Analysis Tools|
Allele Symbol Allele Name Allele ID |
Tg(Alb1-cre)7Gsc transgene insertion 7, Gunther Schutz MGI:2177602 |
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| Summary |
35 genotypes
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• doxycycline-treated mice develop lethal liver dysplasia
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• doxycycline-treated mice develop lethal liver dysplasia
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• doxycycline-treated mice develop lethal liver dysplasia
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• doxycycline-treated mice develop lethal liver dysplasia
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• consistent with the liver damage seen, ALT levels are increased 5-7 fold
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• consistent with the liver damage seen, AST levels are increased 5-7 fold
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• increased liver cell death is seen in 6 week old double hemizygotes
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• die within 8 hours of ConA treatment regardless of pretreatment with Il6
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• liver damage due to ConA treatment regardless of pretreatment with Il6
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• maximal DNA synthesis in hepatocytes after partial hepatectomy and lipopolysaccharide treatment is reduced relative to controls
• 20% of cells as compared to 30% of cells
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• do not suffer liver damage from ConA treatment if pretreated with Il6
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• maximal DNA synthesis in hepatocytes after partial hepatectomy occurs after about 48 hours
• hepatocyte growth factor has no effect on hepatocyte proliferation unless administered with Il6
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• reduced body weight starting around 3 weeks of age
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• reduced body weight starting around 3 weeks of age
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• non-heme splenic iron levels are significantly reduced compared to littermate controls
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• plasma iron levels are significantly elevated compared to age and sex matched controls
• transferrin saturation is significantly elevated and the unsaturated iron binding capacity is significantly reduced
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• iron accumulates in the parenchymal cells of the liver
• iron levels are 3- to 6- fold higher than littermate controls
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• symptoms in mice are consistent with hemocromatosis
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• non-heme splenic iron levels are significantly reduced compared to littermate controls
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• non-heme splenic iron levels are significantly reduced compared to littermate controls
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• iron accumulates in the parenchymal cells of the liver
• iron levels are 3- to 6- fold higher than littermate controls
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mice exhibit biliary lesions
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• mice exhibit necrotic liver injury (three types of injury are seen) which is maximal at 6-8 weeks of age
• 34% of mice exhibit few white liver lesions identified as necrotic areas (type I liver)
• 40% of mice exhibit multilocular, visible white liver lesions with features of parenchymal necroses or bile infarcts and increased liver weight (type II liver)
• 26% of mice exhibit yellow livers, increased liver size, multilocular yellow lesions resulting in massive necrotic destruction of the liver associated with multiple bile infarcts, and exhibit dwarfism (type III liver)
• increase in cell proliferation (not hepatocytes) in the liver
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• hepatomegaly is seen in mice with type II and III livers
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• mice exhibit necrotic liver injury which is maximal at 6-8 weeks of age
• ageing mice recover from necrotic liver injury and are protected from steatosis but develop liver fibrosis
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• ageing mice recover from necrotic liver injury but develop liver fibrosis
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• dwarfism is seen in mice with type III livers
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• hepatomegaly is seen in mice with type II and III livers
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• increase in bilirubin levels in mice with type III livers
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• serum transaminase levels are increased in mice with type II and III livers
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• alkaline phosphatase levels are elevated in correlation to severity of liver injury
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• increase in bile acid levels in mice with type III livers
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N |
• mice do not develop hepatocellular carcinoma are remain tumor free up to 60 weeks of age
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mice exhibit an increase in serum transaminases levels
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• mice are protected from induction of apoptosis and liver injury by Fas or lipopolysaccarides and exhibit 100% survival compared to 90% mortality within 24 horus of liver injury in controls
