Phenotypes associated with this allele

• Allele Symbol: Alb^{tm1(cre/ERT2)Mtz}
• Allele Name: targeted mutation 1, Daniel Metzger
• Allele ID: MGI:3052812
• Summary: 19 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
ht1	Alb^tm1(cre/ERT2)Mtz/Alb^+	involves: 129S2/SvPas * C57BL/6	MGI:3053224
cn2	Uri1^tm1.1Ndj/Uri1^+ Alb^tm1(cre/ERT2)Mtz/Alb^+	B6.Cg-Alb^tm1(cre/ERT2)Mtz Uri1^tm1.1Ndj	MGI:6378450
cn3	Uri1^tm1.1Ndj/Uri1^tm1.1Ndj Alb^tm1(cre/ERT2)Mtz/Alb^+	B6.Cg-Alb^tm1(cre/ERT2)Mtz Uri1^tm1.1Ndj	MGI:6378449
cn4	Gt(ROSA)26Sor^tm2(OVA/EGFP)Dwir/Gt(ROSA)26Sor^+ Alb^tm1(cre/ERT2)Mtz/Alb^+	involves: 129P2/OlaHsd * 129S2/SvPas	MGI:5056503
cn5	Alb^tm1(cre/ERT2)Mtz/Alb^+ Kras^tm4Tyj/Kras^+ Pten^tm2Mak/Pten^tm2Mak	involves: 129P2/OlaHsd * 129S2/SvPas * 129S4/SvJae	MGI:6256733
cn6	Alb^tm1(cre/ERT2)Mtz/Alb^tm1(cre/ERT2)Mtz Slc2a2^tm2Thor/Slc2a2^tm2Thor	involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6	MGI:5514226
cn7	Gt(ROSA)26Sor^tm2(OVA/EGFP)Dwir/Gt(ROSA)26Sor^+ Tg(TcraTcrb)1100Mjb/0 Alb^tm1(cre/ERT2)Mtz/Alb^+	involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6	MGI:5056505
cn8	Mob1a^tm1.1Asuz/Mob1a^tm1.1Asuz Mob1b^Gt(CC0690)Wtsi/Mob1b^Gt(CC0690)Wtsi Alb^tm1(cre/ERT2)Mtz/Alb^+	involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6	MGI:5897810
cn9	Alb^tm1(cre/ERT2)Mtz/Alb^+ Gt(ROSA)26Sor^tm1(Notch1)Dam/Gt(ROSA)26Sor^+	involves: 129S2/SvPas * 129S4/SvJaeSor * C57BL/6	MGI:5506741
cn10	Alb^tm1(cre/ERT2)Mtz/Alb^+ Per2^tm1Jt/Per2^+ Smg6^tm1.1Tac/Smg6^tm1.1Tac	involves: 129S2/SvPas * 129S6/SvEvTac * C57BL/6J	MGI:7571625
cn11	Alb^tm1(cre/ERT2)Mtz/Alb^+ Polr2m^tm1.1Rgr/Polr2m^tm1.1Rgr Trp53^tm1Tyj/Trp53^tm1Tyj	involves: 129S2/SvPas * C57BL/6	MGI:6515759
cn12	Alb^tm1(cre/ERT2)Mtz/Alb^+ Hcfc1^tm1Lwh/Hcfc1^+	involves: 129S2/SvPas * C57BL/6	MGI:5901756
cn13	Slc2a9^tm1.1Thor/Slc2a9^+ Alb^tm1(cre/ERT2)Mtz/Alb^+	involves: 129S2/SvPas * C57BL/6 * C57BL/6N	MGI:4361282
cn14	Slc2a9^tm1.1Thor/Slc2a9^tm1.1Thor Alb^tm1(cre/ERT2)Mtz/Alb^+	involves: 129S2/SvPas * C57BL/6 * C57BL/6N	MGI:4361281
cn15	Alb^tm1(cre/ERT2)Mtz/Alb^+ Hes1^tm1Kag/Hes1^tm1Kag	involves: 129S2/SvPas * C57BL/6 * CBA	MGI:5506744
cn16	G6pc1^tm1.1Ics/G6pc1^tm1.1Ics Alb^tm1(cre/ERT2)Mtz/Alb^+	involves: 129S2/SvPas * C57BL/6J	MGI:5478556
cn17	Orc1^tm1.1Gle/Orc1^tm1.1Gle Alb^tm1(cre/ERT2)Mtz/Alb^+	involves: 129S2/SvPas * C57BL/6 * SJL	MGI:7408241
cn18	Alb^tm1(cre/ERT2)Mtz/Alb^+ Nr5a2^tm1Sjns/Nr5a2^tm1Sjns	involves: 129/Sv * 129S2/SvPas * C57BL/6 * SJL	MGI:3769251
cn19	Alb^tm1(cre/ERT2)Mtz/Alb^+ Fth1^tm1.1Lck/Fth1^tm1.1Lck	involves: 129/Sv * C57BL/6 * SJL	MGI:4848042

