine/exocrine glands

crypts of Lieberkuhn abscesses ( J:175865 )

♂

immune system

colitis ( J:175865 )

♂ • as in Ikbkg^tm1.1Mpa/Ikbkg^tm1.1Mpa Tg(Vil-cre)997Gum

Genotype
MGI:5293401

cn4

• Allelic Composition: Cyld^tm1.1Mpa/Cyld^tm1.1Mpa; Ikbkg^tm1.1Mpa/Ikbkg^tm1.1Mpa; Tg(Vil1-cre)997Gum/0
• Genetic Background: B6.Cg-Cyld^tm1.1Mpa Ikbkg^tm1.1Mpa Tg(Vil1-cre)997Gum

digestive/alimentary system

crypts of Lieberkuhn abscesses ( J:175865 )

♀

colitis ( J:175865 )

♀ • as in Ikbkg^tm1.1Mpa/Ikbkg^tm1.1Mpa Tg(Vil-cre)997Gum

endocrine/exocrine glands

crypts of Lieberkuhn abscesses ( J:175865 )

♀

immune system

colitis ( J:175865 )

♀ • as in Ikbkg^tm1.1Mpa/Ikbkg^tm1.1Mpa Tg(Vil-cre)997Gum

Genotype
MGI:5293400

cn5

• Allelic Composition: Cyld^tm1.1Mpa/Cyld^tm1.1Mpa; Fadd^tm1Mpa/Fadd^tm1Mpa; Tg(Vil1-cre)997Gum/0
• Genetic Background: B6.Cg-Fadd^tm1Mpa Cyld^tm1.1Mpa Tg(Vil1-cre)997Gum

digestive/alimentary system

digestive/alimentary phenotype ( J:175865 )

N • mice do not develop colitis

decreased Paneth cell number ( J:175865 )

• reduced numbers

cecum inflammation ( J:175865 )

endocrine/exocrine glands

decreased Paneth cell number ( J:175865 )

• reduced numbers

immune system

cecum inflammation ( J:175865 )

Genotype
MGI:5293405

cn6

• Allelic Composition: Fadd^tm1Mpa/Fadd^tm1Mpa; Myd88^tm1Aki/Myd88^tm1Aki; Tg(Vil1-cre)997Gum/0
• Genetic Background: B6.Cg-Fadd^tm1Mpa Myd88^tm1Aki Tg(Vil1-cre)997Gum

digestive/alimentary system

digestive/alimentary phenotype ( J:175865 )

N • mice do not develop colitis

decreased Paneth cell number ( J:175865 )

• reduced numbers

cecum inflammation ( J:175865 )

endocrine/exocrine glands

decreased Paneth cell number ( J:175865 )

• reduced numbers

immune system

cecum inflammation ( J:175865 )

Genotype
MGI:5293399

cn7

• Allelic Composition: Fadd^tm1Mpa/Fadd^tm1Mpa; Ripk3^tm1Vmd/Ripk3^tm1Vmd; Tg(Vil1-cre)997Gum/0
• Genetic Background: B6.Cg-Fadd^tm1Mpa Ripk3^tm1Vmd Tg(Vil1-cre)997Gum

mortality/aging

mortality/aging ( J:175865 )

N • mice exhibit normal survival

digestive/alimentary system

digestive/alimentary phenotype ( J:175865 )

N • mice exhibit normal small intestine and colon morphology

Genotype
MGI:5293398

cn8

• Allelic Composition: Fadd^tm1Mpa/Fadd^tm1Mpa; Tg(Vil1-cre)997Gum/0
• Genetic Background: B6.Cg-Fadd^tm1Mpa Tg(Vil1-cre)997Gum

mortality/aging

postnatal lethality, incomplete penetrance ( J:175865 )

• 50% of mice die before weaning

digestive/alimentary system

diarrhea ( J:175865 )

abnormal intestinal mucosa morphology ( J:175865 )

• thickened colon mucosa, ulceration, and altered vascularization

• mucosal edema in the cecum

decreased Paneth cell number ( J:175865 )

• reduced numbers that are not rescued by antibiotic treatment

crypts of Lieberkuhn abscesses ( J:175865 )

intestinal ulcer ( J:175865 )

abnormal cecum morphology ( J:175865 )

• enteritis with blunted and fused villi, mucosal edema, and increased cellularity of the lamina propria

abnormal colon morphology ( J:175865 )

• mice exhibit shorter and thicker colons with thickened colon mucosa, ulceration, and altered vascularization compared with control mice

abnormal enterocyte physiology ( J:175865 )

• caspase-independent cell death occurs in the small intestine

increased enterocyte apoptosis ( J:175865 )

• in the colon

abnormal enterocyte proliferation ( J:175865 )

• increased in the colon and cecum

cecum inflammation ( J:175865 )

• with increased number of granulocytes, blunted and fused villi, mucosal edema, and increased cellularity of the lamina propria that are not rescued by antibiotic treatment

colitis ( J:175865 )

• as early as 2 weeks of age, mice develop T and B cell infiltration-independent colitis with infiltration of F4/80+, Gr-1+, T, and B cells unlike co-housed Fadd^tm1Mpa control mice

• however, colitis is attenuated by treatment with a broad-spectrum antibiotics

growth/size/body

decreased body weight ( J:175865 )

immune system

cecum inflammation ( J:175865 )

• with increased number of granulocytes, blunted and fused villi, mucosal edema, and increased cellularity of the lamina propria that are not rescued by antibiotic treatment

colitis ( J:175865 )

• as early as 2 weeks of age, mice develop T and B cell infiltration-independent colitis with infiltration of F4/80+, Gr-1+, T, and B cells unlike co-housed Fadd^tm1Mpa control mice

• however, colitis is attenuated by treatment with a broad-spectrum antibiotics

endocrine/exocrine glands

decreased Paneth cell number ( J:175865 )

• reduced numbers that are not rescued by antibiotic treatment

crypts of Lieberkuhn abscesses ( J:175865 )

cellular

increased enterocyte apoptosis ( J:175865 )

• in the colon

abnormal enterocyte proliferation ( J:175865 )

• increased in the colon and cecum

Genotype
MGI:5293404

cn9

• Allelic Composition: Fadd^tm1Mpa/Fadd^tm1Mpa; Tnf^tm1Gkl/Tnf^tm1Gkl; Tg(Vil1-cre)997Gum/0
• Genetic Background: B6.Cg-Fadd^tm1Mpa Tnf^tm1Gkl Tg(Vil1-cre)997Gum

digestive/alimentary system

decreased Paneth cell number ( J:175865 )

• reduced numbers

cecum inflammation ( J:175865 )

colitis ( J:175865 )

• less severe than in Fadd^tm1Mpa/Fadd^tm1Mpa Tg(Vil-cre)997Gum mice

endocrine/exocrine glands

decreased Paneth cell number ( J:175865 )

• reduced numbers

immune system

cecum inflammation ( J:175865 )

colitis ( J:175865 )

• less severe than in Fadd^tm1Mpa/Fadd^tm1Mpa Tg(Vil-cre)997Gum mice

Genotype
MGI:5293403

cn10

• Allelic Composition: Ikbkg^tm1.1Mpa/Ikbkg^tm1.1Mpa; Tg(Vil1-cre)997Gum/0
• Genetic Background: B6.Cg-Ikbkg^tm1.1Mpa Tg(Vil1-cre)997Gum

digestive/alimentary system

crypts of Lieberkuhn abscesses ( J:175865 )

♀

colitis ( J:175865 )

♀ • severe and chronic

endocrine/exocrine glands

crypts of Lieberkuhn abscesses ( J:175865 )

♀

immune system

colitis ( J:175865 )

♀ • severe and chronic

Genotype
MGI:5293406

cn11

• Allelic Composition: Ikbkg^tm1.1Mpa/Y; Tg(Vil1-cre)997Gum/0
• Genetic Background: B6.Cg-Ikbkg^tm1.1Mpa Tg(Vil1-cre)997Gum

digestive/alimentary system

crypts of Lieberkuhn abscesses ( J:175865 )

♂

colitis ( J:175865 )

♂ • severe and chronic

endocrine/exocrine glands

crypts of Lieberkuhn abscesses ( J:175865 )

♂

immune system

colitis ( J:175865 )

♂ • severe and chronic

Genotype
MGI:5896658

cn12

• Allelic Composition: Naipc^tm1Kmma/Naipc^tm1Kmma; Tg(Vil1-cre)997Gum/0
• Genetic Background: B6.Cg-Naipc^tm1Kmma Tg(Vil1-cre)997Gum

neoplasm

increased incidence of tumors by chemical induction ( J:222114 )

• in mice treated with azoxymethane and dextran sulfate sodium

digestive/alimentary system

decreased susceptibility to induced colitis ( J:222114 )

• mice treated with DSS exhibit reduced severity of colitis, weight loss and colon shortening compared with control mice

growth/size/body

decreased susceptibility to weight loss ( J:222114 )

• in DSS-treated mice

homeostasis/metabolism

increased incidence of tumors by chemical induction ( J:222114 )

• in mice treated with azoxymethane and dextran sulfate sodium

immune system

decreased susceptibility to induced colitis ( J:222114 )

• mice treated with DSS exhibit reduced severity of colitis, weight loss and colon shortening compared with control mice

Genotype
MGI:5433666

cn13

• Allelic Composition: Slc3a2^tm1.1Merl/Slc3a2^tm1.1Merl; Tg(Vil1-cre)997Gum/0
• Genetic Background: B6.Cg-Slc3a2^tm1.1Merl Tg(Vil1-cre)997Gum

mortality/aging

preweaning lethality, incomplete penetrance ( J:173946 )

• fewer than expected mice are born indicating embryonic of neonatal lethality

Genotype
MGI:5433667

cn14

• Allelic Composition: Slc3a2^tm1.1Merl/Slc3a2⁺; Tg(Vil1-cre)997Gum/0
• Genetic Background: B6.Cg-Slc3a2^tm1.1Merl Tg(Vil1-cre)997Gum

Slc3a2^tm1.1Merl/Slc3a2⁺ Tg(Vil1-cre)997Gum/0 mice are protected from dextran sodium sulfate-induced colitis

mortality/aging

decreased susceptibility to xenobiotic induced morbidity/mortality ( J:173946 )

• in mice treated with azoxymethane and DSS

digestive/alimentary system

abnormal enterocyte proliferation ( J:173946 )

• mice treated with azoxymethane and DSS exhibit reduced colonic epithelial cell proliferation compared with control mice

decreased susceptibility to induced colitis ( J:173946 )

• DSS-treated mice exhibit reduced weight loss, decreased rectal bleeding, no diarrhea, reduced colon shortening, reduced crypt damage and fewer inflammatory infiltrates and ulcerations compared with control mice

neoplasm

decreased incidence of tumors by chemical induction ( J:173946 )

• mice treated with azoxymethane and DSS exhibit fewer and smaller adenomas than in control mice

decreased tumor growth/size ( J:173946 )

• in mice treated with azoxymethane and DSS

growth/size/body

decreased susceptibility to weight loss ( J:173946 )

• in DSS-treated mice or treated with azoxymethane and DSS

homeostasis/metabolism

decreased susceptibility to xenobiotic induced morbidity/mortality ( J:173946 )

• in mice treated with azoxymethane and DSS

decreased incidence of tumors by chemical induction ( J:173946 )

• mice treated with azoxymethane and DSS exhibit fewer and smaller adenomas than in control mice

immune system

decreased susceptibility to induced colitis ( J:173946 )

• DSS-treated mice exhibit reduced weight loss, decreased rectal bleeding, no diarrhea, reduced colon shortening, reduced crypt damage and fewer inflammatory infiltrates and ulcerations compared with control mice

cellular

abnormal enterocyte proliferation ( J:173946 )

• mice treated with azoxymethane and DSS exhibit reduced colonic epithelial cell proliferation compared with control mice

Genotype
MGI:7716851

cn15

• Allelic Composition: Smyd5^{tm1a(EUCOMM)Wtsi}/Smyd5^{tm1a(EUCOMM)Wtsi}; Tg(Vil1-cre)997Gum/0
• Genetic Background: B6.Cg-Smyd5^{tm1a(EUCOMM)Wtsi} Tg(Vil1-cre)997Gum

immune system

decreased susceptibility to induced colitis ( J:339411 )

• mice exhibit protection from dextran sulfate sodium (DSS)-induced colitis, with mice losing less weight than controls, better-shaped stools and less rectal bleeding, less colon shortening, less extensive ulceration and erosion, less severe inflammatory cell infiltration, less thickening of mucosa, and improved epithelial barrier integrity

digestive/alimentary system

abnormal enterocyte morphology ( J:339411 )

• mice show a slight, but significant, increase in the number of mitochondria in intestinal epithelial cells

• however, mitochondrial perimeter and circularity in intestinal epithelial cells do not show any differences

• however, mice show no other abnormalities in the gastrointestinal tract under basal conditions

decreased susceptibility to induced colitis ( J:339411 )

• mice exhibit protection from dextran sulfate sodium (DSS)-induced colitis, with mice losing less weight than controls, better-shaped stools and less rectal bleeding, less colon shortening, less extensive ulceration and erosion, less severe inflammatory cell infiltration, less thickening of mucosa, and improved epithelial barrier integrity

Genotype
MGI:4829679

cn16

• Allelic Composition: Tnfaip3^tm1.1Gvl/Tnfaip3^tm1.1Gvl; Tg(Vil1-cre)997Gum/0
• Genetic Background: B6.Cg-Tnfaip3^tm1.1Gvl Tg(Vil1-cre)997Gum

mortality/aging

increased susceptibility to induced morbidity/mortality ( J:163410 )

• TNF-treated mice exhibit increased mortality compared with similarly treated wild-type mice

• however, mice treated with broad-spectrum antibiotics are protected against TNF toxicity-induced lethality

increased susceptibility to xenobiotic induced morbidity/mortality ( J:163410 )

• in DDS-treated mice during the recovery phase

homeostasis/metabolism

impaired adaptive thermogenesis ( J:163410 )

• TNF-treated mice exhibit hypothermia unlike similarly treated wild-type mice

increased circulating interleukin-6 level ( J:163410 )

• in DDS-treated mice

increased circulating alanine transaminase level ( J:163410 )

• in TNF-treated mice

increased circulating aspartate transaminase level ( J:163410 )

• in TNF-treated mice

abnormal response/metabolism to endogenous compounds ( J:163410 )

• TNF-treated mice exhibit TNF toxicity (including hypothermia, severe diarrhea, and increased mortality) at doses that are sub-lethal in wild-type mice

• however, mice treated with broad-spectrum antibiotics are protected against TNF toxicity-induced mortality, hypothermia, and liver damage

increased susceptibility to xenobiotic induced morbidity/mortality ( J:163410 )

• in DDS-treated mice during the recovery phase

digestive/alimentary system

rectal hemorrhage ( J:163410 )

• in DDS-treated mice

increased enterocyte apoptosis ( J:163410 )

• in DDS-treated mice and more profound in the recovery phase

• in TNF-treated mice

diarrhea ( J:163410 )

• in DDS-treated mice

• in TNF-treated mice

abnormal small intestine crypts of Lieberkuhn morphology ( J:163410 )

• TNF-treated mice exhibit increased intestinal damage with near complete loss of crypt-villus structure unlike in similarly treated wild-type mice

• antibiotic treatment does not rescue TNF-induced intestinal damage

decreased colon length ( J:163410 )

• DDS-treated mice exhibit increased colonic shortening compared with wild-type mice

increased susceptibility to induced colitis ( J:163410 )

• DDS-treated mice exhibit more severe colitis symptoms such as rectal bleeding, diarrhea, colon shortening, colonic inflammation, mucosal damage, crypt loss, immune cell infiltration, increased IL6 serum levels, loss of body weight, increased intestinal epithelial cell apoptosis, and mortality compared with wild-type mice

growth/size/body

increased susceptibility to weight loss ( J:163410 )

• in DDS-treated mice

cardiovascular system

rectal hemorrhage ( J:163410 )

• in DDS-treated mice

liver/biliary system

liver degeneration ( J:163410 )

• in TNF-treated mice

immune system

increased susceptibility to induced colitis ( J:163410 )

• DDS-treated mice exhibit more severe colitis symptoms such as rectal bleeding, diarrhea, colon shortening, colonic inflammation, mucosal damage, crypt loss, immune cell infiltration, increased IL6 serum levels, loss of body weight, increased intestinal epithelial cell apoptosis, and mortality compared with wild-type mice

increased circulating interleukin-6 level ( J:163410 )

• in DDS-treated mice

endocrine/exocrine glands

abnormal small intestine crypts of Lieberkuhn morphology ( J:163410 )

• TNF-treated mice exhibit increased intestinal damage with near complete loss of crypt-villus structure unlike in similarly treated wild-type mice

• antibiotic treatment does not rescue TNF-induced intestinal damage

cellular

increased enterocyte apoptosis ( J:163410 )

• in DDS-treated mice and more profound in the recovery phase

• in TNF-treated mice

Genotype
MGI:6093452

cn17

• Allelic Composition: Gt(ROSA)26Sor^{tm1(CAG-CAMK2G*T287D,-EGFP)Whua}/Gt(ROSA)26Sor⁺; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: 129 * C57BL/6

homeostasis/metabolism

increased incidence of tumors by chemical induction ( J:243363 )