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• mice exhibit increased necrotic damage, reduced survival, increased aspartate aminotransferase and alanine aminotransferase levels, and increased infiltration of CD11b+F4/80+ macrophages in response to acute liver injury induced by concanavalin A
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• livers show small inflammatory infiltrates of granulocytes and monocytes and increased serum transaminases, indicating basal liver inflammation
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• livers show small inflammatory infiltrates of granulocytes and monocytes and increased serum transaminases, indicating basal liver inflammation
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• reduced survival (40% versus 70% WT littermate controls) after two thirds partial hepatectomy
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• mice gain weight at a slower rate compared to controls starting at six weeks of age
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• reduction in number of proliferating cells 36 to 48 hours after two-thirds partial hepatectomy (PH)
• increase in number of proliferating cells 7 days after PH
• 7 days after PH, the liver-to-body weight ratio is lower compared to control mice
• 15 days after PH, there are no significant differences in the liver-to-body weight ratio
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• five-fold increase in serum levels 24 hours after partial hepatectomy
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• five-fold increase in serum levels 24 hours after partial hepatectomy
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• animals displayed reduced body weight at 2 weeks of age that persisted into adulthood
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• reduced liver weight
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• following 70% partial hepatectomy, large areas of necrotic tissues were observed in the regenerating liver
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• maximal DNA synthesis in hepatocytes after partial hepatectomy and lipopolysaccharide treatment is reduced relative to controls
• 10% of cells as compared to 30% of cells
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• mice exhibit normal survival throughout 40 weeks
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• mice exhibit strong dysplasia, absence of small bile ducts, and increased bile duct proliferation compared with wild-type mice
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• mice exhibit hyperproliferation, dysplasia, and reduction of biliary epithelial cells unlike wild-type mice
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• at an earlier age and to a larger extent than in Map3k7tm1Aki/ Map3k7tm1Aki Tg(Alb1-cre)7Gsc mice
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• serum bilirubin levels are increased compared to in wild-type mice and Map3k7tm1Aki/ Map3k7tm1Aki Tg(Alb1-cre)7Gsc mice
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• milder than in Map3k7tm1Aki/ Map3k7tm1Aki Tg(Alb1-cre)7Gsc mice
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• mice exhibit strong dysplasia, absence of small bile ducts, and increased bile duct proliferation compared with wild-type mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mice die between 14 and 36 weeks
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• at 6 to 8 weeks, mice lack biliary epithelial cells and regularly shaped small bile ducts compared with wild-type mice
• biliary ductopenia is pronounced within areas of hepatocyte dysplasia
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• numerous small visible nodules at 6 weeks
• larger nodules and an icteric appearance at 20 weeks
• nodules display cellular features of dysplasia like anisokaryosis unlike wild-type cells
• at 14 weeks, livers exhibit an increase in hydroproline content compared with wild-type liver
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• biliary ductopenia is pronounced within areas of hepatocyte dysplasia
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• starting at 6 weeks
• in 14 of 16 mice at 16 to 33 weeks
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• at 6 weeks, mice exhibit periportal liver fibrosis unlike wild-type mice
• at 20 to 29 weeks, mice exhibit severe diffuse fibrosis unlike wild-type mice
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• at 6 weeks and further at 20 weeks
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• at 6 and 20 weeks
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• at 6 weeks
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• at 6 and 20 weeks
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• at 6 weeks, circulating glutamate dehydrogenase is increased compared to in wild-type mice
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• starting at 6 weeks
• in 14 of 16 mice at 16 to 33 weeks
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• at 6 to 8 weeks, mice lack biliary epithelial cells and regularly shaped small bile ducts compared with wild-type mice
• biliary ductopenia is pronounced within areas of hepatocyte dysplasia
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
 N |
• mice exhibit normal survival throughout 50 weeks
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N |
• bile ducts are normal at 6 weeks
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N |
• mice exhibit normal bilirubin serum levels
