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Allele Symbol Allele Name Allele ID |
Ikbkgtm1.1Chtr targeted mutation 1.1, Christian Trautwein MGI:4355682 |
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| Summary |
6 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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• 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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• 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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• hepatomegaly is seen in mice with type II and III livers
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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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• 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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| ♀ | 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 |
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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• 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 1 year
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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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• 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 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
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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
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• at 1 year
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• 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
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• 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
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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 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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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 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 50 weeks but not at 21 to 26 weeks
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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 04/30/2024 MGI 6.23 |
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