• mice injected with azoxymethane (AOM) followed by DSS administration show increased distal colorectal cancer compared to controls, with higher average tumor number and increased number of small tumors and proportion of high-grade tumors

immune system

decreased susceptibility to induced colitis ( J:243363 )

• mice treated with dextran sodium sulfate (DSS) to induce colitis are protected from colitis-induced injury, showing suppression of weight loss and colonic shortening, decreased rectal bleeding rate, better epithelial crypt morphology, and higher proliferation rates and decreased cell death in colonic epithelial tissue compared to controls

neoplasm

increased incidence of tumors by chemical induction ( J:243363 )

• mice injected with azoxymethane (AOM) followed by DSS administration show increased distal colorectal cancer compared to controls, with higher average tumor number and increased number of small tumors and proportion of high-grade tumors

digestive/alimentary system

digestive/alimentary phenotype ( J:243363 )

N • mice exhibit normal gastrointestinal development and do not show signs of spontaneous colorectal tumor development up to 8 months of age

decreased susceptibility to induced colitis ( J:243363 )

• mice treated with dextran sodium sulfate (DSS) to induce colitis are protected from colitis-induced injury, showing suppression of weight loss and colonic shortening, decreased rectal bleeding rate, better epithelial crypt morphology, and higher proliferation rates and decreased cell death in colonic epithelial tissue compared to controls

Genotype
MGI:5760132

cn18

• Allelic Composition: Slc2a9^tm1Khm/Slc2a9^tm1Khm; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: 129 * C57BL/6 * C57BL/6J

growth/size/body

increased body fat mass ( J:221544 )

• significantly increased body fat mass relative to control mice

digestive/alimentary system

abnormal feces composition ( J:221544 )

• liquid chromatography-mass spectrometry of stool extracts revealed significantly reduced stool urate concentrations relative to controls, suggesting impaired enterocyte uptake and efflux into stool

abnormal enterocyte physiology ( J:221544 )

• isolated villous enterocytes display a ~65% reduction in [14C]-urate uptake relative to control enterocytes

adipose tissue

increased body fat mass ( J:221544 )

• significantly increased body fat mass relative to control mice

increased percent body fat/body weight ( J:221544 )

• significantly increased body fat percentage relative to control mice

homeostasis/metabolism

increased blood uric acid level ( J:221544 )

• significantly higher serum uric acid concentrations in fasting 6-8-week-old mice

• plasma uric acid levels are significantly decreased following allopurinol treatment

increased circulating insulin level ( J:221544 )

• ~40% increase in fasting plasma insulin levels relative to controls

abnormal circulating lipid level ( J:221544 )

• mice exhibit dyslipidemia, unlike control mice

increased circulating cholesterol level ( J:221544 )

• significantly increased total plasma cholesterol levels in fasting mice relative controls

• total plasma cholesterol levels are significantly lowered following allopurinol treatment

increased circulating free fatty acids level ( J:221544 )

• significantly increased plasma free fatty acid levels in fasting mice relative controls

• fasting free fatty acid levels are not significantly affected by allopurinol treatment

increased circulating triglyceride level ( J:221544 )

• significantly increased plasma triglyceride levels in fasting mice relative controls

• fasting triglyceride levels are not significantly affected by allopurinol treatment

increased energy expenditure ( J:221544 )

• higher resting energy expenditure relative to control mice, as determined by indirect calorimetry

increased oxygen consumption ( J:221544 )

• significantly increased volume of inspired oxygen in both 8- and 16-week-old mice relative controls

decreased respiratory quotient ( J:221544 )

• significantly decreased respiratory exchange ratio in 8-week-old mice relative controls

insulin resistance ( J:221544 )

• signs of early insulin resistance, with an ~40% increase in fasting plasma insulin levels in the context of normal fasting blood glucose and insulin tolerance testing

increased liver free fatty acids level ( J:221544 )

• hepatic free fatty acids are elevated in liver homogenates relative to controls

increased liver triglyceride level ( J:221544 )

• hepatic triglycerides are elevated in liver homogenates relative to controls

• hepatic triglyceride content is significantly lowered following allopurinol treatment

increased urine uric acid level ( J:221544 )

• significantly higher urine uric acid concentrations in fasting 6-8-week-old mice

• urine urate concentrations are not significantly altered by allopurinol treatment

abnormal metabolism ( J:221544 )

• mice develop early-onset spontaneous hyperuricemic metabolic syndrome that is partially reversed by allopurinol, a xanthine oxidase inhibitor

increased basal metabolism ( J:221544 )

• significantly increased heat production in 8-week-old mice relative controls

cardiovascular system

abnormal heart echocardiography feature ( J:221544 )

• echocardiography revealed significantly increased basal heart rate, decreased diastolic left ventricular internal diameter with increased relative wall thickness, suggesting cardiac hypertrophic remodeling

• echocardiographic parameters are not significantly altered by allopurinol treatment

increased heart rate ( J:221544 )

• significantly increased basal heart rate relative to controls, as shown by echocardiography

hypertension ( J:221544 )

• baseline hypertension, as shown by significantly increased systolic, diastolic, and mean blood pressure in non-fasting mice relative controls

• blood pressure is significantly lowered following allopurinol treatment

liver/biliary system

increased liver free fatty acids level ( J:221544 )

• hepatic free fatty acids are elevated in liver homogenates relative to controls

increased liver triglyceride level ( J:221544 )

• hepatic triglycerides are elevated in liver homogenates relative to controls

• hepatic triglyceride content is significantly lowered following allopurinol treatment

hepatic steatosis ( J:221544 )

• increased hepatic fat deposition relative to controls

liver fibrosis ( J:221544 )

renal/urinary system

increased urine uric acid level ( J:221544 )

• significantly higher urine uric acid concentrations in fasting 6-8-week-old mice

• urine urate concentrations are not significantly altered by allopurinol treatment

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
abdominal obesity-metabolic syndrome		DOID:0060611	OMIM:PS605552	J:221544
hyperuricemia		DOID:1920		J:221544

Genotype
MGI:5547498

cn19

• Allelic Composition: Apc^Min/Apc⁺; Hsd11b2^tm1.1Mzz/Hsd11b2^tm1.1Mzz; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: 129 * C57BL/6 * C57BL/6J

neoplasm

increased intestinal adenoma incidence ( J:205456 )

• fewer total intestinal adenoma at 20 weeks with prevented initiation of polyp formation compared with Apc^Min heterozygotes

decreased tumor growth/size ( J:205456 )

• reduced proliferation and increased apoptosis compared with tumors from Apc^Min heterozygotes

homeostasis/metabolism

abnormal corticosterone level ( J:205456 )

• 10-fold higher corticosterone (active glucocorticoid) levels in the intestine compared with Apc^Min heterozygotes

• 11-keto-corticosterone (inactive glucocorticoid) levels is lower in the intestine compared with Apc^Min heterozygotes

digestive/alimentary system

increased intestinal adenoma incidence ( J:205456 )

• fewer total intestinal adenoma at 20 weeks with prevented initiation of polyp formation compared with Apc^Min heterozygotes

Genotype
MGI:3771153

cn20

• Allelic Composition: Slc31a1^tm2Djt/Slc31a1^tm2Djt; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: 129 * C57BL/6 * FVB/N * SJL

mortality/aging

postnatal lethality, incomplete penetrance ( J:129741 )

• most mice die by P14 with severe weight loss and nearly all mice die by weaning

• however, postnatal lethality can be rescued by intraperitoneal injection of copper

homeostasis/metabolism

abnormal copper level ( J:129741 )

• copper levels are reduced in the heart, brain, kidney and spleen to 18%, 20%, less than 40% and 70%, respectively, of wild-type levels

• copper levels are over 8-fold higher in intestinal epithelial cells compared to wild-type

decreased circulating copper level ( J:129741 )

• serum copper levels are less than 40% of wild-type

abnormal liver copper level ( J:129741 )

• copper content in the liver reduced to 5% of wild-type

hemosiderosis ( J:129741 )

• iron content in the liver is increased 4-fold compared to in wild-type mice

cardiovascular system

abnormal heart morphology ( J:129741 )

• cardiac tissue exhibits large vacuoles and swollen mitochondria not present in wild-type cardiac tissue

• however, abnormal cardiac tissue morphology can be partially rescued by intraperitoneal injection of copper

enlarged heart ( J:129741 )

• hearts are enlarged 20% compared to wild-type

• cardiac hypertrophy occurs at 2 weeks of age

growth/size/body

enlarged heart ( J:129741 )

• hearts are enlarged 20% compared to wild-type

• cardiac hypertrophy occurs at 2 weeks of age

decreased body weight ( J:129741 )

• at P14, mice weigh 4 g instead 9 g for wild-type mice

weight loss ( J:129741 )

• mice die with severe weight loss

• however, postnatal weight lose can be rescued by intraperitoneal injection of copper

postnatal growth retardation ( J:129741 )

• mice exhibit poor growth beginning at day 10

behavior/neurological

ataxia ( J:129741 )

hematopoietic system

decreased spleen weight ( J:129741 )

• spleen weight adjusted for decreased body weight is less than in wild-type mice

pigmentation

hypopigmentation ( J:129741 )

liver/biliary system

abnormal liver copper level ( J:129741 )

• copper content in the liver reduced to 5% of wild-type

immune system

decreased spleen weight ( J:129741 )

• spleen weight adjusted for decreased body weight is less than in wild-type mice

integument

kinked vibrissae ( J:129741 )

• whiskers are kinked and brittle

loose skin ( J:129741 )

• skin laxity

Genotype
MGI:3799251

cn21

• Allelic Composition: Rela^tm1Asba/Rela^tm1Asba; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: 129 * C57BL/6J * SJL

mortality/aging

increased susceptibility to xenobiotic induced morbidity/mortality ( J:131977 )

• following removal of DSS treatment, mice exhibit increased mortality compared to similarly treated wild-type mice

decreased survivor rate ( J:131977 )

• 10% to 15% of mice develop intestinal problems and die prior to day 25

premature death ( J:131977 )

• mice with abdominal irregularities die prior to day 25

digestive/alimentary system

diarrhea ( J:131977 )

• at 2 to 3 days after birth, 10% to 15% of mice exhibit diarrhea and abdominal discoloration unlike wild-type mice

abnormal intestinal epithelium morphology ( J:131977 )

• cell proliferation and apoptosis of the epithelial layer in the colon is increased compared to in wild-type mice

megacolon ( J:131977 )

• distended with air or dark material in 10% to 15% of mice

abnormal small intestine morphology ( J:131977 )

• 10% to 15% of mice exhibit a thin-walled, pale small intestine

abnormal small intestine crypts of Lieberkuhn morphology ( J:131977 )

• severely affected animals display a nearly complete loss of crypt-villus structure in the ileum

abnormal small intestinal villus morphology ( J:131977 )

• severely affected animals display a nearly complete loss of crypt-villus structure in the ileum

impaired intestine regeneration ( J:131977 )

• despite removal of DSS mice continue to exhibit increased intestinal epithelial apoptosis and fail to recover unlike wild-type mice

increased susceptibility to induced colitis ( J:131977 )

• mice are more susceptible to colitis induced by long term DSS treatment than wild-type mice

• unlike wild-type mice, after 5 to 7 days of treatment with DSS mice exhibit rectal bleeding, more severe weight loss, increased mucosal damage, colon epithelial cell proliferation and apoptosis, increased PGE2, IL-6 and MCP-1 levels, and increased immune response

• following removal of DSS treatment, mice exhibit increased mortality compared to similarly treated wild-type mice

• despite removal of DSS mice continue to exhibit increased intestinal epithelial apoptosis

growth/size/body

slow postnatal weight gain ( J:131977 )

• mice with abdominal irregularities exhibit decreased postnatal weight gain compared to wild-type mice

immune system

increased susceptibility to induced colitis ( J:131977 )

• mice are more susceptible to colitis induced by long term DSS treatment than wild-type mice

• unlike wild-type mice, after 5 to 7 days of treatment with DSS mice exhibit rectal bleeding, more severe weight loss, increased mucosal damage, colon epithelial cell proliferation and apoptosis, increased PGE2, IL-6 and MCP-1 levels, and increased immune response

• following removal of DSS treatment, mice exhibit increased mortality compared to similarly treated wild-type mice

• despite removal of DSS mice continue to exhibit increased intestinal epithelial apoptosis

endocrine/exocrine glands

abnormal small intestine crypts of Lieberkuhn morphology ( J:131977 )

• severely affected animals display a nearly complete loss of crypt-villus structure in the ileum

homeostasis/metabolism

increased susceptibility to xenobiotic induced morbidity/mortality ( J:131977 )

• following removal of DSS treatment, mice exhibit increased mortality compared to similarly treated wild-type mice

Genotype
MGI:4362042

cn22

• Allelic Composition: Dlg1^tm1Jhm/Dlg1^tm1Jhm; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: 129 * C57BL/6 * SJL

digestive/alimentary system

abnormal enterocyte morphology ( J:146174 )

• the upper zone surface of epithelial cells in the cecum and ascending colon are shorter than in wild-type mice

Genotype
MGI:4361214

cn23

• Allelic Composition: St14^tm2Bug/St14^tm3Bug; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: 129P2/OlaHsd * 129S6/SvEvTac * Black Swiss * C57BL/6 * SJL

mortality/aging

premature death ( J:153070 )

• short lifespan of a few weeks to up to a 2 months

digestive/alimentary system

digestive/alimentary phenotype ( J:153070 )

N • mice exhibit normal small intestine morphology

abnormal enterocyte proliferation ( J:153070 )

• mice exhibit hyperproliferation of colonic epithelial cells compared with wild-type mice

chronic diarrhea ( J:153070 )

• persistent prior to weaning

abnormal colon morphology ( J:153070 )

• mice exhibit disruption of the colonic tissue architecture, edema, and pervasive inflammation unlike wild-type mice

megacolon ( J:153070 )

• without obstruction

intestinal edema ( J:153070 )

• in the colon

absent digestive secretion ( J:153070 )

colitis ( J:153070 )

homeostasis/metabolism

intestinal edema ( J:153070 )

• in the colon

growth/size/body

decreased body size ( J:153070 )

immune system

colitis ( J:153070 )

cellular

abnormal enterocyte proliferation ( J:153070 )

• mice exhibit hyperproliferation of colonic epithelial cells compared with wild-type mice

Genotype
MGI:5528298

cn24

• Allelic Composition: Braf^tm1.1Brd/Braf⁺; Cdkn2a^tm1.1Brn/Cdkn2a^tm1.1Brn; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6 * SJL

neoplasm

increased intestinal adenoma incidence ( J:199307 )

• 1.3 fold increase in serrated adenomas relative to mice with unmutated Cdkn2a alleles (not statistically significant)

increased carcinoma incidence ( J:199307 )

• 6.4 fold increase in carcinomas relative to mice with unmutated Cdkn2a alleles

digestive/alimentary system

increased intestinal adenoma incidence ( J:199307 )

• 1.3 fold increase in serrated adenomas relative to mice with unmutated Cdkn2a alleles (not statistically significant)

Genotype
MGI:5573123

cn25

• Allelic Composition: Tnfrsf1a^tm3.1Gkl/Tnfrsf1a^tm3.1Gkl; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6 * C57BL/6J * SJL

mortality/aging

decreased susceptibility to induced morbidity/mortality ( J:210950 )

• in mice challenged with TNF

• in B17BL6 tumor-bearing mice treated with TNF and IFN-gamma

homeostasis/metabolism

abnormal response/metabolism to endogenous compounds ( J:210950 )

• mice subjected to TNF challenge exhibit decreased lethality and a reduced loss of intestinal barrier function compared with wild-type mice

Genotype
MGI:5573122

cn26

• Allelic Composition: Tnfrsf1a^tm3.1Gkl/Tnfrsf1a⁺; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6 * C57BL/6J * SJL

mortality/aging

decreased susceptibility to induced morbidity/mortality ( J:210950 )

• in mice challenged with TNF

homeostasis/metabolism

abnormal response/metabolism to endogenous compounds ( J:210950 )

• mice subjected to TNF challenge exhibit decreased lethality and a reduced loss of intestinal barrier function compared with wild-type mice

Genotype
MGI:7564089

cn27

• Allelic Composition: Atg16l1^{tm1c(EUCOMM)Wtsi}/Atg16l1^{tm1c(EUCOMM)Wtsi}; Tcrd^tm1Mom/Tcrd^tm1Mom; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6J * C57BL/6N * SJL

mortality/aging

increased susceptibility to colitis induced morbidity/mortality ( J:340266 )

• increased susceptibility to mortality following treatment with 5% dextran sulfate sodium even in the absence of mouse norovirus infection

• injection with recombinant Api5 improved survival

digestive/alimentary system

increased small intestinal crypt cell apoptosis ( J:340266 )

abnormal Paneth cell morphology ( J:340266 )

• remaining Paneth cells display abnormal lysozyme staining patterns

decreased Paneth cell number ( J:340266 )