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• reduced body weight starting around 3 weeks of age
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• mice exhibit no significant differences in the acute response to CCl4-induced liver injury and show normal liver regeneration after partial hepatectomy relative to similarly treated control mice
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• at 12 months of age, mice exhibit supernumerary, often dilated bile ducts that are still largely confined to the portal areas
• however, bile ducts show no apparent obstruction
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• at 2 and 12 months of age, mice show an increased number of bile duct epithelial cells (BECs), including periportal patches that represent KRT19-positive liver progenitor cells (LPCs)
• increased BEC proliferation index is confirmed by Ki-67 staining at 12 months of age
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• mice develop bile duct hyperplasia by 2 months of age
• ductular reaction is associated with biliary fibrosis at 2 and 12 months, as shown by collagen staining with Sirius Red; however, no hepatocellular injury or intrahepatic cholangiocarcinoma tumor development is observed over time
• mice fed a diet supplemented with 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DCC) for 3 weeks show enhanced bile duct hyperplasia relative to similarly treated controls, as determined by H&E, KRT19 and BrdU staining
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• mice exhibit supernumerary bile ducts at 12 months of age
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• bile ducts are often dilated at 12 months of age
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• mice show an increased number of F4/80-positive macrophages in the liver at 12 months of age
• however, leukocyte (CD45-positive) and activated hepatic stellate cell (alpha-SMA-positive) numbers remain normal
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• at 2 and 12 months of age, mice show an expansion of the periportal liver progenitor cell (LPC) compartment, as revealed by the KRT19-positive area
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• bile duct hyperplasia is associated with enhanced LPC proliferation
• after 3 weeks on a diet supplemented with 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DCC), mice exhibit a greater increase in chemically induced LPC proliferation relative to similarly treated controls, as determined by KRT19 and BrdU staining
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• mice show an increased number of F4/80-positive macrophages in the liver at 12 months of age
• however, leukocyte (CD45-positive) and activated hepatic stellate cell (alpha-SMA-positive) numbers remain normal
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• at 12 months of age, mice exhibit supernumerary, often dilated bile ducts that are still largely confined to the portal areas
• however, bile ducts show no apparent obstruction
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• at 2 and 12 months of age, mice show an increased number of bile duct epithelial cells (BECs), including periportal patches that represent KRT19-positive liver progenitor cells (LPCs)
• increased BEC proliferation index is confirmed by Ki-67 staining at 12 months of age
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• mice develop bile duct hyperplasia by 2 months of age
• ductular reaction is associated with biliary fibrosis at 2 and 12 months, as shown by collagen staining with Sirius Red; however, no hepatocellular injury or intrahepatic cholangiocarcinoma tumor development is observed over time
• mice fed a diet supplemented with 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DCC) for 3 weeks show enhanced bile duct hyperplasia relative to similarly treated controls, as determined by H&E, KRT19 and BrdU staining
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• mice exhibit supernumerary bile ducts at 12 months of age
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• bile ducts are often dilated at 12 months of age
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• unlike mice that do not carry Casp8tm1.1Yuan, compound heterozygous mutants survive after injection with an anti-Fas Ab
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• unlike mice that do not carry Casp8tm1.1Yuan, compound heterozygous mutants survive and do not display liver damage after injection with an anti-Fas Ab
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• despite the severity of their phenotype, most mutant mice survive for several months
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• mutants exhibit abnormal intrahepatic bile duct (IHBD) differentiation and morphogenesis, resulting in persistence of the ductal plate and a highly disorganized biliary system
• in addition, mutant livers show absence of interlobular arteries in portal tracts, suggesting a link between arterial and biliary development within the liver
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• at 2 months, mutant extrahepatic biliary tracts display epithelial abnormalities
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• in extreme cases, the cystic duct is completely dilated and no duct is clearly identifiable
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• at 2 months, mutants exhibit dysplasia of the larger intrahepatic bile ducts (IHBDs) and a reduction, or paucity, of small IHBDs