Genotype
MGI:3053224

ht1

• Allelic Composition: Alb^{tm1(cre/ERT2)Mtz}/Alb⁺
• Genetic Background: involves: 129S2/SvPas * C57BL/6

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

normal phenotype

no abnormal phenotype detected ( J:92298 )

• cre expression occurred specifically in the hepatocytes of Tam treated mice

Genotype
MGI:6378450

cn2

• Allelic Composition: Uri1^tm1.1Ndj/Uri1⁺; Alb^{tm1(cre/ERT2)Mtz}/Alb⁺
• Genetic Background: B6.Cg-Alb^{tm1(cre/ERT2)Mtz} Uri1^tm1.1Ndj

homeostasis/metabolism

abnormal enzyme/coenzyme level ( J:217463 )

• NAD+ levels are increased in tamoxifen-treated livers

decreased incidence of tumors by chemical induction ( J:217463 )

• tamoxifen-treated mice treated with diethylnitrosamine (DEN) do not show tumors at 24 weeks of age as seen in 60% of control mice and show normal alanine transaminase levels

decreased susceptibility to injury ( J:217463 )

• tamoxifien-treated mice supplied with a liver damage-inducing 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DCC)-supplemented diet present less liver damage and fibrosis

neoplasm

decreased incidence of tumors by chemical induction ( J:217463 )

• tamoxifen-treated mice treated with diethylnitrosamine (DEN) do not show tumors at 24 weeks of age as seen in 60% of control mice and show normal alanine transaminase levels

Genotype
MGI:6378449

cn3

• Allelic Composition: Uri1^tm1.1Ndj/Uri1^tm1.1Ndj; Alb^{tm1(cre/ERT2)Mtz}/Alb⁺
• Genetic Background: B6.Cg-Alb^{tm1(cre/ERT2)Mtz} Uri1^tm1.1Ndj

mortality/aging

postnatal lethality ( J:217463 )

• tamoxifen-treated mice die around 10 days of age probably from fulminant liver failure

liver/biliary system

liver hemorrhage ( J:217463 )

• tamoxifen-treated mice show dilated veins with intrahepatic bleeding

increased hepatocyte apoptosis ( J:217463 )

• Sirius Red staining, collapsed reticulin fibers, and increased ALT levels in tamoxifen-treated mice indicate that hepatocytes undergo massive apoptosis, leading to liver injury

liver inflammation ( J:217463 )

• tamoxifen-treated mice exhibit inflammatory cell infiltration in the liver

abnormal liver morphology ( J:217463 )

• tamoxifen-treated mice exhibit disruption of liver tissue architecture, presence of atypia, dilated veins with intrahepatic bleeding, signs of necrosis and inflammatory cell infiltration

hepatic necrosis ( J:217463 )

• in tamoxifen-treated mice

liver failure ( J:217463 )

homeostasis/metabolism

increased circulating alanine transaminase level ( J:217463 )

• tamoxifen-treated mice show increased alanine transaminase (ALT) levels

cardiovascular system

liver hemorrhage ( J:217463 )

• tamoxifen-treated mice show dilated veins with intrahepatic bleeding

immune system

liver inflammation ( J:217463 )