• spontaneous Paneth cell loss in the absence of infection with murine norovirus

• however, goblet cell numbers are similar to controls

decreased small intestinal villus height ( J:340266 )

increased susceptibility to colitis induced morbidity/mortality ( J:340266 )

• increased susceptibility to mortality following treatment with 5% dextran sulfate sodium even in the absence of mouse norovirus infection

• injection with recombinant Api5 improved survival

homeostasis/metabolism

abnormal cytokine level ( J:340266 )

• increased local levels of cytokine production in the small intestine

immune system

increased susceptibility to colitis induced morbidity/mortality ( J:340266 )

• increased susceptibility to mortality following treatment with 5% dextran sulfate sodium even in the absence of mouse norovirus infection

• injection with recombinant Api5 improved survival

abnormal cytokine level ( J:340266 )

• increased local levels of cytokine production in the small intestine

cellular

increased small intestinal crypt cell apoptosis ( J:340266 )

endocrine/exocrine glands

abnormal Paneth cell morphology ( J:340266 )

• remaining Paneth cells display abnormal lysozyme staining patterns

decreased Paneth cell number ( J:340266 )

• spontaneous Paneth cell loss in the absence of infection with murine norovirus

• however, goblet cell numbers are similar to controls

Genotype
MGI:5751560

cn28

• Allelic Composition: Il10^tm1Cgn/Il10^tm1Cgn; Tg(Vil1-cre)997Gum/?; Tlr5^tm1.1Gewr/Tlr5^tm1.1Gewr
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6J * C57BL/6NTac * SJL

digestive/alimentary system

rectal prolapse ( J:229155 )

• 100% of mice develop rectal prolapse by approximately 75 days

abnormal gut flora balance ( J:229155 )

• increase in levels of fecal bacteria as compared to Il10 mutation alone

colitis ( J:229155 )

• severe uniform colitis in 100% of mice; presence of intestinal endothelial cell (IEC)-specific Tlr5 null mutation exacerbates phenotype

• increased incidence of rectal prolapse; presence of IEC-specific Tlr5 null mutation exacerbates phenotype

immune system

colitis ( J:229155 )

• severe uniform colitis in 100% of mice; presence of intestinal endothelial cell (IEC)-specific Tlr5 null mutation exacerbates phenotype

• increased incidence of rectal prolapse; presence of IEC-specific Tlr5 null mutation exacerbates phenotype

mortality/aging

premature death ( J:229155 )

• mice are euthanized due to rectal prolapse

Genotype
MGI:4838643

cn29

• Allelic Composition: Yap1^tm1.1Dupa/Yap1^tm1.1Dupa; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6J * SJL

mortality/aging

increased susceptibility to xenobiotic induced morbidity/mortality ( J:165471 )

• in DSS-treated mice

digestive/alimentary system

digestive/alimentary phenotype ( J:165471 )

N • mice, whether treated with DSS or not, do not develop colonic polyps

increased enterocyte apoptosis ( J:165471 )

• in DSS-treated mice

abnormal enterocyte proliferation ( J:165471 )

• DSS-treated mice exhibit decreased cell proliferation in the colon compared with similarly treated wild-type mice

increased susceptibility to induced colitis ( J:165471 )

• DSS-treated mice exhibit increased mortality a rapid decrease in body weight, increased apoptotic cells in the colon, and decreased proliferating cells in the colon compared with similarly treated wild-type mice

immune system

increased susceptibility to induced colitis ( J:165471 )

• DSS-treated mice exhibit increased mortality a rapid decrease in body weight, increased apoptotic cells in the colon, and decreased proliferating cells in the colon compared with similarly treated wild-type mice

homeostasis/metabolism

increased susceptibility to xenobiotic induced morbidity/mortality ( J:165471 )

• in DSS-treated mice

growth/size/body

increased susceptibility to weight loss ( J:165471 )

• in DSS-treated mice

cellular

increased enterocyte apoptosis ( J:165471 )

• in DSS-treated mice

abnormal enterocyte proliferation ( J:165471 )

• DSS-treated mice exhibit decreased cell proliferation in the colon compared with similarly treated wild-type mice

Genotype
MGI:4420973

cn30

• Allelic Composition: Gadd45gip1^tm2Kong/Gadd45gip1^tm2Kong; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6J * SJL

Abnormal small intestine morphogenesis in Gadd45gip1^tm2Kong/Gadd45gip1^tm2Kong Tg(Vil1-cre)997Gum/0 embryos

mortality/aging

perinatal lethality, incomplete penetrance ( J:156319 )

• fewer than expected (6 of 52) are found at P1

postnatal lethality, incomplete penetrance ( J:156319 )

• fewer than expected (2 of 157) are found at P21

prenatal lethality, incomplete penetrance ( J:156319 )

• fewer than expected (16 of 83) are found at E18.5

digestive/alimentary system

digestive/alimentary phenotype ( J:156319 )

N • no defect in goblet cell differentiation is detected

abnormal small intestinal crypt cell proliferation ( J:156319 )

• slight but significant decrease in the proliferation of small intestinal crypt cells

abnormal digestive system development ( J:156319 )

• at E18.5, expression analysis indicates that enterocyte differentiation is defective with the cells retaining epithelial characteristics

abnormal enterocyte morphology ( J:156319 )

• at E18.5 small intestine absorptive enterocytes show abnormal tufting of the apical brush border

• at E18 small intestine absorptive enterocytes are irregular in shape and size, have heterogeneously stained cytoplasm and disorganized nuclei

abnormal small intestinal villus morphology ( J:156319 )

• at E18.5 villi are shorter, fewer in number, and abnormally shaped

abnormal small intestinal microvillus morphology ( J:156319 )

• at E18.5 enterocytes contain fewer, shorter microvilli at the apical membranes

decreased small intestinal villus height ( J:156319 )

• at E18.5

decreased small intestinal villus number ( J:156319 )

• at E18.5

cellular

abnormal small intestinal crypt cell proliferation ( J:156319 )

• slight but significant decrease in the proliferation of small intestinal crypt cells

Genotype
MGI:4838642

cn31

• Allelic Composition: Sav1^tm1.1Dupa/Sav1^tm1.1Dupa; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6J * SJL

digestive/alimentary system

abnormal enterocyte proliferation ( J:165471 )

• the colon and small intestine contains increased more and faster proliferating cells compared to in wild-type mice

abnormal large intestine crypts of Lieberkuhn morphology ( J:165471 )

• enlarged in the colon

abnormal small intestine crypts of Lieberkuhn morphology ( J:165471 )

• enlarged

colon polyps ( J:165471 )

• by 13 months of age, all male mice develop colonic polyps with 'saw-tooth' appearance characteristic of sessile serrated polyps unlike wild-type mice

• 3 months after DSS treatment, mice develop colonic polyps unlike similarly treated wild-type mice and well before homozygous mice not treated with DSS

endocrine/exocrine glands

abnormal large intestine crypts of Lieberkuhn morphology ( J:165471 )

• enlarged in the colon

abnormal small intestine crypts of Lieberkuhn morphology ( J:165471 )

• enlarged

cellular

abnormal enterocyte proliferation ( J:165471 )

• the colon and small intestine contains increased more and faster proliferating cells compared to in wild-type mice

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
colonic disease		DOID:5353		J:165471

Genotype
MGI:4838644

cn32

• Allelic Composition: Sav1^tm1.1Dupa/Sav1^tm1.1Dupa; Yap1^tm1.1Dupa/Yap1^tm1.1Dupa; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6J * SJL

digestive/alimentary system

digestive/alimentary phenotype ( J:165471 )

N • mice exhibit normal cell proliferation in the small intestine and colon

N • mice, whether treated with DSS or not, do not develop colonic polyps

Genotype
MGI:5297575

cn33

• Allelic Composition: Myd88^tm1Defr/Myd88^tm1Defr; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6J * SJL

digestive/alimentary system

abnormal gut flora balance ( J:177506 )

• mice exhibit a higher mucosal bacterial loads compared with Myd88^tm1Defr control mice but not as much as in Myd88 null or conditionally knocked-out mice

• however, luminal bacterial loads are normal

Genotype
MGI:5529839

cn34

• Allelic Composition: Ass1^tm1.1Ekoe/Ass1^tm1.1Ekoe; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6 * SJL

homeostasis/metabolism

abnormal amino acid level ( J:203474 )

• citrulline production in the splanchnic region is doubled while arginine production is abolished

• suckling mice exhibit premature induction of the post-weaning pattern of amino acid metabolism in the liver

abnormal circulating amino acid level ( J:203474 )

• aorta veins exhibit increased circulating levels of glutamate, alanine and taurine compared with wild-type mice

• portal veins exhibit increased circulating glutamine, threonine, alanine, taurine, valine and leucine compared with wild-type mice

• renal veins exhibit decreased circulating levels of alanine, taurine, valine, isoleucine and, leucine compared with wild-type mice

• hepatic veins exhibit decreased circulating levels of glutamate, valine, isoleucine. Tryptophan and leucine compared with wild-type mice

• however, circulating lysine levels are normal

decreased circulating arginine level ( J:203474 )

• decreased circulating arginine levels in the hepatic and renal vein but not aorta and portal vein

increased circulating citrulline level ( J:203474 )

• increased circulating citrulline (arginine precursor) levels in the aorta and hepatic vein (1.5-fold) and portal and renal veins (2-fold)

decreased circulating ornithine level ( J:203474 )

• decreased circulating ornithine levels in the hepatic vein

increased circulating ornithine level ( J:203474 )

• increased circulating ornithine levels in the renal vein

decreased circulating taurine level ( J:203474 )

• renal veins exhibit decreased circulating levels of taurine compared with wild-type mice

increased circulating taurine level ( J:203474 )

• aorta veins exhibit increased circulating levels of taurine compared with wild-type mice

• portal veins exhibit increased circulating levels of taurine compared with wild-type mice

digestive/alimentary system

abnormal enterocyte morphology ( J:203474 )

• enterocytes exhibit altered amino acid fluxes compared with wild-type cells

growth/size/body

growth/size/body region phenotype ( J:203474 )

N • normal body weight

immune system

immune system phenotype ( J:203474 )

N • normal Peyer's patch development

integument

integument phenotype ( J:203474 )

N • normal hair growth

Genotype
MGI:3821583

cn35

• Allelic Composition: Hfe^tm1Wsr/Hfe^tm1Wsr; Tg(Vil1-cre)997Gum/?
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6 * SJL

normal phenotype

no abnormal phenotype detected ( J:141745 )

• mice are viable, fertile and have no detectable defects in iron homeostasis

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
NOT	hemochromatosis type 1	DOID:0111029	OMIM:235200	J:141745

Genotype
MGI:4829678

cn36

• Allelic Composition: Myd88^tm1Aki/Myd88^tm1Aki; Tnfaip3^tm1.1Gvl/Tnfaip3^tm1.1Gvl; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6 * SJL

digestive/alimentary system

increased enterocyte apoptosis ( J:163410 )

• in DDS-treated mice

increased susceptibility to induced colitis ( J:163410 )

• mice exhibit increased susceptibility compared to in Myd88^tm1Aki/Myd88⁺ Tnfaip3^tm1.1Gvl Tg(Vil-cre)997Gum mice or Myd88^tm1Aki homozygotes

immune system

increased susceptibility to induced colitis ( J:163410 )

• mice exhibit increased susceptibility compared to in Myd88^tm1Aki/Myd88⁺ Tnfaip3^tm1.1Gvl Tg(Vil-cre)997Gum mice or Myd88^tm1Aki homozygotes

cellular

increased enterocyte apoptosis ( J:163410 )

• in DDS-treated mice

Genotype
MGI:3662654

cn37

• Allelic Composition: Gata6^tm2.1Sad/Gata6^tm2.1Sad; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CD-1 * SJL

mortality/aging

embryonic lethality during organogenesis, complete penetrance ( J:111388 )

• matings of 4 of 5 males carrying the Cre transgene to homozygous females produced no offspring homozygous for the floxed allele and Cre positive

Genotype
MGI:5014229

cn38

• Allelic Composition: Lrp5^tm1Mawa/Lrp5⁺; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ * C57BL/6J * SJL

skeleton

skeleton phenotype ( J:172746 )

N • normal bone mass

Genotype
MGI:5014228

cn39

• Allelic Composition: Lrp5^tm2Mawa/Lrp5⁺; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ * C57BL/6J * SJL

skeleton

skeleton phenotype ( J:172746 )

N • normal bone mass

Genotype
MGI:5014234

cn40

• Allelic Composition: Lrp5^tm3.1Mawa/Lrp5^tm3.1Mawa; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ * C57BL/6J * SJL

skeleton

skeleton phenotype ( J:172746 )

N • normal bone mass

Genotype
MGI:5519892

cn41

• Allelic Composition: Edn2^tm1.1Nat/Edn2^tm1.1Nat; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ * C57BL/6J * SJL

mortality/aging

mortality/aging ( J:201436 )

N • mice exhibit normal survival

digestive/alimentary system

digestive/alimentary phenotype ( J:201436 )

N • mice exhibit normal fat and carbohydrate absorption and excretion

growth/size/body

growth/size/body region phenotype ( J:201436 )

N • mice exhibit normal growth

homeostasis/metabolism

homeostasis/metabolism phenotype ( J:201436 )

N • mice exhibit normal blood glucose levels and body temperature regulation

Genotype
MGI:5902495

cn42

• Allelic Composition: B3gnt6^tm1Lx/B3gnt6^tm1Lx; C1galt1^tm1.1Rpmc/C1galt1^tm1.1Rpmc; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: 129S1/Sv * C57BL/6J * SJL

digestive/alimentary system

abnormal intestinal mucosa morphology ( J:239765 )

• duodenal mucosa is slightly thicker at 5 months of age

abnormal small intestine morphology ( J:239765 )

• moderate thickening in different regions of the small intestinal tract is seen in a subset of mutants that are 12-20 months of age

• thickening of the small intestine is most pronounced in the proximal duodenum

abnormal duodenum morphology ( J:239765 )

• loss of acidic glycans, such as sialic acid and sulfated mucin, and presence of neutral structures, such as Tn antigen in duodenal mucosa

• little secreted mucus is seen in luminal regions or between villi of 5 month old mice

• duodenal mucosa is slightly thicker and the villi wider at 5 months of age

• administration of broad spectrum antibiotics does not increase luminal mucus in the duodenum and does not increase villus spacing

abnormal duodenum crypts of Lieberkuhn morphology ( J:239765 )

• expansion in the proliferative zone of the duodenal crypt in 4 and 8 month old mice

duodenal lesions ( J:239765 )

• numerous lesions within the first 2 cm of the duodenum; these regions are composed of hyperplastic duodenal mucosa overlaying submucosal Brunners glands

• lesions are devoid of villous structures and contain dysplastic epithelium, suggesting adenomatous polyps

abnormal ileum morphology ( J:239765 )

• 30% of mice exhibit thickening in the terminal ileum, although no tumor development is seen in this region

abnormal small intestinal villus morphology ( J:239765 )

• villi are less spaced apart than in wild-type mice and are usually adherent to each other

• duodenal villi are wider at 5 months of age

increased duodenum glandular epithelium tumor incidence ( J:239765 )

• approximately 27% of mice develop spontaneous duodenal tumors, with an average of 4 lesions per mouse, by about 1 year of age

• tumors are epithelial cell-derived

• tumor incidence does not increase with age but aggressiveness of tumors increases over time

small intestinal inflammation ( J:239765 )

• modest spontaneous duodenal inflammation at 5 months of age, with a modest influx of polymorphonuclear cells and leukocytes into the mucosa

endocrine/exocrine glands

abnormal duodenum crypts of Lieberkuhn morphology ( J:239765 )

• expansion in the proliferative zone of the duodenal crypt in 4 and 8 month old mice

immune system

small intestinal inflammation ( J:239765 )

• modest spontaneous duodenal inflammation at 5 months of age, with a modest influx of polymorphonuclear cells and leukocytes into the mucosa

neoplasm

increased duodenum glandular epithelium tumor incidence ( J:239765 )

• approximately 27% of mice develop spontaneous duodenal tumors, with an average of 4 lesions per mouse, by about 1 year of age

• tumors are epithelial cell-derived

• tumor incidence does not increase with age but aggressiveness of tumors increases over time

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
duodenum cancer		DOID:10021		J:239765

Genotype
MGI:4829677

cn43

• Allelic Composition: Tnfaip3^tm1.1Gvl/Tnfaip3^tm1.1Gvl; Tnfrsf1a^tm1Mak/Tnfrsf1a^tm1Mak; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: 129S2/SvPas * C57BL/6 * SJL

digestive/alimentary system

decreased susceptibility to induced colitis ( J:163410 )

• mice exhibit decreased susceptibility compared to Tnfrsf1a^tm1Mak/Tnfrf1⁺ Tnfaip3^tm1.1Gvl Tg(Vil-cre)997Gum mice

increased susceptibility to induced colitis ( J:163410 )

• mice exhibit increased susceptibility compared to in Tnfrsf1a^tm1Mak homozygotes

immune system

decreased susceptibility to induced colitis ( J:163410 )