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• absence of identifiable IHBDs is already evident at P7, indicating lack of formation of interlobular bile ducts
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• at 2 months, mutant gallbladders exhibit epithelial dysplasia
• in the mutant gallbladder, the normal cuboidal epithelium is replaced in some areas by a stratified squamous epithelium or mucus-secreting cells
• nonetheless, mutant gallbladders are filled with bile and communicate with the liver and the duodenum
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• mutant mice exhibit fully penetrant liver hypertrophy
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• at 2 months, mutant livers display hepatocyte necrosis and oval cell proliferation
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• at 2 months, mutant mice exhibit liver inflammation
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• as early as P7, mutant mice show increased plasma levels of bilirubin
• by 2 months, mutant bilirubin and bile acid levels are dramatically increased
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• as early as P7, mutants exhibit significantly increased levels of serum cholesterol; levels become stabilized after P14
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• as early as P7, mutants exhibit significantly increased levels of serum triglycerides, suggesting altered hepatocyte metabolism; levels become stabilized after P14
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• body weight differences are detected as early as P2 and increase with time, reaching a growth plateau at weaning
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• mutant mice display severe postnatal growth retardation
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• mutant mice exhibit fully penetrant liver hypertrophy
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• at 2 months, mutant mice exhibit liver inflammation
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• at 2 months, mutant extrahepatic biliary tracts display epithelial abnormalities
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• in extreme cases, the cystic duct is completely dilated and no duct is clearly identifiable
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• at 2 months, mutants exhibit dysplasia of the larger intrahepatic bile ducts (IHBDs) and a reduction, or paucity, of small IHBDs
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• absence of identifiable IHBDs is already evident at P7, indicating lack of formation of interlobular bile ducts
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• at 2 months, mutant gallbladders exhibit epithelial dysplasia
• in the mutant gallbladder, the normal cuboidal epithelium is replaced in some areas by a stratified squamous epithelium or mucus-secreting cells
• nonetheless, mutant gallbladders are filled with bile and communicate with the liver and the duodenum
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mutants die within 12 hours of birth
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• blood glucose is less than 10 mg/dl shortly after birth compared to 58 mg/dl in controls; however mutants are able to feed as milk is found in the digestive tract
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• total glucose production in the liver is reduced about 3-fold with gluconeogenesis reduced about 2-fold
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• total glucose production in the liver is reduced about 3-fold with glycogenolysis reduced about 3-fold
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• at E17.5, E18.5, and P0, glycogen levels in the liver are severely reduced
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• proliferation in parenchymal cells is increased 1.6-fold and 4- to 5-fold at E17.5 and E18.5, respectively and a 40% increase in parenchymal cells is seen
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• at E17.5, E18.5, and P0, glycogen levels in the liver are severely reduced
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• the cytoplasm contains fewer organelles and mitochondria suggesting a defect in terminal hepatocyte differentiation
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• intermembrane spaces are enlarged and cell-cell junctions are disrupted
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• proliferation in parenchymal cells is increased 1.6-fold and 4- to 5-fold at E17.5 and E18.5, respectively and a 40% increase in parenchymal cells is seen
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mice exhibit an increase in circulating leptin levels in a fasting mouse but leptin levels do not rise when fed unlike wild-type mice
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• in a fasting mouse but not in a fed mouse
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• in a fasting mouse but not in a fed mouse
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• endogenous glucose production is higher than in wild-type mice
• mice fail to exhibit an increase in hepatic glucose production when treated with leptin or adiponectin unlike wild-type mice
• however, mice remain sensitive to the inhibitory effects of hyperinsulinemia on gluconeogenesis and exhibit normal insulin sensitive whole body glucose turnover
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• in a fasting mouse
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• in a fasting mouse but not in a fed mouse
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• in a fasting mouse but not in a fed mouse