• tamoxifen-treated mice exhibit inflammatory cell infiltration in the liver

cellular

increased hepatocyte apoptosis ( J:217463 )

• Sirius Red staining, collapsed reticulin fibers, and increased ALT levels in tamoxifen-treated mice indicate that hepatocytes undergo massive apoptosis, leading to liver injury

Genotype
MGI:5056503

cn4

• Allelic Composition: Gt(ROSA)26Sor^{tm2(OVA/EGFP)Dwir}/Gt(ROSA)26Sor⁺; Alb^{tm1(cre/ERT2)Mtz}/Alb⁺
• Genetic Background: involves: 129P2/OlaHsd * 129S2/SvPas

liver/biliary system

abnormal hepatocyte physiology ( J:173806 )

• hepatocytes from tamoxifen-treated mice are capable of activating OT-I CD8+ T cells unlike cells from un-induced mice

Genotype
MGI:6256733

cn5

• Allelic Composition: Alb^{tm1(cre/ERT2)Mtz}/Alb⁺; Kras^tm4Tyj/Kras⁺; Pten^tm2Mak/Pten^tm2Mak
• Genetic Background: involves: 129P2/OlaHsd * 129S2/SvPas * 129S4/SvJae

neoplasm

increased cholangiocarcinoma incidence ( J:254370 )

• mice injected with tamoxifen at P10 develop liver tumors that are exclusively intrahepatic cholangiocarcinoma

increased hepatocellular carcinoma incidence ( J:254370 )

• mice injected with tamoxifen at 8 weeks after birth develop multiple liver tumors that are all hepatocellular carcinoma and hepatocellular dysplasia, but not intrahepatic cholangiocarcinoma

liver/biliary system

increased cholangiocarcinoma incidence ( J:254370 )

• mice injected with tamoxifen at P10 develop liver tumors that are exclusively intrahepatic cholangiocarcinoma

increased hepatocellular carcinoma incidence ( J:254370 )

• mice injected with tamoxifen at 8 weeks after birth develop multiple liver tumors that are all hepatocellular carcinoma and hepatocellular dysplasia, but not intrahepatic cholangiocarcinoma

endocrine/exocrine glands

increased cholangiocarcinoma incidence ( J:254370 )

• mice injected with tamoxifen at P10 develop liver tumors that are exclusively intrahepatic cholangiocarcinoma

Genotype
MGI:5514226

cn6

• Allelic Composition: Alb^{tm1(cre/ERT2)Mtz}/Alb^{tm1(cre/ERT2)Mtz}; Slc2a2^tm2Thor/Slc2a2^tm2Thor
• Genetic Background: involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6

Suppressed hepatic glucose uptake in Slc2a2^tm2Thor/Slc2a2^tm2Thor Alb^{tm1(cre/ERT2)Mtz}/Alb^{tm1(cre/ERT2)Mtz} mice

homeostasis/metabolism

homeostasis/metabolism phenotype ( J:197607 )

N • tamoxifen-treated mice exhibit normal energy homeostasis and plasma glucagon levels

abnormal glucose homeostasis ( J:197607 )

• tamoxifen-treated mice exhibit reduced hepatic glucose output and rate of glucose disappearance under basal but not insulin clamp conditions

decreased insulin secretion ( J:197607 )

• at 4 months following intraperitoneal glucose injection in tamoxifen-treated mice

• reduced insulin secretory capacity in islets of tamoxifen-treated mice

abnormal circulating glucose level ( J:197607 )

• rapid decrease of serum glucose levels early in the fasting period of tamoxifen-treated mice due to impaired hepatic glycogen mobilization

impaired glucose tolerance ( J:197607 )

• progressive development in tamoxifen-treated mice beginning at 4 months

abnormal glycogen homeostasis ( J:197607 )

• rapid decrease of serum glucose levels early in the fasting period of tamoxifen-treated mice due to impaired hepatic glycogen mobilization

increased liver glycogen level ( J:197607 )

• in fasted mice treated with tamoxifen

abnormal lipid homeostasis ( J:197607 )

• tamoxifen-treated mice exhibit increased VLDL production compared with control mice