• mice exhibit decreased susceptibility compared to Tnfrsf1a^tm1Mak/Tnfrf1⁺ Tnfaip3^tm1.1Gvl Tg(Vil-cre)997Gum mice

increased susceptibility to induced colitis ( J:163410 )

• mice exhibit increased susceptibility compared to in Tnfrsf1a^tm1Mak homozygotes

Genotype
MGI:5559520

cn44

• Allelic Composition: Ern1^tm2.1Tiw/Ern1^tm2.1Tiw; Xbp1^tm2Glm/Xbp1^tm2Glm; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: 129S4/SvJae * 129S6/SvEvTac * C57BL/6 * SJL

immune system

small intestinal inflammation ( J:206084 )

• enteritis is diminished compared to mice with IEC (intestinal epithelial cell) deletion of Xbp1 only

digestive/alimentary system

small intestinal inflammation ( J:206084 )

• enteritis is diminished compared to mice with IEC (intestinal epithelial cell) deletion of Xbp1 only

Genotype
MGI:5528297

cn45

• Allelic Composition: Braf^tm1.1Brd/Braf⁺; Tg(Vil1-cre)997Gum/0; Trp53^tm2Tyj/Trp53^tm2Tyj
• Genetic Background: involves: 129S4/SvJae * 129S7/SvEvBrd * C57BL/6 * SJL

neoplasm

abnormal tumor pathology ( J:199307 )

• invasiveness of cancers considerably increased

• 56% of mice at 10-20 months

increased metastatic potential ( J:199307 )

• 25% of cancerous mice have metastases

Genotype
MGI:4941760

cn46

• Allelic Composition: Pten^tm1Hwu/Pten^tm1Hwu; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: 129S4/SvJae * BALB/c * C57BL/6J * SJL

digestive/alimentary system

abnormal small intestinal crypt cell proliferation ( J:150553 )

• increase in crypt cell proliferation

abnormal intestine morphology ( J:150553 )

• intestine is 1.28-fold longer and weighs 1.58-fold more than controls

• however, mutants do not develop polyps

abnormal intestinal mucosa morphology ( J:150553 )

• thickening of the intestinal mucosa

abnormal intestinal goblet cell morphology ( J:150553 )

• increase in the number and size of goblet cells

abnormal intestinal enteroendocrine cell morphology ( J:150553 )

• decrease in the number of enteroendocrine cells

abnormal small intestine morphology ( J:150553 )

• thickening of the muscular layers of the small intestine

abnormal small intestine crypts of Lieberkuhn morphology ( J:150553 )

• small intestine exhibits an expanded crypt compartment with increased number of crypts per villus

abnormal Paneth cell morphology ( J:150553 )

• marker analysis indicates impaired Paneth cell maturation

abnormal duodenum morphology ( J:150553 )

• total protein content of the duodenum is enhanced by 50%

abnormal jejunum morphology ( J:150553 )

• jejunum exhibits expanded crypt and villus compartments, an increased number of crypts, thickening of the muscular layers and villus branching

abnormal small intestinal villus morphology ( J:150553 )

• small intestine exhibits an expanded villus compartment

branched small intestinal villi ( J:150553 )

• mutants exhibit branching of the villi in the small intestine

endocrine/exocrine glands

abnormal small intestine crypts of Lieberkuhn morphology ( J:150553 )

• small intestine exhibits an expanded crypt compartment with increased number of crypts per villus

abnormal Paneth cell morphology ( J:150553 )

• marker analysis indicates impaired Paneth cell maturation

cellular

abnormal intestinal goblet cell morphology ( J:150553 )

• increase in the number and size of goblet cells

abnormal small intestinal crypt cell proliferation ( J:150553 )

• increase in crypt cell proliferation

Genotype
MGI:4941759

cn47

• Allelic Composition: Apc^Min/Apc⁺; Pten^tm1Hwu/Pten^tm1Hwu; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: 129S4/SvJae * BALB/c * C57BL/6J * SJL

mortality/aging

premature death ( J:150553 )

• all mutants die within 80 days

neoplasm

increased intestinal adenoma incidence ( J:150553 )

• adenomas in the small intestine

digestive/alimentary system

intestine polyps ( J:150553 )

• mutants develop an average of 20.1 intestinal polyps per mouse, an 11.17-fold increase over the numbers seen in heterozygous Apc mice

increased intestinal adenoma incidence ( J:150553 )

• adenomas in the small intestine

Genotype
MGI:5770568

cn48

• Allelic Composition: Ffar2^tm2Soff/Ffar2^tm2Soff; Ffar3^tm2.1Soff/Ffar3^tm2.1Soff; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: 129S4/SvJae * C57BL/6 * C57BL/6J * SJL

homeostasis/metabolism

homeostasis/metabolism phenotype ( J:227939 )

N • plasma insulin levels are normal after acetate treatment

N • mice fed a high-fat diet and treated with either intraperitoneal injection or oral glucose challenge exhibit normal glucose tolerance, plasma free fatty acid levels and insulin secretion

Genotype
MGI:5560214

cn49

• Allelic Composition: Mirc31^tm1.1Aru/Mirc31^tm1.1Aru; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: 129S4/SvJae * C57BL/6 * C57BL/6J * SJL

digestive/alimentary system

abnormal intestine morphology ( J:202923 )

• modest but significant intestinal hypertrophy

abnormal crypts of Lieberkuhn morphology ( J:202923 )

• increase in the fraction of fissile crypts

abnormal small intestine morphology ( J:202923 )

• thicker

decreased Paneth cell number ( J:202923 )

• modest decrease in the number of Paneth cells

endocrine/exocrine glands

abnormal crypts of Lieberkuhn morphology ( J:202923 )

• increase in the fraction of fissile crypts

decreased Paneth cell number ( J:202923 )

• modest decrease in the number of Paneth cells

Genotype
MGI:5560215

cn50

• Allelic Composition: Mirc31^tm1.1Aru/Mirc31^tm1.1Aru; Tg(Vil1-cre)997Gum/0; Tg(Vil1-Lin28b,-tdTomato)LoAru/0
• Genetic Background: involves: 129S4/SvJae * C57BL/6 * C57BL/6J * SJL

digestive/alimentary system

abnormal crypts of Lieberkuhn morphology ( J:202923 )

• crypt hyperplasia and expanded crypts

decreased Paneth cell number ( J:202923 )

• significant reduction in the number of Paneth cells

endocrine/exocrine glands

abnormal crypts of Lieberkuhn morphology ( J:202923 )

• crypt hyperplasia and expanded crypts

decreased Paneth cell number ( J:202923 )

• significant reduction in the number of Paneth cells

Genotype
MGI:4430578

cn51

• Allelic Composition: Apc^Min/Apc⁺; Col1a1^{tm1(CAG-Sirt1)Dsin}/Col1a1⁺; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: 129S4/SvJae * C57BL/6 * C57BL/6J * SJL

neoplasm

decreased tumor incidence ( J:134301 )

• mice do not develop tumors morbidities, including anemia and cachaxia, unlike Col1a1^{tm1(CAG-Sirt1)Dsin} Apc^Min heterozygotes

• mice develop fewer intestinal tumors than Col1a1^{tm1(CAG-Sirt1)Dsin} Apc^Min heterozygotes

Genotype
MGI:5608787

cn52

• Allelic Composition: Rab11a^tm1.1Ngao/Rab11a^tm1.1Ngao; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: 129S4/SvJae * C57BL/6J * SJL

mortality/aging

increased susceptibility to induced morbidity/mortality ( J:278932 )

• mice show higher mortality rate 8 weeks after azoxymethane-dextran sulfate sodium (AOM-DSS) treatment

premature death ( J:215917 )

• survivors show a higher mortality with aging

• germ-free mice show reduced mortality

postnatal lethality, incomplete penetrance ( J:215917 )

• about 40% mortality rate at weaning

• males show a higher mortality rate than females

homeostasis/metabolism

increased cytokine level ( J:278932 )

• mice exhibit a higher baseline level of inflammatory cytokines than wild-type mice

increased incidence of tumors by chemical induction ( J:278932 )

• mice show increased susceptibility to AOM-DSS-induced tumorigenesis

• AOM-DSS-treated mice that survive post 8 weeks form 2 to 6 poorly differentiated c-Myc+ and BrdUrd+ tubular adenomas in the ileum that are not seen in wild-type mice; tumors show complex glandular (cribriforming) structures, marked nuclear pleiomorphism, necrosis, increased mitotic activities, and single infiltrating cells in mucosa, best classified as intramucosal carcinoma

neoplasm

increased intestinal adenoma incidence ( J:278932 )

• mice develop tubular adenomas (low-grade epithelial dysplasia) at juvenile ages

• at 1 year, the distal intestines of approximately 30% of mice develop 2 to 3 well-demarcated tubular adenomas and high-grade dysplasia that exhibit complex glandular (cribriforming) structures, marked pleiomorphism, necrosis, and increased mitotic activities

increased incidence of tumors by chemical induction ( J:278932 )

• mice show increased susceptibility to AOM-DSS-induced tumorigenesis

• AOM-DSS-treated mice that survive post 8 weeks form 2 to 6 poorly differentiated c-Myc+ and BrdUrd+ tubular adenomas in the ileum that are not seen in wild-type mice; tumors show complex glandular (cribriforming) structures, marked nuclear pleiomorphism, necrosis, increased mitotic activities, and single infiltrating cells in mucosa, best classified as intramucosal carcinoma

growth/size/body

decreased body size ( J:215917 )

• runting is seen at a young age

digestive/alimentary system

abnormal intestine morphology ( J:215917 )

• dilated intestinal lumen

abnormal intestinal goblet cell morphology ( J:215917 )

• reduction in goblet cells

abnormal intestinal epithelium morphology ( J:215917 )

• epithelial hyperplasia and dysplasia continue to be present at 5 months of age

abnormal crypts of Lieberkuhn morphology ( J:215917 )

• increase in numbers of cycling crypt cells at all postnatal stages indicating crypt hyperplasia

• enlarged crypt

• however, differentiation of enterocytes and intestinal secretory cell lineages is unaffected

decreased colon length ( J:215917 )

• shortened colon

abnormal small intestinal villus morphology ( J:215917 )

• in neonates, the intestinal villi frequently fuse and branch

decreased small intestinal villus size ( J:215917 )

• intestines show blunted villi

increased intestinal adenoma incidence ( J:278932 )

• mice develop tubular adenomas (low-grade epithelial dysplasia) at juvenile ages

• at 1 year, the distal intestines of approximately 30% of mice develop 2 to 3 well-demarcated tubular adenomas and high-grade dysplasia that exhibit complex glandular (cribriforming) structures, marked pleiomorphism, necrosis, and increased mitotic activities

abnormal digestive system physiology ( J:215917 )

• mice show a stronger intestinal epithelial barrier function than wild-type mice

abnormal intestine physiology ( J:215917 , J:278932 )

• intestinal organoid cultures initiate bud outgrowths more rapidly and contain a larger population of proliferative cells than wild-type cultures (J:215917)

• intestinal organoid cultures from germ-free mice show decreased proliferation (J:215917)

• treatment of intestinal organoids with an NF-kappaB pathway inhibitor, BAY11-0782, results in reduction of cell proliferation (J:215917)

• all mice exhibit irregular cribriform proliferation in villi at 150 days (J:278932)

abnormal small intestinal crypt cell physiology ( J:278932 )

• crypt hyperproliferation and low-grade dysplasia is seen throughout the small intestine from birth

abnormal small intestinal crypt cell proliferation ( J:215917 )

• increase in numbers of cycling crypt cells at all postnatal stages

• germ-free mice show an overall reduction of crypt cell proliferation compared to specific pathogen free conditions

intestinal inflammation ( J:215917 )

• macrophage infiltration into the intestinal submucosa

endocrine/exocrine glands

abnormal crypts of Lieberkuhn morphology ( J:215917 )

• increase in numbers of cycling crypt cells at all postnatal stages indicating crypt hyperplasia

• enlarged crypt

• however, differentiation of enterocytes and intestinal secretory cell lineages is unaffected

immune system

intestinal inflammation ( J:215917 )

• macrophage infiltration into the intestinal submucosa

increased cytokine level ( J:278932 )

• mice exhibit a higher baseline level of inflammatory cytokines than wild-type mice

abnormal cytokine secretion ( J:215917 )

• intestinal organoid cultures produce higher levels of cytokines, including interleukin-6, interleukin-1 beta, and CXCL12

• luminal perfusion of TLR9 (endotoxin-free E.coli DNA) or TLR4 (LPS) agonists drastically activates cytokine responses in germ-free mutants compared to wild-type controls, indicating that intestinal epithelial cells show impaired tolerance to microbial TLR agonists

increased interleukin-1 beta secretion ( J:215917 )

• by intestinal organoid cultures

increased interleukin-6 secretion ( J:215917 )

• by intestinal organoid cultures

• intestinal organoid cultures from germ-free mice show reduced IL-6 secretion

• treatment of intestinal organoids with an NF-kappaB pathway inhibitor, BAY11-0782, results in a reduction of IL-6 production

cellular

abnormal intestinal goblet cell morphology ( J:215917 )

• reduction in goblet cells

abnormal small intestinal crypt cell proliferation ( J:215917 )

• increase in numbers of cycling crypt cells at all postnatal stages

• germ-free mice show an overall reduction of crypt cell proliferation compared to specific pathogen free conditions

Genotype
MGI:5306895

cn53

• Allelic Composition: Casr^tm1Wch/Casr^tm1Wch; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: 129S4/SvJae * C57BL/6J * SJL

digestive/alimentary system

abnormal enterocyte proliferation ( J:179672 )

• cell proliferation in colonic crypts is increased compared to in control mice

abnormal large intestine crypts of Lieberkuhn morphology ( J:179672 )

• colon crypt height and number of cells per crypt are increased compared to in control mice

endocrine/exocrine glands

abnormal large intestine crypts of Lieberkuhn morphology ( J:179672 )

• colon crypt height and number of cells per crypt are increased compared to in control mice

cellular

abnormal enterocyte proliferation ( J:179672 )

• cell proliferation in colonic crypts is increased compared to in control mice

Genotype
MGI:7642164

cn54

• Allelic Composition: Apc^Min/Apc⁺; Rab11a^tm1.1Ngao/Rab11a^tm1.1Ngao; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: 129S4/SvJae * C57BL/6J * SJL/J

mortality/aging

decreased tumor-free survival time ( J:278932 )

• mice show higher mortality due to increased tumor burden compared to single Apc^Min mice

neoplasm

increased intestinal adenoma incidence ( J:278932 )

• 2-month-old mice develop twice the number of adenomas that are 5 times larger and occupy larger epithelial fields as compared with tumor fields in single Apc^Min mice

• mice show higher mortality due to increased tumor burden compared to single Apc^Min mice

digestive/alimentary system

increased intestinal adenoma incidence ( J:278932 )

• 2-month-old mice develop twice the number of adenomas that are 5 times larger and occupy larger epithelial fields as compared with tumor fields in single Apc^Min mice

• mice show higher mortality due to increased tumor burden compared to single Apc^Min mice

Genotype
MGI:6459274

cn55

• Allelic Composition: Cc2d1a^tm1.1Thkn/Cc2d1a^tm1.1Thkn; Hes1^tm1.1Sat/Hes1⁺; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: 129S4/SvJae * C57BL/6NTac * SJL

digestive/alimentary system

digestive/alimentary phenotype ( J:236761 )

N • mice exhibit normal intestinal Notch signaling

Genotype
MGI:3844315

cn56

• Allelic Composition: Apc^tm1Tno/Apc^tm1Tno; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: 129S4/SvJae * C57BL/6 * SJL

mortality/aging

embryonic lethality, complete penetrance ( J:126018 )

• embryonic lethality is observed

Genotype
MGI:3844314

cn57

• Allelic Composition: Apc^tm1Tno/Apc⁺; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: 129S4/SvJae * C57BL/6 * SJL

growth/size/body

postnatal growth retardation ( J:126018 )

• male and female animals display growth inhibition compared to controls

hematopoietic system

anemia ( J:126018 )

• mice exhibit severe anemia

neoplasm

increased gastrointestinal tumor incidence ( J:126018 )

• about 36 tumors are observed per mouse; most tumors are located in the small intestine

• cecal and colon tumors are small than those in age-matched in CDX2-cre/APC mice

increased small intestine adenocarcinoma incidence ( J:126018 )

digestive/alimentary system

increased gastrointestinal tumor incidence ( J:126018 )

• about 36 tumors are observed per mouse; most tumors are located in the small intestine

• cecal and colon tumors are small than those in age-matched in CDX2-cre/APC mice

increased small intestine adenocarcinoma incidence ( J:126018 )

Genotype
MGI:6459275

cn58

• Allelic Composition: Cc2d1a^tm1.1Thkn/Cc2d1a^tm1.1Thkn; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: 129S4/SvJae * C57BL/6 * SJL

digestive/alimentary system

digestive/alimentary phenotype ( J:236761 )

N • mice exhibit normal intestine morphology

Genotype
MGI:4360363

cn59

• Allelic Composition: Apc^Min/Apc⁺; Erbb3^tm1.1Dwt/Erbb3^tm2.1Dwt; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: 129S6/SvEvTac * C57BL/6 * C57BL/6J * SJL

digestive/alimentary system

digestive/alimentary phenotype ( J:152703 )