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• reduced body weight starting around 3 weeks of age
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• reduced body weight starting around 3 weeks of age
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• at 10 weeks
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• at P14 and further at 22 and 52 weeks
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• at P14 and further at 22 and 52 weeks
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| N |
• adult mice exhibit normal hematologic values
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• mice exhibit normal leptin levels, respiratory exchange rate, and homeostasis of oxygen and carbon dioxide
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• in cultured islets under high glucose conditions
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• in cultured islets under low glucose conditions
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• in mice infected with P. chabaudi
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• during the steady state
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• in mice infected with P. chabaudi
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• 2.5-fold
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• mice exhibit impaired glucose tolerance compared with wild-type mice
• however, depletion of TNF or treatment with clodronate liposomes to deplete Kupffer cells normalizes glucose clearance
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• mice exhibit increased hepatic glycogen synthesis and glycogenolysis compared with wild-type mice
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• in steady state
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• in steady state, mice exhibit a reduction in hepatic glycogen levels compared with wild-type mice
• however, fasted mice exhibit normal hepatic glycogen levels
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• in an insulin tolerance test, insulin treatment fails to lower serum glucose levels as in similarly treated wild-type mice
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| N |
• mice exhibit normal epigonadal fat pad weight and total body fat content
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• glucose uptake in white adipose tissue is reduced compared to in wild-type tissue
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• in mice infected with P. chabaudi
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• during the steady state
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• in mice infected with P. chabaudi
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• 2.5-fold
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• mice infected with P. chabaudi exhibit lower IL1b and TNF-alpha levels compared with control mice
• however, lethality is normal
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| N |
• mice exhibit normal body weight
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| N |
• mice exhibit normal food intake and activity levels
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• in steady state, mice exhibit a reduction in hepatic glycogen levels compared with wild-type mice
• however, fasted mice exhibit normal hepatic glycogen levels
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• in cultured islets under high glucose conditions
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• in cultured islets under low glucose conditions
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• glucose uptake in white adipose tissue is reduced compared to in wild-type tissue
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• most mice die by 7 months of age
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• most mice die by 7 months of age
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• the number of intact small portal bile ducts is reduced compared to in wild-type mice and exhibit signs of severe chronic cholestasis
• unobstructed bile ducts exhibit damaged, flattened epithelium surrounded by inflammatory foci with lymphocyte and ceroid macrophage infiltrate unlike in wild-type mice
• however, small bile duct development is normal at birth
• as the portal bile ducts are destroyed bile leaks between neighboring cells and the blood-bile barrier is disrupted
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• altered tubular arrangements of hepatocytes and severe dilations of the bile canaliculi are observed along with the disappearance of microvilli, formation of blebs and thickening of the pericanalicular ectoplasm
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• severe chronic cholestasis in the liver
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• following exposure to LPS, mice exhibit increased liver failure and hepatocyte apoptosis compared to similarly treated wild-type mice or single homozygous mice
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• the number of intact small portal bile ducts is reduced compared to in wild-type mice and exhibit signs of severe chronic cholestasis
• unobstructed bile ducts exhibit damaged, flattened epithelium surrounded by inflammatory foci with lymphocyte and ceroid macrophage infiltrate unlike in wild-type mice
• however, small bile duct development is normal at birth
• as the portal bile ducts are destroyed bile leaks between neighboring cells and the blood-bile barrier is disrupted
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• spontaneous serum ALT levels are decreased compared to single Ikbkg mutants at 8 weeks of age
