Analysis Tools|
Allele Symbol Allele Name Allele ID |
Alb+ wild type MGI:2440246 |
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| Summary |
22 genotypes
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• cre expression occurred specifically in the hepatocytes of Tam treated mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• tamoxifen-treated mice die around 10 days of age probably from fulminant liver failure
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• tamoxifen-treated mice show dilated veins with intrahepatic bleeding
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• Sirius Red staining, collapsed reticulin fibers, and increased ALT levels in tamoxifen-treated mice indicate that hepatocytes undergo massive apoptosis, leading to liver injury
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• tamoxifen-treated mice exhibit inflammatory cell infiltration in the liver
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• tamoxifen-treated mice exhibit disruption of liver tissue architecture, presence of atypia, dilated veins with intrahepatic bleeding, signs of necrosis and inflammatory cell infiltration
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• in tamoxifen-treated mice
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• tamoxifen-treated mice show increased alanine transaminase (ALT) levels
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• tamoxifen-treated mice show dilated veins with intrahepatic bleeding
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• tamoxifen-treated mice exhibit inflammatory cell infiltration in the liver
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• Sirius Red staining, collapsed reticulin fibers, and increased ALT levels in tamoxifen-treated mice indicate that hepatocytes undergo massive apoptosis, leading to liver injury
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• NAD+ levels are increased in tamoxifen-treated livers
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• 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
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• tamoxifien-treated mice supplied with a liver damage-inducing 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DCC)-supplemented diet present less liver damage and fibrosis
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• 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
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• UDCA (hydrophilic non-12alpha-OH BA) is significantly decreased by CDAHFD feeding, such that CDAHFD-fed males show a further reduction in UDCA content relative to SC-fed males and CDAHFD-fed wild-type controls
• male mice fed either a standard control (SC) diet or a choline-deficient, L-amino acid-defined, high-fat diet (CDAHFD) for 8 weeks show hepatic bile acid (BA) pools that are more conducive to liver fibrosis development, with significantly increased hydrophobic 12alpha-OH BAs [cholic acids (CAs) and deoxycholic acids (DCAs)] and decreased hydrophilic non-12alpha-OH BAs [muricholic acids (MCAs), hyodeoxycholic acids (HDCAs) and ursodeoxycholic acids (UDCAs)]
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• male mice fed a CDAHFD for 8 weeks show more severe liver fibrosis, an increased number of hepatic alpha-SMA-positive cells, and higher mRNA expression levels of hepatic fibrosis factors (Acta2, Col1a1, and Tgfb1) than CDAHFD-fed wild-type controls
• however, CDAHFD-fed males show no differences in the severity of liver steatosis and inflammation, as indicated by similar gross liver morphology, liver weight/body weight index, serum transaminase levels, liver histology, and expression of hepatic inflammatory factors relative to CDAHFD-fed controls
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• CDAHFD-fed males show more severe liver fibrosis than CDAHFD-fed wild-type controls, as determined by Masson and Sirius red staining
• profibrotic effect might be attributed to inhibition of BA alternative synthesis pathway
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• males fed either a SC diet or a CDAHFD show a significant decrease in hepatic mRNA and protein levels of Cyp27a1 (a key enzyme in the alternative pathway of bile acid synthesis) relative to diet-matched controls
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mice fed a high-fat diet (HFD) for 12 weeks exhibit significantly lower hepatic cholesterol levels than diet-matched control mice
• however, hepatic cholesterol levels are relatively normal under standard-fat diet (SFD) conditions
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• HFD-fed mice exhibit significantly lower hepatic TG levels than diet-matched control mice
• however, hepatic TG levels are normal under SFD conditions
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• HFD-fed mice exhibit a significantly lower liver weight to body weight ratio (LW/BW) than diet-matched controls
• however, LW/BW ratio is normal under SFD conditions
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• mice fed a HFD for 12 weeks show significantly less hepatic steatosis than diet-matched controls, as determined by liver macroscopic appearance, H&E staining, Oil Red O staining, LW/BW ratio, and hepatic lipid contents
• administration of Ad-shRNA targeting INSIG1 (insulin induced gene 1, a direct target of Mir32) abrogates the alleviation of hepatic steatosis, insulin resistance, hyperlipidemia, and overexpression of lipogenic genes in HFD-fed mice
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• HFD-fed mice show activation of AKT signaling in the liver while mRNA and protein levels of hepatic genes involved in fatty acyl-CoA, triglyceride, and cholesterol biosynthesis are markedly reduced
• HFD-fed mice show significantly alleviated hepatic endoplasmic reticulum stress relative to diet-matched control mice
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| N |
• mice exhibit normal oxygen consumption, carbon dioxide production, respiratory exchange rate (RER), and heat generation regardless of whether they are fed a HFD or SFD
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• HFD-fed mice exhibit significantly lower total serum cholesterol levels than diet-matched control mice