N • unlike Apc^Min heterozygotes, mice do not develop colonic polyps

intestine polyps ( J:152703 )

• mice develop fewer intestinal polyps compared to in Apc^Min heterozygotes

neoplasm

decreased tumor incidence ( J:152703 )

• the number and size of microadenomas in the intestine are decreased compared to in Apc^Min heterozygotes due to an increased in Caspase-3 dependent apoptosis

• mice fail to develop colon tumors unlike Apc^Min heterozygotes

Genotype
MGI:5629980

cn60

• Allelic Composition: Tg(Vil1-cre)997Gum/0; Tnfrsf11a^tm1.1Irw/Tnfrsf11a^tm1.1Irw
• Genetic Background: involves: 129S6/SvEvTac * C57BL/6 * C57BL/6NTac * SJL

immune system

decreased plasma cell number ( J:226603 )

• reduced numbers of IgA+ antibody secreting cells in intestinal lamina propria 1 week after weaning as compared to controls

• number of IgA+ cells increases by 3 weeks, but remains less than controls

decreased IgA level ( J:226603 )

• fecal IgA production is reduced as compared to controls

• serum IgA levels are lower through the first 1 to 3 weeks after weaning, but increase to same levels of control 3 weeks after weaning

• following exposure to foreign antigen (horse ferritin), anti-ferritin IgA levels are similar to unimmunized controls

abnormal Peyer's patch morphology ( J:226603 )

• uptake of bacteria into Peyer's patches is less than 1% of control uptake; most section exhibit no bacterial uptake

• uptake of particulates (polystyrene beads) into Peyer's patches is reduced by over 90%

abnormal Peyer's patch epithelium morphology ( J:219915 , J:226603 )

• absent M cells from follicle-associated epithelium overlying the Peyer's patch resulting in impeded uptake of amorphous Mg-substituted calcium phosphate (AMCP) nanomineral from the gut (J:219915)

• M cells are not deteced in Peyer's patch domes (J:226603)

abnormal Peyer's patch follicle morphology ( J:226603 )

• reduction in size of Peyers patch B cell follicles 1 week after weaning as compared to control

• follicle size increases by 3 weeks, but remains smaller than controls

abnormal Peyer's patch T cell area morphology ( J:226603 )

• Peyers patches contain fewer follicular helper T cells than controls 2 weeks after weaning, however, by 6 weeks numbers are comparable

abnormal Peyer's patch germinal center morphology ( J:226603 )

• Peyers patches contain fewer germinal center B cells than controls 2 weeks after weaning, however, by 6 weeks numbers are comparable.

• germinal cell development is delayed

digestive/alimentary system

abnormal Peyer's patch epithelium morphology ( J:219915 , J:226603 )

• absent M cells from follicle-associated epithelium overlying the Peyer's patch resulting in impeded uptake of amorphous Mg-substituted calcium phosphate (AMCP) nanomineral from the gut (J:219915)

• M cells are not deteced in Peyer's patch domes (J:226603)

hematopoietic system

decreased plasma cell number ( J:226603 )

• reduced numbers of IgA+ antibody secreting cells in intestinal lamina propria 1 week after weaning as compared to controls

• number of IgA+ cells increases by 3 weeks, but remains less than controls

decreased IgA level ( J:226603 )

• fecal IgA production is reduced as compared to controls

• serum IgA levels are lower through the first 1 to 3 weeks after weaning, but increase to same levels of control 3 weeks after weaning

• following exposure to foreign antigen (horse ferritin), anti-ferritin IgA levels are similar to unimmunized controls

Genotype
MGI:5559519

cn61

• Allelic Composition: Atg7^tm1Tchi/Atg7^tm1Tchi; Xbp1^tm2Glm/Xbp1^tm2Glm; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: 129S6/SvEvTac * C57BL/6 * CBA * SJL

immune system

intestinal inflammation ( J:206084 )

• with Atg7 and Xbp1 deletion in IECs (intestinal epithelial cells), most mice (>70%) develop discontinuous or transmural inflammation with acute and chronic inflammation ending in an abrupt fashion to muscularis propria and serosa resembling pathologies seen in human patients with Crohn's disease

• enteritis progresses such that it is present in all animals by 18 weeks

• dextran sodium sulfate treatment induces greater inflammation that in wild-type mice

ileum inflammation ( J:206084 )

• ileitis is more severe than in animals with IEC deletion of Xbp1 only

cellular

abnormal autophagy ( J:206084 )

digestive/alimentary system

abnormal enterocyte physiology ( J:206084 )

• intestinal epithelial cells (IECs) completely lack unfolded protein response (UPR)-induced autophagy

• more apoptotic IEC cells are detected than in mice having only Xbp1 deletion in IECs

intestinal inflammation ( J:206084 )

• with Atg7 and Xbp1 deletion in IECs (intestinal epithelial cells), most mice (>70%) develop discontinuous or transmural inflammation with acute and chronic inflammation ending in an abrupt fashion to muscularis propria and serosa resembling pathologies seen in human patients with Crohn's disease

• enteritis progresses such that it is present in all animals by 18 weeks

• dextran sodium sulfate treatment induces greater inflammation that in wild-type mice

ileum inflammation ( J:206084 )

• ileitis is more severe than in animals with IEC deletion of Xbp1 only

homeostasis/metabolism

abnormal autophagy ( J:206084 )

Genotype
MGI:4358977

cn62

• Allelic Composition: Abca1^tm1Jp/Abca1^tm1Jp; Speer6-ps1^{Tg(Alb-cre)21Mgn}/Speer6-ps1⁺; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: 129S6/SvEvTac * C57BL/6 * DBA * SJL

homeostasis/metabolism

decreased circulating HDL cholesterol level ( J:107802 )

• plasma HDL levels are reduced by 90%

Genotype
MGI:5767208

cn63

• Allelic Composition: Il25^tm1Cdon/Il25^tm1Cdon; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: 129S6/SvEvTac * C57BL/6J * C57BL/6N * SJL

digestive/alimentary system

abnormal colon morphology ( J:229778 )

• reduced DSS-induced colon shortening compared with wild-type mice

decreased susceptibility to induced colitis ( J:229778 )

• DSS-treated mice exhibit reduced weight loss, inflammation and colon length shortening compared with wild-type mice

growth/size/body

decreased susceptibility to weight loss ( J:229778 )

• in DSS-treated mice

immune system

decreased susceptibility to induced colitis ( J:229778 )

• DSS-treated mice exhibit reduced weight loss, inflammation and colon length shortening compared with wild-type mice

Genotype
MGI:6358742

cn64

• Allelic Composition: Slc52a3^tm1.1Said/Slc52a3^tm1.1Said; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: 129S6/SvEvTac * C57BL/6J * C57BL/6N * SJL

mortality/aging

postnatal lethality, incomplete penetrance ( J:278571 )

• two-thirds of mice die between 6 and 12 weeks

• however, drinking water supplementation with riboflavin reverses phenotype

skeleton

short femur ( J:278571 )

short tibia ( J:278571 )

abnormal pelvic girdle bone morphology ( J:278571 )

• short pelvic bone

decreased bone mineral density ( J:278571 )

• in femur and tibia

• however, drinking water supplementation with riboflavin reverses phenotype

decreased bone mineral density of femur ( J:278571 )

growth/size/body

decreased body weight ( J:278571 )

• however, drinking water supplementation with riboflavin reverses phenotype

postnatal growth retardation ( J:278571 )

behavior/neurological

lethargy ( J:278571 )

hunched posture ( J:278571 )

homeostasis/metabolism

abnormal vitamin level ( J:278571 )

• reduced serum riboflavin (vitamin B2) levels and reduced uptake levels in the jejunal loops, isolated enterocytes and colon

• however, biotin uptake levels are normal

vision/eye

abnormal ocular surface morphology ( J:278571 )

• however, drinking water supplementation with riboflavin reverses phenotype

limbs/digits/tail

short femur ( J:278571 )

short tibia ( J:278571 )

Genotype
MGI:5441532

cn65

• Allelic Composition: Xbp1^tm2Glm/Xbp1^tm2Glm; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: 129S6/SvEvTac * C57BL/6J * FVB/N * SJL

digestive/alimentary system

rectal hemorrhage ( J:188627 )

• in DSS-treated mice

abnormal small intestine goblet cell morphology ( J:188627 )

• reduced number and size in the small intestine with reduced secretory granules

absent Paneth cells ( J:188627 )

• absent with barely detectable lysozyme and pro-forms of cryptdin stores

crypts of Lieberkuhn abscesses ( J:188627 )

• in some mice

intestinal ulcer ( J:188627 )

• in some mice

abnormal intestine physiology ( J:188627 )

• mice exhibit an increase in the migration rate of proliferating cells in the crypt-villus compared with control mice

increased susceptibility to induced colitis ( J:188627 )

• mice treated with DSS exhibit more severe wasting and rectal bleeding and increased areas of mucosal erosions, edema and cellular infiltration compared with control mice

• however, antibiotic treatment rescues increased sensitivity

small intestinal inflammation ( J:188627 )

• small intestine inflammation with endoplasmic reticulum stress in 19 of 31 mice

• inflammation is patchy and ranges in severity from lamina propria polymorphpnuclear infiltration to crypt abscesses and ulceration without granulomas

• however, mice do not exhibit reduced villus length

immune system

increased susceptibility to induced colitis ( J:188627 )

• mice treated with DSS exhibit more severe wasting and rectal bleeding and increased areas of mucosal erosions, edema and cellular infiltration compared with control mice

• however, antibiotic treatment rescues increased sensitivity

small intestinal inflammation ( J:188627 )

• small intestine inflammation with endoplasmic reticulum stress in 19 of 31 mice

• inflammation is patchy and ranges in severity from lamina propria polymorphpnuclear infiltration to crypt abscesses and ulceration without granulomas

• however, mice do not exhibit reduced villus length

increased susceptibility to bacterial infection ( J:188627 )

• mice infected with Listeria monocytogenes exhibit increased bacterial burden in the feces and liver compared with control mice

• however, bacterial burden in the spleen is normal

cardiovascular system

rectal hemorrhage ( J:188627 )

• in DSS-treated mice

cellular

abnormal small intestine goblet cell morphology ( J:188627 )

• reduced number and size in the small intestine with reduced secretory granules

abnormal endoplasmic reticulum morphology ( J:188627 )

• small intestine inflammation with endoplasmic reticulum stress in 19 of 31 mice

abnormal cell migration ( J:188627 )

• mice exhibit an increase in the migration rate of proliferating cells in the crypt-villus compared with control mice

growth/size/body

cachexia ( J:188627 )

• in DSS-treated mice

endocrine/exocrine glands

absent Paneth cells ( J:188627 )

• absent with barely detectable lysozyme and pro-forms of cryptdin stores

crypts of Lieberkuhn abscesses ( J:188627 )

• in some mice

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
inflammatory bowel disease		DOID:0050589	OMIM:PS266600	J:188627

Genotype
MGI:5441533

cn66

• Allelic Composition: Xbp1^tm2Glm/Xbp1⁺; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: 129S6/SvEvTac * C57BL/6J * FVB/N * SJL

digestive/alimentary system

small intestinal inflammation ( J:188627 )

• mild in 5 of 16 mice

immune system

small intestinal inflammation ( J:188627 )

• mild in 5 of 16 mice

Genotype
MGI:4358974

cn67

• Allelic Composition: Abca1^tm1Jp/Abca1⁺; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: 129S6/SvEvTac * C57BL/6 * SJL

homeostasis/metabolism

decreased circulating cholesterol level ( J:107802 )

• total cholesterol levels are reduced due to decreases in HDL

decreased circulating HDL cholesterol level ( J:107802 )

• fasting plasma HDL levels are reduced about 15%

Genotype
MGI:4358973

cn68

• Allelic Composition: Abca1^tm1Jp/Abca1^tm1Jp; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: 129S6/SvEvTac * C57BL/6 * SJL

cellular

decreased cholesterol efflux ( J:107802 )

• enterocytes have decreased efflux of cholesterol in vitro

• in vivo, uptake of cholesterol in the gut is unaffected by cholesterol fails to get transported to the circulatory system

digestive/alimentary system

abnormal enterocyte physiology ( J:107802 )

• cholesterol uptaken from the lumen of the gut is retained in the enterocytes instead of being transported to the blood

homeostasis/metabolism

decreased cholesterol efflux ( J:107802 )

• enterocytes have decreased efflux of cholesterol in vitro

• in vivo, uptake of cholesterol in the gut is unaffected by cholesterol fails to get transported to the circulatory system

decreased circulating cholesterol level ( J:107802 )

• total cholesterol levels are reduced

decreased circulating HDL cholesterol level ( J:107802 )

• fasting plasma HDL levels are reduced about 30%

• serum levels of Apo-AI, Apo-AII and ApoB are also reduced by about 25-35%

decreased circulating LDL cholesterol level ( J:107802 )

• serum levels of Apo-AI, Apo-AII and ApoB are also reduced by about 25-35%

Genotype
MGI:5559521

cn69

• Allelic Composition: Xbp1^tm2Glm/Xbp1^tm2Glm; Tnfrsf1a^tm1Imx/Tnfrsf1a^tm1Imx; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: 129S6/SvEvTac * C57BL/6 * SJL

immune system

small intestinal inflammation ( J:206084 )

• enteritis is diminished compared to mice with IEC (intestinal epithelial cell) deletion of Xbp1 only

digestive/alimentary system

small intestinal inflammation ( J:206084 )

• enteritis is diminished compared to mice with IEC (intestinal epithelial cell) deletion of Xbp1 only

Genotype
MGI:5559517

cn70

• Allelic Composition: Xbp1^tm2Glm/Xbp1^tm2Glm; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: 129S6/SvEvTac * C57BL/6 * SJL

immune system

small intestinal inflammation ( J:206084 )

• limited to the mucosa

• treatment of mice with rapamycin reduces severity of enteritis

digestive/alimentary system

abnormal enterocyte physiology ( J:206084 )

• intenstinal epithelial cells exhibit ER (endoplamic reticulum) stress

small intestinal inflammation ( J:206084 )

• limited to the mucosa

• treatment of mice with rapamycin reduces severity of enteritis

cellular

abnormal autophagy ( J:206084 )

• autophagy is induced in enterocytes, most notably in Paneth cells

homeostasis/metabolism

abnormal autophagy ( J:206084 )

• autophagy is induced in enterocytes, most notably in Paneth cells

Genotype
MGI:4360362

cn71

• Allelic Composition: Erbb3^tm1.1Dwt/Erbb3^tm2.1Dwt; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: 129S6/SvEvTac * C57BL/6 * SJL

digestive/alimentary system

increased susceptibility to induced colitis ( J:152703 )

• following treatment with DSS, mice exhibit greater weight loss than similarly treated control mice and mild lesions with loss of mucus cells, glandular hyperplasia, and increased leukocyte levels in the lamina propria to severe lesions with complete loss of glandular epithelium, followed by collapse of denuded lamina propria, submucosal edema, fibrinoid necrosis of lamina propria vessels, and infiltration of neutrophils and plasma cells

immune system

increased susceptibility to induced colitis ( J:152703 )

• following treatment with DSS, mice exhibit greater weight loss than similarly treated control mice and mild lesions with loss of mucus cells, glandular hyperplasia, and increased leukocyte levels in the lamina propria to severe lesions with complete loss of glandular epithelium, followed by collapse of denuded lamina propria, submucosal edema, fibrinoid necrosis of lamina propria vessels, and infiltration of neutrophils and plasma cells

Genotype
MGI:5559514

cn72

• Allelic Composition: Atg16l1^tm1Kuv/Atg16l1^tm1Kuv; Xbp1^tm2Glm/Xbp1^tm2Glm; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: 129S6/SvEvTac * C57BL/6 * SJL

digestive/alimentary system

abnormal enterocyte physiology ( J:206084 )

• intestinal epithelial cells (IECs) completely lack unfolded protein response (UPR)-induced autophagy

• more apoptotic IEC cells are detected than in mice having only Xbp1 deletion in IECs

intestinal inflammation ( J:206084 )

ileum inflammation ( J:206084 )

• with Atg16l1 and Xbp1 deletion in IECs, most mice (>70%) develop discontinuous or transmural inflammation by 18 weeks, with similar features to IECs with Atg7/Xbp1 deletion

immune system

intestinal inflammation ( J:206084 )

ileum inflammation ( J:206084 )

• with Atg16l1 and Xbp1 deletion in IECs, most mice (>70%) develop discontinuous or transmural inflammation by 18 weeks, with similar features to IECs with Atg7/Xbp1 deletion

Genotype
MGI:3767180

cn73

• Allelic Composition: Atoh1^tm2Hzo/Atoh1^tm3Hzo; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: 129S7/SvEvBrd * C57BL/6J * SJL

mortality/aging

postnatal lethality, complete penetrance ( J:128312 )