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• mice show increased JNK kinase activity
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• completely absent compared to single Ikbkg mutants at 8 weeks of age
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N |
• liver inflammation, hepatocyte apoptosis, increased hepatocyte proliferation, and focal lipid accumulation are inhibited in mutants compared to Ikbkg single mutants
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• completely absent compared to single Ikbkg mutants at 8 weeks of age
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• double mutants are protected from LPS-induced hepatocyte apoptosis
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• 8 week old mice show signs of steatohepatitis in the liver, characterized by immune cell infiltration into the parenchyma
• in 8-week old mice, hepatocytes show features of large-cell dysplasia with strong anisokaryosis; large areas of irregularly shaped glycogen deposits are detected
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• at 6 months, livers show macroscopic nodules
• focal areas of lipid accumulation and low-grade dysplastic nodules with expansive growth are observed
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• at 6 months, hepatocytes show lipid deposition and ballooning
• in 8-week old mice, hepatocytes show features of large-cell dysplasia with strong anisokaryosis; large areas of irregularly shaped glycogen deposits are detected
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• mitochondria of hepatocytes appear swollen and display a reduction in mitochondrial crests compared to wild-type at 8 weeks of age
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• at 6 months, mice show signs of steatosis and increased lipid deposition in hepatocytes
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• multiple tumors are found in livers of 12-month old males; malignant liver tumors are present in all mice examined
• average number of tumors per mouse is 5.75 with average size of 8.58 mm
• tumors show expansive growth, increased cellularity, broad trabecular growth pattern in 4 to 6 layers, eosinophilia, higher cytoplasmic index compared to non malignant areas, and complete absence of portal tracts
• tumors show increased proliferation and higher mitotic indices (~1.44 per high-power field)
• tumors at 9 months show dysplastic foci and nodules
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• multiple tumors are found in livers of 12-month old males; malignant liver tumors are present in all mice examined
• average number of tumors per mouse is 5.75 with average size of 8.58 mm
• tumors show expansive growth, increased cellularity, broad trabecular growth pattern in 4 to 6 layers, eosinophilia, higher cytoplasmic index compared to non malignant areas, and complete absence of portal tracts
• tumors show increased proliferation and higher mitotic indices (~1.44 per high-power field)
• tumors at 9 months show dysplastic foci and nodules
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• cytokine expression is upregulated in mutants
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• upon LPS injection, NF kappa b activation is completely absent
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• following exposure to LPS, mice exhibit increased liver failure and hepatocyte apoptosis compared to similarly treated wild-type mice
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• 8 week old mice show signs of steatohepatitis in the liver, characterized by immune cell infiltration into the parenchyma
• in 8-week old mice, hepatocytes show features of large-cell dysplasia with strong anisokaryosis; large areas of irregularly shaped glycogen deposits are detected
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• mitochondria of hepatocytes appear swollen and display a reduction in mitochondrial crests compared to wild-type at 8 weeks of age
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• 8-week old mice show an increase in apoptotic cells in the liver
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• livers show increased proliferation
• at 8 weeks, there is a significant increase in progenitor cells and activation of oval cells in the liver
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• mice show a decrease in spontaneous serum glucose levels compared to controls
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• mice show elevated serum levels of alanine aminotransferase (ALT) at 3 weeks, indicative of hepatocyte damage; ALT levels are further increased at 8 weeks
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• mice show increased JNK kinase activity
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Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| steatotic liver disease | DOID:9452 |
OMIM:228100 |
J:118336 | |
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• NF kappa b activation is completely blocked
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| N |
• mice do not develop liver tumors or show liver steatosis in contrast to Ikbkg conditional mutants
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
Inflammation and steatohepatitis in 12 week old Ikbkgtm1.1Chtr/Ikbkgtm1.1Chtr Tg(Alb1-cre)7Gsc/0 and Ikbkgtm1.1Chtr/Y Tg(Alb1-cre)7Gsc/0 mice
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• all mice treated with concanavalin A die unlike similarly treated mice not carrying the cre transgene
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• NK1.1+ cells have a higher level of annexin V than in NK1.1+ cells from Ikbkgtm1.1Chtr mice