• however, plasma triglycerides and cholesterol levels are normal

abnormal bile salt level ( J:197607 )

• decreased bile acid with altered composition in the feces of tamoxifen-treated mice

• however, serum levels are normal

decreased liver cholesterol level ( J:197607 )

• in fasted tamoxifen-treated mice

decreased liver triglyceride level ( J:197607 )

• in fasted mice treated with tamoxifen

cellular

increased skeletal muscle cell glucose uptake ( J:197607 )

• increased uptake in the extensor digitorum longus muscle of tamoxifen-treated mice during hyperinsulinemic clamp

decreased cellular glucose uptake ( J:197607 )

• in the liver of tamoxifen-treated mice

• however, fasted glucose production in the liver is normal

liver/biliary system

increased liver glycogen level ( J:197607 )

• in fasted mice treated with tamoxifen

decreased liver cholesterol level ( J:197607 )

• in fasted tamoxifen-treated mice

decreased liver triglyceride level ( J:197607 )

• in fasted mice treated with tamoxifen

muscle

increased skeletal muscle cell glucose uptake ( J:197607 )

• increased uptake in the extensor digitorum longus muscle of tamoxifen-treated mice during hyperinsulinemic clamp

endocrine/exocrine glands

decreased insulin secretion ( J:197607 )

• at 4 months following intraperitoneal glucose injection in tamoxifen-treated mice

• reduced insulin secretory capacity in islets of tamoxifen-treated mice

Genotype
MGI:5056505

cn7

• Allelic Composition: Gt(ROSA)26Sor^{tm2(OVA/EGFP)Dwir}/Gt(ROSA)26Sor⁺; Tg(TcraTcrb)1100Mjb/0; Alb^{tm1(cre/ERT2)Mtz}/Alb⁺
• Genetic Background: involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6

homeostasis/metabolism

increased circulating alanine transaminase level ( J:173806 )

• tamoxifen-treated mice exhibit increased serum alanine transaminase levels compared with un-induced mice

• however, un-induced mice exhibit normal alanine transaminase levels

Genotype
MGI:5897810

cn8

• Allelic Composition: Mob1a^tm1.1Asuz/Mob1a^tm1.1Asuz; Mob1b^{Gt(CC0690)Wtsi}/Mob1b^{Gt(CC0690)Wtsi}; Alb^{tm1(cre/ERT2)Mtz}/Alb⁺
• Genetic Background: involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6

liver/biliary system

increased hepatobiliary system tumor incidence ( J:228499 )

• at 5 weeks, tamoxifen-treated mice exhibit milder combined hepatocellular and cholangiocarcinomas, hepatocellular carcinoma and intrahepatic cholangiocellular carcinoma compared with conditional mice with Tg(Alb-cre)21Mgn transgene

neoplasm

increased hepatobiliary system tumor incidence ( J:228499 )

• at 5 weeks, tamoxifen-treated mice exhibit milder combined hepatocellular and cholangiocarcinomas, hepatocellular carcinoma and intrahepatic cholangiocellular carcinoma compared with conditional mice with Tg(Alb-cre)21Mgn transgene

Genotype
MGI:5506741

cn9

• Allelic Composition: Alb^{tm1(cre/ERT2)Mtz}/Alb⁺; Gt(ROSA)26Sor^{tm1(Notch1)Dam}/Gt(ROSA)26Sor⁺
• Genetic Background: involves: 129S2/SvPas * 129S4/SvJaeSor * C57BL/6

neoplasm

increased cholangiocarcinoma incidence ( J:192740 )

• after 14 weeks of tamoxifen administration, neoplastic nodules form rapidly in the liver, presumably due to increased Notch1 signaling

liver/biliary system

increased cholangiocarcinoma incidence ( J:192740 )

• after 14 weeks of tamoxifen administration, neoplastic nodules form rapidly in the liver, presumably due to increased Notch1 signaling

endocrine/exocrine glands

increased cholangiocarcinoma incidence ( J:192740 )

• after 14 weeks of tamoxifen administration, neoplastic nodules form rapidly in the liver, presumably due to increased Notch1 signaling