• no mutants are found at P14

Genotype
MGI:5528296

cn74

• Allelic Composition: Braf^tm1.1Brd/Braf⁺; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: 129S7/SvEvBrd * C57BL/6 * SJL

digestive/alimentary system

abnormal intestinal epithelium morphology ( J:199307 )

abnormal intestinal mucosa morphology ( J:199307 )

• increased number of proliferating cells (hyperproliferation) in the mucosa

• levels of apoptosis are unchanged

abnormal crypts of Lieberkuhn morphology ( J:199307 )

• generalized crypt hyperplasia affecting almost all crypts

abnormal large intestine crypts of Lieberkuhn morphology ( J:199307 )

• crypt hyperplasia and mucosal protrusions

abnormal large intestine morphology ( J:199307 )

• significantly elongated and thickened

increased large intestine length ( J:199307 )

• significantly elongated

abnormal small intestine morphology ( J:199307 )

• significantly elongated and thickened

abnormal small intestinal villus morphology ( J:199307 )

• villi are thickened and deformed

branched small intestinal villi ( J:199307 )

• villi are often branched

increased small intestine length ( J:199307 )

• significantly elongated

intestine polyps ( J:199307 )

• focal serrated epithelial formations with cytomorphologic features of human microvesicular or goblet rich hyperplastic polyps

• predominantly in the small intestine

increased gastrointestinal tumor incidence ( J:199307 )

• macroscopic tumors and dysplasia in some mice at 2-3 months of age

• all mice with dysplastic lesions by 10 months

increased intestinal adenoma incidence ( J:199307 )

• dysplastic lesions in 10 month old mice with features of human serrated adenomas

• crypt elongation and serrated eosinophilic adenomatous epithelium

• only 5 of 95 tumors found were in the large intestine

• increased proliferation in murine adenoma with dysplasia

neoplasm

increased gastrointestinal tumor incidence ( J:199307 )

• macroscopic tumors and dysplasia in some mice at 2-3 months of age

• all mice with dysplastic lesions by 10 months

increased intestinal adenoma incidence ( J:199307 )

• dysplastic lesions in 10 month old mice with features of human serrated adenomas

• crypt elongation and serrated eosinophilic adenomatous epithelium

• only 5 of 95 tumors found were in the large intestine

• increased proliferation in murine adenoma with dysplasia

increased carcinoma incidence ( J:199307 )

• in 8.3% of mice under 10 months of age

• in 13.8% of mice older than 10 months

endocrine/exocrine glands

abnormal crypts of Lieberkuhn morphology ( J:199307 )

• generalized crypt hyperplasia affecting almost all crypts

abnormal large intestine crypts of Lieberkuhn morphology ( J:199307 )

• crypt hyperplasia and mucosal protrusions

Genotype
MGI:6151440

cn75

• Allelic Composition: Ano1^tm2Jrr/Ano1^tm2Jrr; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: 129S7/SvEvBrd * C57BL/6 * SJL

digestive/alimentary system

decreased intestinal epithelial chloride transmembrane transport ( J:260534 )

• calcium-activated chloride ion secretion and effects of niflumic acid are almost completely abolished in the ileum and proximal and distal colon compared with wild-type mice

• however, transport in the jejunum is normal

Genotype
MGI:3797771

cn76

• Allelic Composition: Nr5a2^tm1Sakl/Nr5a2^tm1Sakl; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: 129S/SvEv * 129S4/SvJaeSor * C57BL/6J * SJL

homeostasis/metabolism

decreased circulating cholesterol level ( J:135822 )

decreased circulating aspartate transaminase level ( J:135822 )

digestive/alimentary system

digestive/alimentary phenotype ( J:135822 )

N • unlike heterozygous null mice, villus length, crypt depth and intestinal proliferation are normal

Genotype
MGI:5426956

cn77

• Allelic Composition: Soat2^tm1.1Llr/Soat2^tm1.1Llr; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: 129S/SvEv * 129S4/SvJaeSor * C57BL/6J * SJL

homeostasis/metabolism

decreased intestinal cholesterol absorption ( J:184908 )

• regardless of dietary cholesterol percentage, mice exhibit decreased cholesterol absorption compared with control mice

• when fed 0.05% or 0.1% dietary cholesterol, mice exhibit increased fecal cholesterol loss compared with control mice

increased circulating triglyceride level ( J:184908 )

• in mice fed a 0.05% or 0.5% dietary cholesterol

decreased cholesterol level ( J:184908 )

• decreased biliary cholesterol regardless of dietary cholesterol percentage

• decreased cholesteryl ester in intestinal enterocytes regardless of dietary cholesterol percentage

decreased circulating cholesterol level ( J:184908 )

• in mice fed a 0.05% or 0.5% dietary cholesterol

decreased circulating VLDL cholesterol level ( J:184908 )

• in mice fed a 0.1% or 0.5% dietary cholesterol

decreased liver cholesterol level ( J:184908 )

• total cholesterol and cholesteryl ester regardless of dietary cholesterol percentage

• free cholesterol when fed a 0.5% cholesterol diet

increased cholesterol level ( J:184908 )

• total and free cholesterol are increased in intestinal enterocytes of mice fed a 0.5% cholesterol diet

decreased liver triglyceride level ( J:184908 )

• when fed a 0.5% cholesterol diet

digestive/alimentary system

decreased intestinal cholesterol absorption ( J:184908 )

• regardless of dietary cholesterol percentage, mice exhibit decreased cholesterol absorption compared with control mice

• when fed 0.05% or 0.1% dietary cholesterol, mice exhibit increased fecal cholesterol loss compared with control mice

liver/biliary system

decreased liver cholesterol level ( J:184908 )

• total cholesterol and cholesteryl ester regardless of dietary cholesterol percentage

• free cholesterol when fed a 0.5% cholesterol diet

decreased liver triglyceride level ( J:184908 )

• when fed a 0.5% cholesterol diet

Genotype
MGI:5573126

cn78

• Allelic Composition: Tnfrsf1a^tm2Gkl/Tnfrsf1a⁺; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: 129S/SvEv * C57BL/6J * SJL

mortality/aging

increased susceptibility to induced morbidity/mortality ( J:210950 )

• in mice challenged with TNF

digestive/alimentary system

abnormal intestine physiology ( J:210950 )

• increased intestinal permeability in mice challenged with TNF

Genotype
MGI:3818605

cn79

• Allelic Composition: Atg5^tm1Myok/Atg5^tm1Myok; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: 129S/SvEv * C57BL/6 * SJL

digestive/alimentary system

abnormal Paneth cell morphology ( J:141419 )

• aberrant, disorganized granules as well as decreased granule numbers are observed in these mice

• virtually all Paneth cells have lysozyme localized throughout the cell instead of being discretely packaged within vesicles

• Paneth cells also have degenerating mitochondria, loss of granules and the frequent absence of apical microvilli

• adjacent crypt lumen often contains intact Paneth granules and cytoplasm, which is a phenomenon not observed in wild-type controls

homeostasis/metabolism

impaired autophagy ( J:141419 )

• autophagy by the ileal epithelium is severely reduced in these mice

cellular

impaired autophagy ( J:141419 )

• autophagy by the ileal epithelium is severely reduced in these mice

endocrine/exocrine glands

abnormal Paneth cell morphology ( J:141419 )

• aberrant, disorganized granules as well as decreased granule numbers are observed in these mice

• virtually all Paneth cells have lysozyme localized throughout the cell instead of being discretely packaged within vesicles

• Paneth cells also have degenerating mitochondria, loss of granules and the frequent absence of apical microvilli

• adjacent crypt lumen often contains intact Paneth granules and cytoplasm, which is a phenomenon not observed in wild-type controls

Genotype
MGI:3703443

cn80

• Allelic Composition: Itgb1^tm1Efu/Itgb1^tm1Efu; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: 129X1/SvJ * C57BL/6J * SJL

Crypt hyperplasia and dysplasia and villous enlargement in Itgb1^tm1Efu/Itgb1^tm1Efu Tg(Vil1-cre)997Gum/0 mice

mortality/aging

postnatal lethality, complete penetrance ( J:119155 )

• die between P7 and P14 from severe malnutrition

growth/size/body

decreased body weight ( J:119155 )

• by P4, mutants are less than half the body weight of controls

digestive/alimentary system

steatorrhea ( J:119155 )

• fat malabsorption as indicated by the presence of large fat droplets in the intestinal contents

abnormal intestine morphology ( J:119155 )

• expansion of the intestinal stroma, muscularis, and extracellular matrix

abnormal intestinal epithelium morphology ( J:119155 )

• mutants exhibit an increase in intestinal epithelial cell proliferation in the crypts with dysplasia and polyps, resulting in an expanded epithelium

• the small intestinal epithelium shows a defective microvillus brush border on the apical surfaces of the villous enterocytes

abnormal enterocyte morphology ( J:119155 )

• the intestinal epithelium shows large lipid inclusions within the villous enterocytes that are not seen in controls

• the intestinal microvilli are diminished in size and poorly formed, indicatiang defective enterocyte differentiation

abnormal crypts of Lieberkuhn morphology ( J:119155 )

• intestinal crypt and villi expansion, enlargement, and dysplasia at P16

• crypt hyperplasia is most severe in the distal small intestine, proximal large intestine, and cecum

abnormal large intestine morphology ( J:119155 )

• proximal large intestine is larger in external diameter than in controls

abnormal small intestine morphology ( J:119155 )

• distal small intestine is larger in external diameter than in controls

intestine polyps ( J:119155 )

• multiple juvenile-like polyps in the small intestinal mucosa

abnormal intestinal absorption ( J:119155 )

• although mutants can feed, they are malnourished due to intestinal epithelium defects

homeostasis/metabolism

steatorrhea ( J:119155 )

• fat malabsorption as indicated by the presence of large fat droplets in the intestinal contents

abnormal circulating lipid level ( J:119155 )

• total serum lipid levels are reduced

endocrine/exocrine glands

abnormal crypts of Lieberkuhn morphology ( J:119155 )

• intestinal crypt and villi expansion, enlargement, and dysplasia at P16

• crypt hyperplasia is most severe in the distal small intestine, proximal large intestine, and cecum

Genotype
MGI:5504261

cn81

• Allelic Composition: Fpr2^tm1.1Jimw/Fpr2^tm1.1Jimw; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: 129X1/SvJ * C57BL/6J * SJL

Decreased colon crypt length in Fpr2^tm1.1Jimw/Fpr2^tm1.1Jimw Tg(Vil1-cre)997Gum/0 mice

digestive/alimentary system

abnormal large intestine crypts of Lieberkuhn morphology ( J:197568 )

• shorter than normal colonic crypts

endocrine/exocrine glands

abnormal large intestine crypts of Lieberkuhn morphology ( J:197568 )

• shorter than normal colonic crypts

Genotype
MGI:3806161

cn82

• Allelic Composition: Nr1h4^tm1.1Gonz/Nr1h4^tm1.1Gonz; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: 129X1/SvJ * C57BL/6 * SJL

homeostasis/metabolism

abnormal bile salt homeostasis ( J:129978 )

• mice have almost double the loss of deoxycholic acid in the feces compared to control mice

increased bile salt level ( J:129978 )

• total bile acid pool collected from liver, gallbladder and small intestine trends towards being higher than in controls

• the increases in the bile acid pool consist of increases in cholate and its derivates including taurocholic acid and taurodeoxycholic acid

Genotype
MGI:5493511

cn83

• Allelic Composition: Slc5a6^tm1.1Said/Slc5a6^tm1.1Said; Tg(Vil1-cre)997Gum/?
• Genetic Background: involves: C57BL/6

mortality/aging

premature death ( J:194700 )

• about 2/3 of mice die prematurely between 6 and 10 weeks of age

growth/size/body

postnatal growth retardation ( J:194700 )

• significant postnatal growth retardation

slow postnatal weight gain ( J:194700 )

• mean body weight at 6-10 weeks of age is significantly lower than sex matched control litter mates

skeleton

abnormal appendicular skeleton morphology ( J:194700 )

decreased bone mineral density of humerus ( J:194700 )

• decreased bone density of the humoral heads

short femur ( J:194700 )

short tibia ( J:194700 )

abnormal pelvic girdle bone morphology ( J:194700 )

• shorter pelvic bones

decreased bone mineral density of femur ( J:194700 )

• decreased bone density of the femoral heads

behavior/neurological

lethargy ( J:194700 )

hunched posture ( J:194700 )

• hunched back posture

digestive/alimentary system

abnormal intestinal mucosa morphology ( J:194700 )

• increased neutrophiles in mucosa

• mucosal edema

abnormal large intestine morphology ( J:194700 )

abnormal large intestine crypts of Lieberkuhn morphology ( J:194700 )

• chronic focal cryptitis/crypt abscesses

distended cecum ( J:194700 )

• distended and thinned walls

abnormal small intestine morphology ( J:194700 )

• focal areas of low grade dysplasia

distended ileum ( J:194700 )

• distended and thinned walls

decreased small intestinal villus size ( J:194700 )

• shorter small intestine villi

abnormal vitamin absorption ( J:194700 )

• no biotin or pantothenic acid uptake in the jejunum

endocrine/exocrine glands

endocrine/exocrine gland phenotype ( J:194700 )

N • pancreas normal

abnormal large intestine crypts of Lieberkuhn morphology ( J:194700 )

• chronic focal cryptitis/crypt abscesses

homeostasis/metabolism

abnormal vitamin absorption ( J:194700 )

• no biotin or pantothenic acid uptake in the jejunum

abnormal vitamin level ( J:194700 )

• lower biotin levels in the liver

nervous system

nervous system phenotype ( J:194700 )

N • brain normal

cardiovascular system

cardiovascular system phenotype ( J:194700 )

N • heart normal

respiratory system

respiratory system phenotype ( J:194700 )

N • lungs normal

liver/biliary system

liver/biliary system phenotype ( J:194700 )

N • liver normal

immune system

immune system phenotype ( J:194700 )

N • spleen normal

renal/urinary system

renal/urinary system phenotype ( J:194700 )

N • kidneys normal

limbs/digits/tail

decreased bone mineral density of humerus ( J:194700 )

• decreased bone density of the humoral heads

short femur ( J:194700 )

short tibia ( J:194700 )

Genotype
MGI:5774438

cn84

• Allelic Composition: Lmna^tm4Stw/Lmna^tm4Stw; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: C57BL/6 * C57BL/6J

normal phenotype

no abnormal phenotype detected ( J:220874 )

• mice are born at normal Mendelian ratios and survive for >1 year with no gross defects, such as shortened lifespan or reduced weight

• H&E staining showed normal gastrointestinal (GI) tract histology (duodenum, jejunum, ileum and colon) at 10 weeks of age

• Ki67 staining revealed normal GI epithelial proliferation at 1 year of age

Genotype
MGI:5774439

cn85

• Allelic Composition: Apc^Min/Apc⁺; Lmna^tm4Stw/Lmna^tm4Stw; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: C57BL/6 * C57BL/6J

digestive/alimentary system

duodenum polyps ( J:220874 )

• at 16-32 weeks of age, mice show a 1.5-fold increase in the frequency of larger polyps (2-5 mm) in the duodenum relative to Apc^Min heterozygous controls

jejunum polyps ( J:220874 )

• mice show a 3-fold increase in the frequency of larger polyps (2-5 mm) in the proximal jejunum relative to Apc^Min heterozygous controls

• however, the total number of polyps found in the gastrointestinal tract (duodenum, proximal and distal jejunum, ileum and colon) is not significantly altered relative to ApcMin heterozygous controls

Genotype
MGI:5904968

cn86

• Allelic Composition: Atp2b1^tm1.1Raku/Atp2b1^tm1.1Raku; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: C57BL/6 * C57BL/6J

mortality/aging

prenatal lethality, incomplete penetrance ( J:232942 )

• mice are born at a lower than the expected 25% Mendelian frequency

growth/size/body

decreased birth body size ( J:232942 )

• mice are smaller than control mice at birth

decreased body size ( J:232942 )

• adult mice are smaller than control mice

skeleton

decreased bone mineral density ( J:232942 )

• at 2 months of age, mice fed a 0.81% calcium, 0.34% phosphorus, normal vitamin D diet show a reduction in whole body bone mineral density relative to control mice

decreased bone mineral density of femur ( J:232942 )

• femoral bone mineral density is reduced relative to than in control mice

decreased bone mineralization ( J:232942 )

• mice exhibit reduced bone mineral deposition

homeostasis/metabolism

decreased urine calcium level ( J:232942 )

• urinary calcium concentrations tend to be lower than those in control mice (P = 0.15)

abnormal urine phosphate level ( J:232942 )

• urinary phosphorus concentrations tend to be lower than those in control mice (P = 0.08)

• the urinary phosphorus concentration normalized for creatinine is higher than that in control mice

digestive/alimentary system

decreased intestinal calcium absorption ( J:232942 )

• following i.p. administration of 1alpha,25(OH)₂D₃, mice fail to show an increase in active intestinal calcium transport in everted gut sacs, unlike similarly treated wild-type controls where a ~2-fold increase is observed

renal/urinary system

decreased urine calcium level ( J:232942 )

• urinary calcium concentrations tend to be lower than those in control mice (P = 0.15)

abnormal urine phosphate level ( J:232942 )