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• NK1.1+ cells have a higher level of annexin V than in NK1.1+ cells from Ikbkgtm1.1Chtr mice
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• before and after treatment with concanavalin A compared with Ikbkgtm1.1Chtr mice
• however, depletion of NK/NKT cells with NK1.1 lowers TNF levels
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• before and after treatment with concanavalin A compared with Ikbkgtm1.1Chtr mice
• however, depletion of NK/NKT cells with NK1.1 or ASIALO antibodies lowers IFN-gamma levels induced by concanavalin A
• mice treated with concanavalin A, NK1.1 antibodies, and wild-type mononuclear cells exhibit elevated serum IFN-gamma levels compared to mice treated with concanavalin A and NK1.1 antibodies
• however, mice treated with concanavalin A, NK1.1 antibodies and Tnfsf10tm1Mjs mononuclear or NK/NKT cells exhibit reduced IFN-gamma levels
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• at 12 weeks, mice exhibit liver inflammation unlike in Ikbkgtm1.1Chtr mice
• mice treated with concanavalin A develop more severe hepatitis than similarly treated Ikbkgtm1.1Chtr mice
• however, depletion of NK/NKT cells with NK1.1 antibodies decreases liver damage in untreated and concanavalin A treated mice
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• mice treated with concanavalin A exhibit increased apoptosis compared to similarly treated Ikbkgtm1.1Chtr mice
• however, depletion of NK/NKT cells with NK1.1 or ASIALO antibodies reduces apoptosis induced by concanavalin A
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• at 12 weeks, mice exhibit liver inflammation unlike in Ikbkgtm1.1Chtr mice
• mice treated with concanavalin A develop more severe hepatitis than similarly treated Ikbkgtm1.1Chtr mice
• however, depletion of NK/NKT cells with NK1.1 antibodies decreases liver damage in untreated and concanavalin A treated mice
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• at 12 weeks, livers are dysplastic and display anisokaryosis unlike in wild-type mice
• however, depletion of NK/NKT cells with NK1.1 antibodies decreases liver damage in untreated mice and mice treated with concanavalin A
• however, depletion of NK/NKT cells with ASIALO antibodies decreases liver damage induced by concanavalin A
• mice treated with concanavalin A, NK1.1 antibodies, and wild-type mononuclear cells exhibit increased liver damage compared to mice treated with concanavalin A and NK1.1 antibodies
• however, mice treated with concanavalin A, NK1.1 antibodies and Tnfsf10tm1Mjs mononuclear or NK/NKT cells exhibit reduced liver damage
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• at 1 year
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• hepatic necrosis is observed in mice treatment with concanavalin A unlike in similarly treated Ikbkgtm1.1Chtr mice
• however, depletion of NK/NKT cells with NK1.1 improves necrosis induced by concanavalin A
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• at 12 weeks
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• at 1 year
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• before and after treatment with concanavalin A compared with Ikbkgtm1.1Chtr mice
• however, depletion of NK/NKT cells with NK1.1 lowers TNF levels
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• at 12 weeks, mice exhibit elevated serum alanine transaminase (ALT) levels compared to in Ikbkgtm1.1Chtr mice
• mice treated with concanavalin A exhibit increased serum ALT levels compared with similarly treated Ikbkgtm1.1Chtr mice
• however, depletion of NK/NKT cells with NK1.1 antibodies decreases ALT levels in untreated mice and mice treated with concanavalin A
• however, depletion of NK/NKT cells with ASIALO antibodies decreases ALT levels mice treated with concanavalin A
• mice treated with concanavalin A, NK1.1 antibodies, and wild-type mononuclear cells exhibit elevated ALT levels compared to mice treated with concanavalin A and NK1.1 antibodies
• however, mice treated with concanavalin A, NK1.1 antibodies and Tnfsf10tm1Mjs mononuclear or NK/NKT cells exhibit reduced ALT levels
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• all mice treated with concanavalin A die unlike similarly treated mice not carrying the cre transgene
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• mice treated with concanavalin A develop more severe hepatitis, high ALT, necrosis, and apoptosis than similarly treated Ikbkgtm1.1Chtr mice
• all mice treated with concanavalin A exhibit increased interferon-gamma and TNF levels compared to in similarly treated Ikbkgtm1.1Chtr mice
• however, depletion of NK/NKT cells with ASIALO antibodies decreases liver damage, liver apoptosis, ALT levels, and IFN-gamma levels induced by concanavalin A
• mice treated with concanavalin A, NK1.1 antibodies, and wild-type mononuclear cells exhibit elevated ALT and IFN-gamma levels and liver damage compared to mice treated with concanavalin A and NK1.1 antibodies
• however, mice treated with concanavalin A, NK1.1 antibodies and Tnfsf10tm1Mjs mononuclear or NK/NKT cells exhibit reduced ALT and IFN-gamma levels and liver damage
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• at 1 year
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• NK1.1+ cells have a higher level of annexin V than in NK1.1+ cells from Ikbkgtm1.1Chtr mice
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• NK1.1+ cells have a higher level of annexin V than in NK1.1+ cells from Ikbkgtm1.1Chtr mice