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• HFD-fed mice exhibit significantly lower serum LDL cholesterol levels than diet-matched control mice
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• HFD-fed mice exhibit significantly lower serum ALT levels than diet-matched control mice
• however, serum ALT levels are relatively normal under SFD conditions
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• HFD-fed mice exhibit significantly lower serum AST levels than diet-matched control mice
• however, serum AST levels are not significantly altered under SFD conditions
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• HFD-fed mice show improved glucose tolerance relative to diet-matched control mice, as indicated by an intraperitoneal glucose tolerance test (IPGTT)
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• HFD-fed mice show enhanced insulin sensitivity relative to diet-matched control mice, as indicated by an insulin tolerance test (IPITT
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• mice fed a high-fat diet (HFD) for 12 weeks exhibit significantly lower hepatic cholesterol levels than diet-matched control mice
• however, hepatic cholesterol levels are relatively normal under standard-fat diet (SFD) conditions
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• HFD-fed mice exhibit significantly lower hepatic TG levels than diet-matched control mice
• however, hepatic TG levels are normal under SFD conditions
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• lipidomic analysis of livers from HFD-fed mice showed a significant reduction in triglyceride and cholesterol ester species relative to diet-matched controls; specifically, TG_48:1, TG_48:2, TG_48:3, TG_49:1, TG_50:1, TG_50:2, TG_50:3, TG_52:1, TG_54:2, CE_22:6, and CE_18:2 are dramatically reduced
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• HFD-fed mice show significantly alleviated hepatic endoplasmic reticulum stress relative to diet-matched control mice
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| N |
• mice exhibit normal body weight regardless of whether they are fed a HFD or SFD
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| N |
• mice exhibit normal food intake and total activity regardless of whether they are fed a HFD or SFD
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• after the injection of pyruvate
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• in hepatocytes due to a lack of glucagon signaling inhibition
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• in a glucose tolerance test after the injection of pyruvate
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• hepatocytes from tamoxifen-treated mice are capable of activating OT-I CD8+ T cells unlike cells from un-induced mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mice injected with tamoxifen at P10 develop liver tumors that are exclusively intrahepatic cholangiocarcinoma
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• 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
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• mice injected with tamoxifen at P10 develop liver tumors that are exclusively intrahepatic cholangiocarcinoma
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• 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
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• mice injected with tamoxifen at P10 develop liver tumors that are exclusively intrahepatic cholangiocarcinoma
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• tamoxifen-treated mice exhibit increased serum alanine transaminase levels compared with un-induced mice
• however, un-induced mice exhibit normal alanine transaminase levels
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• 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
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• 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
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• after 14 weeks of tamoxifen administration, neoplastic nodules form rapidly in the liver, presumably due to increased Notch1 signaling
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• after 14 weeks of tamoxifen administration, neoplastic nodules form rapidly in the liver, presumably due to increased Notch1 signaling
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• after 14 weeks of tamoxifen administration, neoplastic nodules form rapidly in the liver, presumably due to increased Notch1 signaling
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• when entrained on a light phase feeding regimen
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• 3-hours longer period in liver explants
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• phase differences at the pre-mRNA level for many core clock genes in liver
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• when entrained on a light phase feeding regimen
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• after induction with tamoxifen and partial hepatectomy, Hcfc1-negative cells do not display cell proliferation markers
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• following tamoxifen injection, nuclei are enlarged compared to cells from Trp53 null mice
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• expression analysis indicates hepatocytes rapidly reenter the cell cycle after tamoxifen treatment
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• following tamoxifen injection, nuclei are enlarged compared to cells from Trp53 null mice
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• expression analysis indicates hepatocytes rapidly reenter the cell cycle after tamoxifen treatment
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• 2 weeks after tamoxifen treatment, plasma urate levels are increased
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• after tamoxifen treatment
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• mild increase in Mg2+ fractional excretion after tamoxifen treatment
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• after tamoxifen treatment, urine osmolality is decreased and water deprivation fails to increase urine osmolality
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• after tamoxifen treatment