Genotype
MGI:7571625

cn10

• Allelic Composition: Alb^{tm1(cre/ERT2)Mtz}/Alb⁺; Per2^tm1Jt/Per2⁺; Smg6^tm1.1Tac/Smg6^tm1.1Tac
• Genetic Background: involves: 129S2/SvPas * 129S6/SvEvTac * C57BL/6J

behavior/neurological

abnormal locomotor circadian rhythm ( J:342742 )

• when entrained on a light phase feeding regimen

prolonged circadian behavior period ( J:342742 )

• 3-hours longer period in liver explants

abnormal circadian behavior phase ( J:342742 )

• phase differences at the pre-mRNA level for many core clock genes in liver

abnormal circardian behavior entrainment ( J:342742 )

• when entrained on a light phase feeding regimen

Genotype
MGI:6515759

cn11

• Allelic Composition: Alb^{tm1(cre/ERT2)Mtz}/Alb⁺; Polr2m^tm1.1Rgr/Polr2m^tm1.1Rgr; Trp53^tm1Tyj/Trp53^tm1Tyj
• Genetic Background: involves: 129S2/SvPas * C57BL/6

liver/biliary system

increased hepatocyte karyomegaly ( J:291184 )

• following tamoxifen injection, nuclei are enlarged compared to cells from Trp53 null mice

increased hepatocyte proliferation ( J:291184 )

• expression analysis indicates hepatocytes rapidly reenter the cell cycle after tamoxifen treatment

cellular

increased hepatocyte karyomegaly ( J:291184 )

• following tamoxifen injection, nuclei are enlarged compared to cells from Trp53 null mice

increased hepatocyte proliferation ( J:291184 )

• expression analysis indicates hepatocytes rapidly reenter the cell cycle after tamoxifen treatment

Genotype
MGI:5901756

cn12

• Allelic Composition: Alb^{tm1(cre/ERT2)Mtz}/Alb⁺; Hcfc1^tm1Lwh/Hcfc1⁺
• Genetic Background: involves: 129S2/SvPas * C57BL/6

liver/biliary system

impaired liver regeneration ( J:231596 )

♀ • after induction with tamoxifen and partial hepatectomy, Hcfc1-negative cells do not display cell proliferation markers

Genotype
MGI:4361282

cn13

• Allelic Composition: Slc2a9^tm1.1Thor/Slc2a9⁺; Alb^{tm1(cre/ERT2)Mtz}/Alb⁺
• Genetic Background: involves: 129S2/SvPas * C57BL/6 * C57BL/6N

homeostasis/metabolism

increased urine magnesium level ( J:153089 )

• mild increase in Mg2+ fractional excretion after tamoxifen treatment

increased urine phosphate level ( J:153089 )

• mild increase in urine Pi levels after tamoxifen treatment

renal/urinary system

increased urine magnesium level ( J:153089 )

• mild increase in Mg2+ fractional excretion after tamoxifen treatment

increased urine phosphate level ( J:153089 )

• mild increase in urine Pi levels after tamoxifen treatment

Genotype
MGI:4361281

cn14

• Allelic Composition: Slc2a9^tm1.1Thor/Slc2a9^tm1.1Thor; Alb^{tm1(cre/ERT2)Mtz}/Alb⁺
• Genetic Background: involves: 129S2/SvPas * C57BL/6 * C57BL/6N

homeostasis/metabolism

increased blood uric acid level ( J:153089 )

• 2 weeks after tamoxifen treatment, plasma urate levels are increased

increased urine potassium level ( J:153089 )

• after tamoxifen treatment

increased urine magnesium level ( J:153089 )

• mild increase in Mg2+ fractional excretion after tamoxifen treatment

decreased urine osmolality ( J:153089 )

• after tamoxifen treatment, urine osmolality is decreased and water deprivation fails to increase urine osmolality

decreased urine pH ( J:153089 )

• after tamoxifen treatment

increased urine phosphate level ( J:153089 )

• mild increase in urine Pi levels after tamoxifen treatment

uraturia ( J:153089 )

• 2 weeks after tamoxifen treatment, urine urate levels are increased about 20 fold