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• mice treated with concanavalin A exhibit increased apoptosis compared to similarly treated Ikbkgtm1.1Chtr mice
• however, depletion of NK/NKT cells with NK1.1 or ASIALO antibodies reduces apoptosis induced by concanavalin A
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• at 1 year
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
Ikbkgtm1.1Chtr/Y Tg(Alb1-cre)7Gsc/0 mice are protected from anti-Fas mAb stimulated development of hepatitis
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• 90% of mice treated with anti-Fas mAB (Jo2) survive where as all similarly treated Ikbkgtm1.1Chtr mice die
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• NK1.1+ cells have a higher level of annexin V than in NK1.1+ cells from Ikbkgtm1.1Chtr mice
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• NK1.1+ cells have a higher level of annexin V than in NK1.1+ cells from Ikbkgtm1.1Chtr mice
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• at 12 weeks, mice exhibit liver inflammation unlike in Ikbkgtm1.1Chtr mice
• mice treated with TRAIL (Tnfsf10) exhibit by profuse PMN infiltration in the liver compared to in similarly treated Ikbkgtm1.1Chtr mice
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• mice treated with TRAIL (Tnfsf10) exhibit increased apoptosis compared to similarly treated Ikbkgtm1.1Chtr mice
• however, treatment with JNK inhibitor AS600125 prevents TRAIL (Tnfsf10) induced liver apoptosis
|
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|
• at 12 weeks, mice exhibit liver inflammation unlike in Ikbkgtm1.1Chtr mice
• mice treated with TRAIL (Tnfsf10) exhibit by profuse PMN infiltration in the liver compared to in similarly treated Ikbkgtm1.1Chtr mice
|
|
|
• at 12 weeks, livers are dysplastic and display anisokaryosis unlike in wild-type mice
• however, depletion of NK/NKT cells with NK1.1 antibodies decreases liver damage
|
|
|
• at 1 year
|
|
|
• at 12 weeks, mice exhibit elevated serum alanine transaminase (ALT) levels compared to in Ikbkgtm1.1Chtr mice
• mice treated with TRAIL (Tnfsf10) exhibit increased serum ALT levels compared with similarly treated Ikbkgtm1.1Chtr mice
• however, depletion of NK/NKT cells with NK1.1 antibodies decreases ALT levels
|
|
|
• hepatic necrosis is observed in mice treatment with TRAIL (Tnfsf10) unlike in similarly treated Ikbkgtm1.1Chtr mice
• however, depletion of NK/NKT cells with NK1.1 improves necrosis induced by TRAIL (Tnfsf10)
|
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• 90% of mice treated with anti-Fas mAB (Jo2) survive where as all similarly treated Ikbkgtm1.1Chtr mice die
|
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• anti-Fas mAB (Jo2)-treated mice do not exhibit hepatic blood accumulation, further increased liver weight, further increased alanine transaminase serum levels, hepatic necrosis, or hepatic apoptosis as observed in similarly treated Ikbkgtm1.1Chtr mice
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• at 1 year
|
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• NK1.1+ cells have a higher level of annexin V than in NK1.1+ cells from Ikbkgtm1.1Chtr mice
|
|
|
• NK1.1+ cells have a higher level of annexin V than in NK1.1+ cells from Ikbkgtm1.1Chtr mice
|
|
|
• mice treated with TRAIL (Tnfsf10) exhibit increased apoptosis compared to similarly treated Ikbkgtm1.1Chtr mice
• however, treatment with JNK inhibitor AS600125 prevents TRAIL (Tnfsf10) induced liver apoptosis
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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 are only subtly protected from diet-induced body weight gain
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• mice fed a high-fat diet are only subtly protected from diet-induced body weight gain
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• mice fed a high-fat diet show improved glucose tolerance, but not insulin sensitivity
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• reduction in hepatic C(16:0) ceramides and dihydroceramides
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• following exposure to LPS, mice exhibit increased liver failure and hepatocyte apoptosis compared to similarly treated wild-type mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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N |
• mice exhibit normal bile ducts and no liver necrosis
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• at 14 weeks, livers exhibit an increase in hydroproline content compared with wild-type liver
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• at 50 weeks but not at 21 to 26 weeks
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• at 6 weeks, mice exhibit periportal liver fibrosis unlike wild-type mice
• at 20 to 29 weeks, mice exhibit severe diffuse fibrosis unlike wild-type mice
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N |
• mice exhibit normal bilirubin serum levels
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• milder than in Map3k7tm1Aki/ Map3k7tm1Aki Tg(Alb1-cre)7Gsc mice
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• milder than in Map3k7tm1Aki/ Map3k7tm1Aki Tg(Alb1-cre)7Gsc mice
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• at 6 weeks, circulating glutamate dehydrogenase is increased compared to in wild-type mice
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• at 50 weeks but not at 21 to 26 weeks
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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 11/12/2024 MGI 6.24 |
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