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• mild increase in urine Pi levels after tamoxifen treatment
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• 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
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| N |
• unlike in germline null mice, liver specific null mice have normal kidney histology
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• after tamoxifen treatment
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• mild increase in Mg2+ fractional excretion after tamoxifen treatment
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• after tamoxifen treatment, urine osmolality is decreased and water deprivation fails to increase urine osmolality
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• after tamoxifen treatment
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• mild increase in urine Pi levels after tamoxifen treatment
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• 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
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mild increase in Mg2+ fractional excretion after tamoxifen treatment
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• mild increase in urine Pi levels after tamoxifen treatment
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• mild increase in Mg2+ fractional excretion after tamoxifen treatment
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• mild increase in urine Pi levels after tamoxifen treatment
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• unlike in global knock-out mice, glycogen accumulation is not observed in the kidney or intestine of tamoxifen-treated mice
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• increased serum lactic acid in tamoxifen-treated mice after 10 day or 1 month
• however, levels are normal at 6 and 18 months
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• 3-fold in tamoxifen-treated mice after 10 day or 1 month
• however, levels are normal at 6 and 18 months
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• twice as high in tamoxifen-treated mice
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• 3-fold in tamoxifen-treated mice
• however, levels at 18 months are normal
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• in tamoxifen-treated mice
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• in tamoxifen-treated mice
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• in tamoxifen-treated mice
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• in tamoxifen-treated mice
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• in tamoxifen-treated mice
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• in tamoxifen-treated mice
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• large hepatocyte containing large lipid vacuoles in tamoxifen-treated mice
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• in tamoxifen-treated mice
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• in tamoxifen-treated mice after a year
• however, no hepatocellular carcinoma is observed
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• in tamoxifen-treated mice
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• in tamoxifen-treated mice after a year
• however, no hepatocellular carcinoma is observed
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• in tamoxifen-treated mice
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• in tamoxifen-treated mice
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Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| glycogen storage disease Ia | DOID:2749 |
OMIM:232200 |
J:195257 | |
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| 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
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• mice fed tamoxifen chow at birth (preweaning) exhibit livers with fewer hepatocytes containing visibly larger nuclei at 3 weeks of age
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• mice fed tamoxifen chow at birth (preweaning) exhibit livers with fewer hepatocytes at 3 weeks of age
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| 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
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• mice fed tamoxifen chow at birth (preweaning) exhibit hepatocytes accumulating 4C or greater DNA content by 3 weeks of age
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• mice fed tamoxifen chow at birth (preweaning) exhibit livers with fewer hepatocytes containing visibly larger nuclei at 3 weeks of age
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• following treatment with tamoxifen, bile acid in the feces is almost doubled in Nr5a2tm2Sjns homozygotes due to an increase in lithocholic acid and hydrophobic secondary bile acids produced in the intestine by bacteria
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• following treatment with tamoxifen, mice exhibit lipid malabsorption
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• 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
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• following treatment with tamoxifen, feces lipid and bile acid content is increased
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• following treatment with tamoxifen, bile acid in the feces is almost doubled in Nr5a2tm2Sjns homozygotes due to an increase in lithocholic acid and hydrophobic secondary bile acids produced in the intestine by bacteria
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• following treatment with tamoxifen, mice exhibit lipid malabsorption
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• 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 Fth1tm1.1Lck homozygotes
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| N |
• no liver damage is observed in tamoxifen-treated mice fed standard chow
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• 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 Fth1tm1.1Lck homozygotes
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Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO) |
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last database update 03/18/2025 MGI 6.24 |
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