• after tamoxifen treatment, fractional excretion of urate is about 25% in both males and females and daily urate excretion is elevated

renal/urinary system

renal/urinary system phenotype ( J:153089 )

N • unlike in germline null mice, liver specific null mice have normal kidney histology

increased urine potassium level ( J:153089 )

• after tamoxifen treatment

increased urine magnesium level ( J:153089 )

• mild increase in Mg2+ fractional excretion after tamoxifen treatment

decreased urine osmolality ( J:153089 )

• after tamoxifen treatment, urine osmolality is decreased and water deprivation fails to increase urine osmolality

decreased urine pH ( J:153089 )

• after tamoxifen treatment

increased urine phosphate level ( J:153089 )

• mild increase in urine Pi levels after tamoxifen treatment

uraturia ( J:153089 )

• 2 weeks after tamoxifen treatment, urine urate levels are increased about 20 fold

• after tamoxifen treatment, fractional excretion of urate is about 25% in both males and females and daily urate excretion is elevated

polyuria ( J:153089 )

• after tamoxifen treatment, urine volume is increased about 2 fold

Genotype
MGI:5506744

cn15

• Allelic Composition: Alb^{tm1(cre/ERT2)Mtz}/Alb⁺; Hes1^tm1Kag/Hes1^tm1Kag
• Genetic Background: involves: 129S2/SvPas * C57BL/6 * CBA

neoplasm

neoplasm ( J:192740 )

N • after 14 weeks of tamoxifen administration, neoplastic nodules are not found in livers of mice; intrahepatic cholangiocarcinoma (ICC) does not develop in absence of Notch1- mediated conversion of hepatocytes into biliary lineage cells

Genotype
MGI:5478556

cn16

• Allelic Composition: G6pc1^tm1.1Ics/G6pc1^tm1.1Ics; Alb^{tm1(cre/ERT2)Mtz}/Alb⁺
• Genetic Background: involves: 129S2/SvPas * C57BL/6J

homeostasis/metabolism

homeostasis/metabolism phenotype ( J:195257 )

N • unlike in global knock-out mice, glycogen accumulation is not observed in the kidney or intestine of tamoxifen-treated mice

abnormal blood homeostasis ( J:195257 )

• increased serum lactic acid in tamoxifen-treated mice after 10 day or 1 month

• however, levels are normal at 6 and 18 months

increased blood uric acid level ( J:195257 )

• 3-fold in tamoxifen-treated mice after 10 day or 1 month

• however, levels are normal at 6 and 18 months

increased circulating cholesterol level ( J:195257 )

• twice as high in tamoxifen-treated mice

increased circulating triglyceride level ( J:195257 )

• 3-fold in tamoxifen-treated mice

• however, levels at 18 months are normal

increased liver glycogen level ( J:195257 )

• in tamoxifen-treated mice

increased liver triglyceride level ( J:195257 )

• in tamoxifen-treated mice

liver/biliary system

enlarged liver ( J:195257 )

• in tamoxifen-treated mice

increased liver weight ( J:195257 )

• in tamoxifen-treated mice

increased liver glycogen level ( J:195257 )

• in tamoxifen-treated mice

increased liver triglyceride level ( J:195257 )

• in tamoxifen-treated mice

abnormal hepatocyte morphology ( J:195257 )

• large hepatocyte containing large lipid vacuoles in tamoxifen-treated mice

hepatic steatosis ( J:195257 )

• in tamoxifen-treated mice

increased liver adenoma incidence ( J:195257 )

• in tamoxifen-treated mice after a year

• however, no hepatocellular carcinoma is observed

pale liver ( J:195257 )

• in tamoxifen-treated mice

neoplasm

increased liver adenoma incidence ( J:195257 )

• in tamoxifen-treated mice after a year

• however, no hepatocellular carcinoma is observed

growth/size/body

enlarged liver ( J:195257 )

• in tamoxifen-treated mice

increased liver weight ( J:195257 )

• in tamoxifen-treated mice

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
glycogen storage disease Ia		DOID:2749	OMIM:232200	J:195257