• urinary phosphorus concentrations tend to be lower than those in control mice (P = 0.08)

• the urinary phosphorus concentration normalized for creatinine is higher than that in control mice

Genotype
MGI:5898003

cn87

• Allelic Composition: Apc^Min/Apc⁺; Elp3^tm1.1Tac/Elp3^tm1.1Tac; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: C57BL/6 * C57BL/6J * C57BL/6NTac * SJL

cellular

abnormal gastrointestinal brush cell morphology ( J:227334 )

• the number of Tuft cells in the intestinal epithelium are slightly decreased

digestive/alimentary system

digestive/alimentary phenotype ( J:227334 )

N • crypt cell proliferation and cell apoptosis at the top of the villi remain unchanged compared to single Apc^Min mutants

abnormal gastrointestinal brush cell morphology ( J:227334 )

• the number of Tuft cells in the intestinal epithelium are slightly decreased

abnormal intestinal epithelium morphology ( J:227334 )

• the number of Dclk1+ cells in both tumors and adjacent regions are decreased in the intestine

• the number of Tuft cells are slightly decreased

• the number of Dckl1+/acetylated alpha-tubulin-negative cells are highly decreased

decreased intestinal adenoma incidence ( J:227334 )

• mice exhibit decreased tumor number in proximal, middle, and distal intestines compared to single Apc^Min mutants and expanded life span

neoplasm

decreased intestinal adenoma incidence ( J:227334 )

• mice exhibit decreased tumor number in proximal, middle, and distal intestines compared to single Apc^Min mutants and expanded life span

increased tumor latency ( J:227334 )

• mice exhibit delayed tumor appearance in intestinal epithelia compared to single Apc^Min mutants

hematopoietic system

hematopoietic system phenotype ( J:227334 )

N • mice do not exhibit decreased hematocrit levels as seen in single Apc^Min mutants

immune system

immune system phenotype ( J:227334 )

N • mice do not exhibit splenomegaly

Genotype
MGI:5898002

cn88

• Allelic Composition: Elp3^tm1.1Tac/Elp3^tm1.1Tac; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: C57BL/6 * C57BL/6J * C57BL/6NTac * SJL

cellular

abnormal gastrointestinal brush cell morphology ( J:227334 )

• the number of Tuft cells is decreased in intestinal epithelium

digestive/alimentary system

abnormal gastrointestinal brush cell morphology ( J:227334 )

• the number of Tuft cells is decreased in intestinal epithelium

abnormal intestinal epithelium morphology ( J:227334 )

• the number of Dclk1+ cells is decreased in intestinal crypts, suggesting impaired Tuft cell differentiation

• the number of Tuft cells is decreased in intestinal epithelium

impaired intestine regeneration ( J:227334 )

• the number of regenerating crypts following irradiation is decreased compared to controls

Genotype
MGI:5520917

cn89

• Allelic Composition: Tlr4^tm1Djh/Tlr4^tm1Djh; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: C57BL/6 * C57BL/6J * FVB/N * SJL

homeostasis/metabolism

abnormal bile salt level ( J:193668 )

• reduced in the ileal lumen and stool

decreased susceptibility to injury ( J:193668 )

• following induction of necrotizing enterocolitis, mice exhibit preservation of the small intestinal mucosa and minimal cytokine elevation compared with wild-type mice

digestive/alimentary system

abnormal intestinal goblet cell morphology ( J:193668 )

• increased goblet-like cells, more apparent along the duodenum-jejunum-ileum axis

cellular

abnormal intestinal goblet cell morphology ( J:193668 )

• increased goblet-like cells, more apparent along the duodenum-jejunum-ileum axis

Genotype
MGI:6251480

cn90

• Allelic Composition: Pkd2^tm1.1Gwu/Pkd2^tm1.1Gwu; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: C57BL/6 * C57BL/6J * SJL

mortality/aging

premature death ( J:265516 )

• most mice die between 4 and 6 months of age

• more than 50% of females survive to 5 months of age, approximately 1 month longer than males, indicating better survival for females

• treatment with rapamycin from P10 to P60 improves survival, with female rapamycin-treated mice having a median survival of about 7 months and male rapamycin-treated mice 6 months

• enhanced rapamycin treatment (extended duration) improves lifespan even more to a median survival of about 8 months

renal/urinary system

increased kidney cell proliferation ( J:265516 )

• mice show increased proliferation in renal epithelia

• rapamycin treatment suppresses the increased proliferation in renal epithelia

abnormal kidney morphology ( J:265516 )

• by 4 months of age, normal parenchyma is almost completely lost in the kidney

kidney cyst ( J:265516 )

• mice develop severe cysts in the kidneys

• renal cysts derive from all nephronic segments of the kidney

• renal cytogenesis is more severe in males than females

• treatment with rapamycin from P10 to P60 reduces growth of renal cysts, with treatment response better in females than males

• enhanced rapamycin treatment (extended duration) reduces renal cyst growth even more

enlarged kidney ( J:265516 )

• mice exhibit a larger kidney/body weight ratio by P15

kidney failure ( J:265516 )

endocrine/exocrine glands

pancreas cyst ( J:265516 )

• cysts in the pancreas are seen starting at 4 months of age

liver/biliary system

liver cyst ( J:265516 )

• cysts in liver are seen starting at 2 months of age with the cystic liver worsening rapidly with age

• however, the liver/body weight ratio and alanine aminotransferase levels are not different from wild-type

homeostasis/metabolism

increased circulating creatinine level ( J:265516 )

• mice show a higher creatinine level at 1 month of age

• creatinine levels are more elevated in males than in females at 4 months of age

• treatment with rapamycin improves creatinine levels but not completely to normal levels

• enhanced rapamycin treatment improves creatinine levels further

increased blood urea nitrogen level ( J:265516 )

• mice show a higher blood urea nitrogen level at 2 months of age

• blood urea nitrogen levels are more elevated in males than in females at 4 months of age

• treatment with rapamycin or enhanced rapamycin (extended duration) improves BUN levels to normal

cellular

increased kidney cell proliferation ( J:265516 )

• mice show increased proliferation in renal epithelia

• rapamycin treatment suppresses the increased proliferation in renal epithelia

growth/size/body

pancreas cyst ( J:265516 )

• cysts in the pancreas are seen starting at 4 months of age

kidney cyst ( J:265516 )

• mice develop severe cysts in the kidneys

• renal cysts derive from all nephronic segments of the kidney

• renal cytogenesis is more severe in males than females

• treatment with rapamycin from P10 to P60 reduces growth of renal cysts, with treatment response better in females than males

• enhanced rapamycin treatment (extended duration) reduces renal cyst growth even more

liver cyst ( J:265516 )

• cysts in liver are seen starting at 2 months of age with the cystic liver worsening rapidly with age

• however, the liver/body weight ratio and alanine aminotransferase levels are not different from wild-type

enlarged kidney ( J:265516 )

• mice exhibit a larger kidney/body weight ratio by P15

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
autosomal dominant polycystic kidney disease		DOID:898		J:265516

Genotype
MGI:5304853

cn91

• Allelic Composition: Spint1^tm2.1Hk/Spint1^tm2.1Hk; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: C57BL/6 * C57BL/6J * SJL

mortality/aging

increased susceptibility to xenobiotic induced morbidity/mortality ( J:179937 )

• in DSS-treated mice

digestive/alimentary system

abnormal large intestine crypts of Lieberkuhn morphology ( J:179937 )

• mice exhibit dissolution of crypt architecture with reduced crypt size and crypt disorganization unlike in control mice

intestinal ulcer ( J:179937 )

• cecum ulcers in DSS-treated mice

small cecum ( J:179937 )

• in DSS-treated mice

abnormal defecation ( J:179937 )

• bloody stool in DSS-treated mice

diarrhea ( J:179937 )

• in DSS-treated mice

abnormal intestine physiology ( J:179937 )

• mice exhibit increased intestinal permeability compared with control mice

increased enterocyte apoptosis ( J:179937 )

• in colon, suggested by increased epithelial cell shedding

abnormal enterocyte proliferation ( J:179937 )

• increased in the colon

increased susceptibility to induced colitis ( J:179937 )

• DSS-treated mice exhibit delayed mucosal regeneration, short cecum length, cecum ulceration, more severe diarrhea, bloody stool, increased weight loss, and increased mortality compared with control mice

homeostasis/metabolism

increased susceptibility to xenobiotic induced morbidity/mortality ( J:179937 )

• in DSS-treated mice

immune system

increased susceptibility to induced colitis ( J:179937 )

• DSS-treated mice exhibit delayed mucosal regeneration, short cecum length, cecum ulceration, more severe diarrhea, bloody stool, increased weight loss, and increased mortality compared with control mice

cellular

increased enterocyte apoptosis ( J:179937 )

• in colon, suggested by increased epithelial cell shedding

abnormal enterocyte proliferation ( J:179937 )

• increased in the colon

growth/size/body

increased susceptibility to weight loss ( J:179937 )

• in DSS-treated mice

endocrine/exocrine glands

abnormal large intestine crypts of Lieberkuhn morphology ( J:179937 )

• mice exhibit dissolution of crypt architecture with reduced crypt size and crypt disorganization unlike in control mice

Genotype
MGI:5502215

cn92

• Allelic Composition: Zfp148^tm1.1Jmer/Zfp148^tm1.1Jmer; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: C57BL/6 * C57BL/6J * SJL

mortality/aging

increased susceptibility to bacterial infection induced morbidity/mortality ( J:198847 )

• in mice infected with Salmonella typhimurium

immune system

increased inflammatory response ( J:198847 )

• slightly prior to infection

increased susceptibility to bacterial infection ( J:198847 )

• mice infected with Salmonella typhimurium exhibit increased weight loss, earlier lethality and increased colonic and systemic bacterial load compared with wild-type mice

increased susceptibility to bacterial infection induced morbidity/mortality ( J:198847 )

• in mice infected with Salmonella typhimurium

homeostasis/metabolism

decreased serotonin level ( J:198847 )

• in the enteroendocrine cells of the colons and plasma

growth/size/body

increased susceptibility to weight loss ( J:198847 )

• in mice infected with Salmonella typhimurium

Genotype
MGI:6456093

cn93

• Allelic Composition: Mcc^tm1.1Maija/Mcc^tm1.1Maija; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: C57BL/6 * C57BL/6J * SJL

digestive/alimentary system

increased large intestine adenocarcinoma incidence ( J:294342 )

• increased mucinous or non-mucinous adenocarcinomas following drug-induced lesions in colon

neoplasm

increased large intestine adenocarcinoma incidence ( J:294342 )

• increased mucinous or non-mucinous adenocarcinomas following drug-induced lesions in colon

Genotype
MGI:5822876

cn94

• Allelic Composition: Lpcat3^{tm1c(EUCOMM)Wtsi}/Lpcat3^{tm1c(EUCOMM)Wtsi}; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: C57BL/6 * C57BL/6N * SJL
• Cell Lines: EPD0455_5_A07

growth/size/body

decreased body weight ( J:220827 )

• decreased body weight at 1 week of age

• however, body weight is normal at birth

postnatal growth retardation ( J:220827 )

• pups fail to thrive and exhibit severe growth retardation

• however, suckling is normal

homeostasis/metabolism

decreased circulating glucose level ( J:220827 )

• blood glucose levels are very low at 1 week of age

decreased circulating insulin level ( J:220827 )

• plasma insulin levels are significantly lower at 1 week of age

abnormal lipid level ( J:220827 )

• massive accumulation of cytosolic lipid droplets in intestinal enterocytes at 1 week of age

decreased circulating triglyceride level ( J:220827 )

• plasma triglyceride (TG) levels are significantly lower at 1 week of age

digestive/alimentary system

abnormal enterocyte morphology ( J:220827 )

• massive accumulation of cytosolic lipid droplets in intestinal enterocytes at 1 week of age

Genotype
MGI:5476714

cn95

• Allelic Composition: Map3k8^tm1.1Gkl/Map3k8^tm1.1Gkl; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: C57BL/6 * FVB/N * SJL

homeostasis/metabolism

homeostasis/metabolism phenotype ( J:193546 )

N • mice treated with AOM/DSS exhibit normal body weight loss, decreased colon length, inflammation and tissue damage

neoplasm

neoplasm ( J:193546 )

N • mice treated with AOM/DSS exhibit normal tumor formation

Genotype
MGI:6362927

cn96

• Allelic Composition: Rdh7^{tm1c(KOMP)Wtsi}/Rdh7^{tm1c(KOMP)Wtsi}; Tg(RARE-Hspa1b/lacZ)12Jrt/0; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: C57BL/6J * C57BL/6N * CD-1 * SJL

immune system

immune system phenotype ( J:279231 )

N • mice exhibit normal numbers of TH17 and T regulatory cells in the small intestine and colon

decreased lymphocyte cell number ( J:279231 )

• reduced NCR+ IL22-producing RORgammat+ innate lymphoid cells (ILC3s) in the small intestinal lamina propria

• however, the number of NCR- ILC3s and lymphoid tissue inducer (LTi) cells are normal

decreased susceptibility to bacterial infection ( J:279231 )

• enhanced resistance to colonization by gut pathogens (C. rodentium and S. Typhimurium) with reduced colony forming units in the feces and spleen

• however, IL22 supplementation reverses resistance

hematopoietic system

decreased lymphocyte cell number ( J:279231 )

• reduced NCR+ IL22-producing RORgammat+ innate lymphoid cells (ILC3s) in the small intestinal lamina propria

• however, the number of NCR- ILC3s and lymphoid tissue inducer (LTi) cells are normal

Genotype
MGI:5696541

cn97

• Allelic Composition: Atg16l1^{tm1c(EUCOMM)Wtsi}/Atg16l1^{tm1c(EUCOMM)Wtsi}; Tg(Vil1-cre)997Gum/?
• Genetic Background: involves: C57BL/6J * C57BL/6N * SJL

cellular

abnormal autophagy ( J:221019 )

• reduced expression of autophagy regulators in intestinal epithelia, the mesenchymal compartment, and in cecal patches after infection with Salmonella typhimurium

immune system

cecum inflammation ( J:221019 )

• increased inflammation after infection

increased macrophage cell number ( J:221019 )

• greater number of CD11c+ mononuclear cells found in mesenteric lymph nodes after infection

abnormal cytokine level ( J:221019 )

abnormal circulating interleukin level ( J:221019 )

increased circulating interleukin-1 beta level ( J:221019 )

• significantly increased levels in the terminal Ileum and the cecum

increased circulating interleukin-6 level ( J:221019 )

• significantly increased levels in the terminal Ileum and the cecum

abnormal chemokine level ( J:221019 )

• higher levels of CXCL1 and CCL2 in epithelial cells after infection

increased susceptibility to bacterial infection ( J:221019 )

• reduced up-regulation of antimicrobial proteins in intestinal epithelium of Salmonella typhimurium infected mice

• increased numbers of Salmonella in the spleen and mesenteric lymph nodes

digestive/alimentary system

abnormal Paneth cell morphology ( J:221019 )

• abnormal Paneth cell granules before and after infection

decreased Paneth cell number ( J:221019 )

• fewer Paneth cells/ crypt both before and after infection

cecum inflammation ( J:221019 )

• increased inflammation after infection

homeostasis/metabolism

abnormal autophagy ( J:221019 )

• reduced expression of autophagy regulators in intestinal epithelia, the mesenchymal compartment, and in cecal patches after infection with Salmonella typhimurium

abnormal cytokine level ( J:221019 )

abnormal circulating interleukin level ( J:221019 )

increased circulating interleukin-1 beta level ( J:221019 )

• significantly increased levels in the terminal Ileum and the cecum

increased circulating interleukin-6 level ( J:221019 )

• significantly increased levels in the terminal Ileum and the cecum

abnormal chemokine level ( J:221019 )

• higher levels of CXCL1 and CCL2 in epithelial cells after infection

hematopoietic system

increased macrophage cell number ( J:221019 )

• greater number of CD11c+ mononuclear cells found in mesenteric lymph nodes after infection

endocrine/exocrine glands

abnormal Paneth cell morphology ( J:221019 )

• abnormal Paneth cell granules before and after infection

decreased Paneth cell number ( J:221019 )

• fewer Paneth cells/ crypt both before and after infection

Genotype
MGI:7564126

cn98

• Allelic Composition: Api5^em1Cad/Api5⁺; Atg16l1^{tm1c(EUCOMM)Wtsi}/Atg16l1^{tm1c(EUCOMM)Wtsi}; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: C57BL/6J * C57BL/6N * SJL

digestive/alimentary system

abnormal Paneth cell morphology ( J:340266 )

• increased proportion of abnormal Paneth cells

decreased Paneth cell number ( J:340266 )

endocrine/exocrine glands

abnormal Paneth cell morphology ( J:340266 )

• increased proportion of abnormal Paneth cells

decreased Paneth cell number ( J:340266 )

Genotype
MGI:7564119

cn99

• Allelic Composition: Api5^em1Cad/Api5^em1Cad; Atg16l1^{tm1c(EUCOMM)Wtsi}/Atg16l1^{tm1c(EUCOMM)Wtsi}; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: C57BL/6J * C57BL/6N * SJL

mortality/aging

preweaning lethality, incomplete penetrance ( J:340266 )

