Analysis Tools
normal phenotype
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• cre expression occurred specifically in the hepatocytes of Tam treated mice
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Allele Symbol Allele Name Allele ID |
Albtm1(cre/ERT2)Mtz targeted mutation 1, Daniel Metzger MGI:3052812 |
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| Summary |
19 genotypes
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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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• 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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• 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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• in tamoxifen-treated mice
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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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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
Suppressed hepatic glucose uptake in Slc2a2tm2Thor/Slc2a2tm2Thor Albtm1(cre/ERT2)Mtz/Albtm1(cre/ERT2)Mtz mice
| N |
• tamoxifen-treated mice exhibit normal energy homeostasis and plasma glucagon levels
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• tamoxifen-treated mice exhibit reduced hepatic glucose output and rate of glucose disappearance under basal but not insulin clamp conditions
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• at 4 months following intraperitoneal glucose injection in tamoxifen-treated mice
• reduced insulin secretory capacity in islets of tamoxifen-treated mice
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• rapid decrease of serum glucose levels early in the fasting period of tamoxifen-treated mice due to impaired hepatic glycogen mobilization
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• progressive development in tamoxifen-treated mice beginning at 4 months
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• rapid decrease of serum glucose levels early in the fasting period of tamoxifen-treated mice due to impaired hepatic glycogen mobilization
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• in fasted mice treated with tamoxifen
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• tamoxifen-treated mice exhibit increased VLDL production compared with control mice
• however, plasma triglycerides and cholesterol levels are normal
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• decreased bile acid with altered composition in the feces of tamoxifen-treated mice
• however, serum levels are normal
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• in fasted tamoxifen-treated mice
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• in fasted mice treated with tamoxifen
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• increased uptake in the extensor digitorum longus muscle of tamoxifen-treated mice during hyperinsulinemic clamp
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• in the liver of tamoxifen-treated mice
• however, fasted glucose production in the liver is normal
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• in fasted mice treated with tamoxifen
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• in fasted tamoxifen-treated mice
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• in fasted mice treated with tamoxifen
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• increased uptake in the extensor digitorum longus muscle of tamoxifen-treated mice during hyperinsulinemic clamp
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• at 4 months following intraperitoneal glucose injection in tamoxifen-treated mice
• reduced insulin secretory capacity in islets of tamoxifen-treated mice
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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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| ♀ | 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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• 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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• 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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• 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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• 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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| ♀ | 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
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• in tamoxifen-treated mice after a year
• however, no hepatocellular carcinoma is observed
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• however, no hepatocellular carcinoma is observed
• in tamoxifen-treated mice after a year
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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, 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, 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, feces lipid and bile acid content is increased
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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 04/23/2024 MGI 6.23 |
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