Genotype
MGI:7408241

cn17

• Allelic Composition: Orc1^tm1.1Gle/Orc1^tm1.1Gle; Alb^{tm1(cre/ERT2)Mtz}/Alb⁺
• Genetic Background: involves: 129S2/SvPas * C57BL/6 * SJL

liver/biliary system

liver/biliary system phenotype ( J:272584 )

N • mice fed tamoxifen chow at 6 weeks of age (postweaning) show no significant differences in hepatocyte nuclear size or ploidy levels at 9 weeks of age relative to controls

increased hepatocyte karyomegaly ( J:272584 )

• mice fed tamoxifen chow at birth (preweaning) exhibit livers with fewer hepatocytes containing visibly larger nuclei at 3 weeks of age

decreased hepatocyte number ( J:272584 )

• mice fed tamoxifen chow at birth (preweaning) exhibit livers with fewer hepatocytes at 3 weeks of age

cellular

cellular phenotype ( J:272584 )

N • mice fed tamoxifen chow at 6 weeks of age (postweaning) show no significant differences in hepatocyte ploidy levels at 9 weeks of age relative to controls

polyploidy ( J:272584 )

• mice fed tamoxifen chow at birth (preweaning) exhibit hepatocytes accumulating 4C or greater DNA content by 3 weeks of age

increased hepatocyte karyomegaly ( J:272584 )

• mice fed tamoxifen chow at birth (preweaning) exhibit livers with fewer hepatocytes containing visibly larger nuclei at 3 weeks of age

Genotype
MGI:3769251

cn18

• Allelic Composition: Alb^{tm1(cre/ERT2)Mtz}/Alb⁺; Nr5a2^tm1Sjns/Nr5a2^tm1Sjns
• Genetic Background: involves: 129/Sv * 129S2/SvPas * C57BL/6 * SJL

homeostasis/metabolism

abnormal feces lipid level ( J:129068 )

increased feces bile salt level ( J:129068 )

• following treatment with tamoxifen, bile acid in the feces is almost doubled in Nr5a2^tm2Sjns homozygotes due to an increase in lithocholic acid and hydrophobic secondary bile acids produced in the intestine by bacteria

abnormal intestinal lipid absorption ( J:129068 )

• following treatment with tamoxifen, mice exhibit lipid malabsorption

abnormal bile salt level ( J:129068 )

• following treatment with tamoxifen, the bile acid pool size is reduced as is the levels in the livers /gallbladders and intestines due to a reduction in cholic acid and tauroconjugated cholic acid while the levels of muricholic acid, ursodeoxycholic acid and their taurine conjugates are increased

digestive/alimentary system

abnormal feces composition ( J:129068 )

• following treatment with tamoxifen, feces lipid and bile acid content is increased

abnormal feces lipid level ( J:129068 )

increased feces bile salt level ( J:129068 )

• following treatment with tamoxifen, bile acid in the feces is almost doubled in Nr5a2^tm2Sjns homozygotes due to an increase in lithocholic acid and hydrophobic secondary bile acids produced in the intestine by bacteria

abnormal intestinal lipid absorption ( J:129068 )

• following treatment with tamoxifen, mice exhibit lipid malabsorption

Genotype
MGI:4848042

cn19

• Allelic Composition: Alb^{tm1(cre/ERT2)Mtz}/Alb⁺; Fth1^tm1.1Lck/Fth1^tm1.1Lck
• Genetic Background: involves: 129/Sv * C57BL/6 * SJL

homeostasis/metabolism

abnormal liver iron level ( J:166515 )

• iron-loaded, tamoxifen-treated mice exhibit absence of iron staining from hepatocytes but some strongly stained cells, mainly identified as macrophages, unlike in similarly treated Fth1^tm1.1Lck homozygotes

liver/biliary system

liver/biliary system phenotype ( J:166515 )

N • no liver damage is observed in tamoxifen-treated mice fed standard chow

abnormal liver iron level ( J:166515 )

• iron-loaded, tamoxifen-treated mice exhibit absence of iron staining from hepatocytes but some strongly stained cells, mainly identified as macrophages, unlike in similarly treated Fth1^tm1.1Lck homozygotes