• fewer than expected are recovered

Genotype
MGI:5751557

cn100

• Allelic Composition: Tg(Vil1-cre)997Gum/?; Tlr4^lps-del/Tlr4^lps-del; Tlr5^tm1.1Gewr/Tlr5^tm1.1Gewr
• Genetic Background: involves: C57BL/6J * C57BL/6NTac * C57BL/10ScN * SJL

homeostasis/metabolism

homeostasis/metabolism phenotype ( J:229155 )

N • mice do not exhibit symptoms of metabolic syndrome

N • fat pad weight, body weight, spleen weight, colon weight, and fasting glucose levels are similar to wild-type

behavior/neurological

polyphagia ( J:229155 )

digestive/alimentary system

abnormal colon morphology ( J:229155 )

• increased colon weight

decreased colon length ( J:229155 )

large intestinal inflammation ( J:229155 )

• low grade inflammation, however, phenotype is less severe than in mice with wild-type Tlr4

immune system

large intestinal inflammation ( J:229155 )

• low grade inflammation, however, phenotype is less severe than in mice with wild-type Tlr4

Genotype
MGI:5751550

cn101

• Allelic Composition: Tg(Vil1-cre)997Gum/?; Tlr5^tm1.1Gewr/Tlr5^tm1.1Gewr
• Genetic Background: involves: C57BL/6J * C57BL/6NTac * SJL/J

adipose tissue

increased total fat pad weight ( J:229155 )

• increased adiposity on chow and high fat diet

behavior/neurological

polyphagia ( J:229155 )

digestive/alimentary system

abnormal colon morphology ( J:229155 )

• shorter and heavier colons on chow diet

• increased colon weight on high fat diet, length is similar to wild-type

decreased colon length ( J:229155 )

abnormal gut flora balance ( J:229155 )

• increase in levels of fecal bacteria

• increase in levels of bacteria adherent to the colonic mucosa

• decreased distance of bacteria from intestinal epithelial cells

• delayed clearance of pathobiont bacteria

• alteration in microbiota composition as compared to controls

large intestinal inflammation ( J:229155 )

• low grade inflammation, however mice do not develop spontaneous colitis

increased susceptibility to colitis induced morbidity/mortality ( J:229155 )

• increased mortality observed in mice on low dose DSS

growth/size/body

increased body weight ( J:229155 )

• on chow and high fat diet

enlarged spleen ( J:229155 )

• mild splenomegaly on chow and high fat diet

hematopoietic system

enlarged spleen ( J:229155 )

• mild splenomegaly on chow and high fat diet

homeostasis/metabolism

increased fasting circulating glucose level ( J:229155 )

• increased levels of blood glucose in males following 15 hr fast

• high fat diet compounds hyperglycemia especially in female mice

increased circulating cholesterol level ( J:229155 )

♂ • in males

increased circulating triglyceride level ( J:229155 )

♂ • in males

immune system

large intestinal inflammation ( J:229155 )

• low grade inflammation, however mice do not develop spontaneous colitis

increased susceptibility to colitis induced morbidity/mortality ( J:229155 )

• increased mortality observed in mice on low dose DSS

enlarged spleen ( J:229155 )

• mild splenomegaly on chow and high fat diet

increased interleukin-1 beta secretion ( J:229155 )

• increased levels of colonic IL1B secretion in males treated with DSS

mortality/aging

increased susceptibility to colitis induced morbidity/mortality ( J:229155 )

• increased mortality observed in mice on low dose DSS

Genotype
MGI:6151439

cn102

• Allelic Composition: Ano10^tm1Jrr/Ano10^tm1Jrr; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: C57BL/6J * SJL

digestive/alimentary system

decreased intestinal epithelial chloride transmembrane transport ( J:260534 )

• calcium-activated chloride ion secretion is abolished in the jejunum compared with wild-type mice

• however, transport in the large intestine is normal

Genotype
MGI:4417845

cn103

• Allelic Composition: Il15ra^tm1Ama/Il15ra^tm2.1Ama; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: C57BL/6J * SJL

hematopoietic system

decreased CD8-positive, gamma-delta intraepithelial T cell number ( J:155298 )

• marked reduction

immune system

decreased CD8-positive, gamma-delta intraepithelial T cell number ( J:155298 )

• marked reduction

Genotype
MGI:4453319

cn104

• Allelic Composition: Ltbr^tm1Avt/Ltbr^tm1Avt; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: C57BL/6J * SJL

immune system

decreased neutrophil cell number ( J:158663 )

• neutrophil numbers are greatly reduced in the lamina propria

increased susceptibility to bacterial infection ( J:158663 )

• show a deficiency in clearing Citrobacter rodentium infection, and display 15-20 times higher bacterial titers in the spleen and feces compared to wild-type mice at days 10 and 14 after infection

• despite this most mice survive the infection

hematopoietic system

decreased neutrophil cell number ( J:158663 )

• neutrophil numbers are greatly reduced in the lamina propria

Genotype
MGI:7549294

cn105

• Allelic Composition: Frmd8^em2Smoc/Frmd8^em2Smoc; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: C57BL/6J * SJL

mortality/aging

increased susceptibility to colitis induced morbidity/mortality ( J:338904 )

• in AOM/DSS-treated mice

digestive/alimentary system

increased colon length ( J:338904 )

• in AOM/DSS-treated mice

increased susceptibility to induced colitis ( J:338904 )

• AOM/DSS-treated mice exhibit increased weight loss, increased tumor burden, shortened colorectum length, and poor survival associated with increased intestinal mucosal barrier damage compared with control mice

increased susceptibility to colitis induced morbidity/mortality ( J:338904 )

• in AOM/DSS-treated mice

neoplasm

increased incidence of tumors by chemical induction ( J:338904 )

• AOM/DSS-treated mice exhibit increased total tumor count and tumor burden with more adenoma formation compared with control mice

growth/size/body

increased susceptibility to weight loss ( J:338904 )

• in AOM/DSS-treated mice

increased spleen weight ( J:338904 )

• with greater lymphocyte infiltration in AOM/DSS-treated mice

hematopoietic system

increased spleen weight ( J:338904 )

• with greater lymphocyte infiltration in AOM/DSS-treated mice

homeostasis/metabolism

increased incidence of tumors by chemical induction ( J:338904 )

• AOM/DSS-treated mice exhibit increased total tumor count and tumor burden with more adenoma formation compared with control mice

immune system

increased susceptibility to induced colitis ( J:338904 )

• AOM/DSS-treated mice exhibit increased weight loss, increased tumor burden, shortened colorectum length, and poor survival associated with increased intestinal mucosal barrier damage compared with control mice

increased susceptibility to colitis induced morbidity/mortality ( J:338904 )

• in AOM/DSS-treated mice

increased spleen weight ( J:338904 )

• with greater lymphocyte infiltration in AOM/DSS-treated mice

Genotype
MGI:5523866

cn106

• Allelic Composition: Apc^Min/Apc⁺; Igf2bp1^tm1Vssp/Igf2bp1^tm1Vssp; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: C57BL/6J * SJL

neoplasm

abnormal tumor incidence ( J:202774 )

• mice develop reduced number of intestinal tumors compared with Apc^min heterozygotes at 90 days

Genotype
MGI:5427871

cn107

• Allelic Composition: Cdc42^tm1Brak/Cdc42⁺; Rab8a^tm1.1Aha/Rab8a⁺; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: C57BL/6J * SJL

digestive/alimentary system

abnormal crypts of Lieberkuhn morphology ( J:184563 )

• greatly expanded or elongated crypts with large lumens and vacuoles

• the inner surfaces of cryptic lumina/values are lined by microvilli

abnormal Paneth cell morphology ( J:184563 )

• electron densities of Paneth cell granules are reduced in crypts

intestinal edema ( J:184563 )

• increase in intestinal tissue weight per surface area, indicating tissue edema

abnormal intestine physiology ( J:184563 )

• mutant intestines exhibit a reduction in glucose uptake compared to either single mutant

endocrine/exocrine glands

abnormal crypts of Lieberkuhn morphology ( J:184563 )

• greatly expanded or elongated crypts with large lumens and vacuoles

• the inner surfaces of cryptic lumina/values are lined by microvilli

abnormal Paneth cell morphology ( J:184563 )

• electron densities of Paneth cell granules are reduced in crypts

homeostasis/metabolism

intestinal edema ( J:184563 )

• increase in intestinal tissue weight per surface area, indicating tissue edema

cellular

abnormal cellular glucose uptake ( J:184563 )

• mutant intestines exhibit a reduction in glucose uptake compared to either single mutant

Genotype
MGI:5427868

cn108

• Allelic Composition: Cdc42^tm1Brak/Cdc42^tm1Brak; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: C57BL/6J * SJL

mortality/aging

premature death ( J:184563 )

• approximately 10% of mutants die at 6 months of age, with an average body weight of about 1/3 that of controls

growth/size/body

decreased body size ( J:184563 )

• mutants appear smaller in size starting at P9

postnatal growth retardation ( J:184563 )

• mutants become severely growth-retarded after weaning, with weight plateauing around 3 months of age

digestive/alimentary system

abnormal anus morphology ( J:184563 )

• at 3 months of age, mutants exhibit anal swelling, however no intestinal bleeding is seen

abnormal intestine morphology ( J:184563 )

abnormal intestinal goblet cell morphology ( J:184563 )

• intestinal crypts contain increased numbers of goblet cells

abnormal intestinal enteroendocrine cell morphology ( J:184563 )

• intestinal crypts contain increased numbers of enteroendocrine cells

abnormal intestinal epithelium morphology ( J:184563 )

• at E16.5, intervillus epithelial cells display abnormalities in cytoplasmic division and nuclear organization

• postnatally, villus epithelial cells show an accumulation of vacuoles in their cytoplasm, which persists throughout adulthood with increased severity

• fetal and adult intestines show disruptions of basolateral plasma membrane in villus epithelia with frequent inclusions of lectin Dolichos biflorus agglutinin to the basolaterally located inter- or intracellular regions

abnormal enterocyte morphology ( J:184563 )

• inclusion bodies become enlarged with age

• mutants exhibit formation of large intracellular vacuolar structures containing microvilli (microvillus inclusion bodies) in epithelial enterocytes as early as P7

abnormal crypts of Lieberkuhn morphology ( J:184563 )

• progenitor cells in intestinal crypts are intermingled and become indistinguishable from transit amplifying cells

• marker analysis indicates decreased stem and Paneth cell populations in crypts

decreased Paneth cell number ( J:184563 )

• complete absence of typical Paneth cell granules in 99% of intestinal crypts at 1 month of age and marker analysis indicates decreased Paneth cell population in crypts

intestinal edema ( J:184563 )

• increase in intestinal tissue weight per surface area, indicating tissue edema

abnormal defecation ( J:184563 )

• soft stools are frequently detected at 3 months of age

abnormal intestine physiology ( J:184563 )

• intestines show reduced nutrient uptake (of glucose, carnosine and proline), with almost no absorption of proline

abnormal small intestinal crypt cell physiology ( J:184563 )

• increase in number of cells undergoing mitosis in intestinal crypts

increased small intestinal crypt cell apoptosis ( J:184563 )

• increase in apoptotic cell number in intestinal crypts

endocrine/exocrine glands

abnormal crypts of Lieberkuhn morphology ( J:184563 )

• progenitor cells in intestinal crypts are intermingled and become indistinguishable from transit amplifying cells

• marker analysis indicates decreased stem and Paneth cell populations in crypts

decreased Paneth cell number ( J:184563 )

• complete absence of typical Paneth cell granules in 99% of intestinal crypts at 1 month of age and marker analysis indicates decreased Paneth cell population in crypts

cellular

abnormal intestinal goblet cell morphology ( J:184563 )

• intestinal crypts contain increased numbers of goblet cells

increased small intestinal crypt cell apoptosis ( J:184563 )

• increase in apoptotic cell number in intestinal crypts

homeostasis/metabolism

intestinal edema ( J:184563 )

• increase in intestinal tissue weight per surface area, indicating tissue edema

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
microvillus inclusion disease		DOID:0060775	OMIM:251850	J:184563

Genotype
MGI:5486337

cn109

• Allelic Composition: Nox1^tm1.1Anrt/Nox1^tm1.1Anrt; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: C57BL/6J * SJL

homeostasis/metabolism

abnormal wound healing ( J:194294 )

♀ • in a wounded healing assay, colonic epithelial cells treated with Ac2-26 do not exhibit an increase in reactive oxygen species generation unlike wild-type cells

♀ • wound healing is not enhanced by treatment with ANXA1 unlike wounded wild-type colonic epithelium

immune system

colitis ( J:194294 )

♀ • DSS-induced colitis is not improved by ANXA1 treatment unlike in wild-type mice

cellular

abnormal redox activity ( J:194294 )

♀ • in a wounded healing assay, colonic epithelial cells treated with Ac2-26 do not exhibit an increase in reactive oxygen species generation unlike wild-type cells

digestive/alimentary system

colitis ( J:194294 )

♀ • DSS-induced colitis is not improved by ANXA1 treatment unlike in wild-type mice

Genotype
MGI:5896385

cn110

• Allelic Composition: Sec24c^{tm1c(EUCOMM)Wtsi}/Sec24c^{tm1c(EUCOMM)Wtsi}; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: C57BL/6 * SJL

growth/size/body

growth/size/body region phenotype ( J:232065 )

N • no abnormalities in growth or weight gain are detected on either a normal chow or high fat diet compared to diet-matched controls

homeostasis/metabolism

homeostasis/metabolism phenotype ( J:232065 )

N • no differences in plasma cholesterol or triglyceride levels

Genotype
MGI:3720321

cn111

• Allelic Composition: Rab8a^tm1.1Aha/Rab8a^tm1.1Aha; Tg(Vil1-cre)997Gum/?
• Genetic Background: involves: C57BL/6 * SJL

mortality/aging

premature death ( J:123415 )

• mice die within 12 weeks of birth

Genotype
MGI:3821726

cn112

• Allelic Composition: Arfrp1^tm2Asch/Arfrp1^tm2Asch; Tg(Vil1-cre)997Gum/?
• Genetic Background: involves: C57BL/6 * SJL

cellular

abnormal cell physiology ( J:142321 )

• disruption of the trans-Golgi to plasma membrane trafficking of E-cadherin in enterocytes

Genotype
MGI:3720322

cn113

• Allelic Composition: Rab8a^tm1.1Aha/Rab8a^tm1.2Aha; Tg(Vil1-cre)997Gum/?
• Genetic Background: involves: C57BL/6 * SJL

mortality/aging

premature death ( J:123415 )

• mice die along a similar time course (3 to 4 weeks) as Rab8a^tm1.2Aha homozygotes

Genotype
MGI:5559513

cn114

• Allelic Composition: Atg16l1^tm1Kuv/Atg16l1^tm1Kuv; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: C57BL/6 * SJL

digestive/alimentary system

abnormal enterocyte morphology ( J:206084 )

• IECs (intestinal epithelial cells) have distended endoplasmic reticula, and reduced size and number of secretory granules

abnormal Paneth cell morphology ( J:206084 )

• cells display reduced overall size and number of secretory granules

abnormal enterocyte physiology ( J:206084 )

• IECs display loss of homeostatic autophagy

cellular

abnormal autophagy ( J:206084 )

• IECs (intestinal epithelial cells) display loss of homeostatic autophagy

endocrine/exocrine glands

abnormal Paneth cell morphology ( J:206084 )

• cells display reduced overall size and number of secretory granules

homeostasis/metabolism

abnormal autophagy ( J:206084 )

• IECs (intestinal epithelial cells) display loss of homeostatic autophagy

Genotype
MGI:5607632

cn115

• Allelic Composition: Abcg5^tm1.1Hobb/Abcg5^tm1.1Hobb; Abcg8^tm1.1Hobb/Abcg8^tm1.1Hobb; Tg(Vil1-cre)997Gum/?
• Genetic Background: involves: C57BL/6 * SJL

cellular

abnormal cellular cholesterol metabolism ( J:215443 )

decreased cholesterol efflux ( J:215443 )

• decreased amount of cholesterol is excreted into the feces as compared to controls

digestive/alimentary system

abnormal feces composition ( J:215443 )

increased intestinal phytosterol absorption ( J:215443 )

• rate of clearance of sitosterol from circulation is decreased

• fractional absorption of the phytosterol, campesterol, is increased

homeostasis/metabolism

abnormal cellular cholesterol metabolism ( J:215443 )

decreased cholesterol efflux ( J:215443 )

• decreased amount of cholesterol is excreted into the feces as compared to controls

increased intestinal phytosterol absorption ( J:215443 )

• rate of clearance of sitosterol from circulation is decreased

• fractional absorption of the phytosterol, campesterol, is increased

increased phytosterol level ( J:215443 )

♀ • increased levels of phytosterols in enterocytes

♀ • increased levels of biliary plant sterols (sitosterol and campesterol) as compared to controls

increased circulating phytosterol level ( J:215443 )

♀ • mean plasma levels of sitosterol and campesterol are increased as compared to controls, but are not as high as mice that carry null alleles for both Abcg5 and Abcg8