About   Help   FAQ
Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Tg(Alb1-cre)1Khk
transgene insertion 1, Klaus H Kaestner
MGI:2664969
Summary 10 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
cn1
Foxa1tm1Khk/Foxa1tm1Khk
Foxa2tm1Khk/Foxa2tm1Khk
Tg(Alb1-cre)1Khk/0
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL MGI:5314251
cn2
Akt2tm1.2Mbb/Akt2tm1.2Mbb
Lepob/Lepob
Tg(Alb1-cre)1Khk/0
involves: 129P2/OlaHsd * 129S4/SvJaeSor * C57BL/6 * SJL MGI:4889115
cn3
Akt2tm1.2Mbb/Akt2tm1.2Mbb
Tg(Alb1-cre)1Khk/0
involves: 129P2/OlaHsd * 129S4/SvJaeSor * C57BL/6 * SJL MGI:4889114
cn4
Hhextm1Cwb/Hhextm2Cwb
Tg(Alb1-cre)1Khk/?
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL MGI:3721920
cn5
Jag1tm1.1Loo/Jag1tm1.1Loo
Tg(Alb1-cre)1Khk/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL MGI:3848168
cn6
Jag1tm1.1Loo/Jag1+
Notch2tm1Grid/Notch2+
Tg(Alb1-cre)1Khk/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL MGI:3848170
cn7
Jag1tm1Grid/Jag1tm1.1Loo
Tg(Alb1-cre)1Khk/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL MGI:3848171
cn8
Hhextm2Cwb/Hhextm2Cwb
Tg(Alb1-cre)1Khk/?
involves: 129S1/Sv * C57BL/6 * SJL MGI:3721919
cn9
Foxm1tm1Rhc/Foxm1tm1Rhc
Tg(Alb1-cre)1Khk/0
involves: 129X1/SvJ * C57BL/6 * SJL MGI:3522668
cn10
Hnf4atm1Sad/Hnf4atm1Sad
Tg(Alb1-cre)1Khk/0
involves: C57BL/6 * SJL MGI:2665532


Genotype
MGI:5314251
cn1
Allelic
Composition
Foxa1tm1Khk/Foxa1tm1Khk
Foxa2tm1Khk/Foxa2tm1Khk
Tg(Alb1-cre)1Khk/0
Genetic
Background
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Foxa1tm1Khk mutation (0 available); any Foxa1 mutation (21 available)
Foxa2tm1Khk mutation (1 available); any Foxa2 mutation (28 available)
Tg(Alb1-cre)1Khk mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• male mutants injected with DEN followed by TCPOBOP (carcinogen treatment) show reduced tumor growth compared to control males that develop severe hepatocellular carcinoma
• female mutants injected with DEN followed by TCPOBOP (carcinogen treatment) to induce rapid hepatocellular carcinoma formation, develop multiple and large liver tumors unlike control females that are resistant to hepatocellular carcinoma development
• in females treated with fulverstrant to block estrogen signaling, DEN-induced liver injury is significantly attenuated
• estrogen treatment of male mutants enhances liver injury in DEN-treated males while in DEN-treated controls estrogen treatment prevents liver injury and carcinogenesis
• female mutants injected with N,N-diethylnitrosamine (DEN) followed by TCPOBOP two-step strategy (carcinogen treatment) to induce rapid hepatocellular carcinoma formation, develop multiple and large liver tumors unlike control females that are resistant to hepatocellular carcinoma development
• male mutants injected with DEN followed by TCPOBOP show reduced tumor growth compared to control males that develop severe hepatocellular carcinoma

homeostasis/metabolism
• male mutants injected with DEN followed by TCPOBOP (carcinogen treatment) show reduced tumor growth compared to control males that develop severe hepatocellular carcinoma
• female mutants injected with DEN followed by TCPOBOP (carcinogen treatment) to induce rapid hepatocellular carcinoma formation, develop multiple and large liver tumors unlike control females that are resistant to hepatocellular carcinoma development
• in females treated with fulverstrant to block estrogen signaling, DEN-induced liver injury is significantly attenuated
• estrogen treatment of male mutants enhances liver injury in DEN-treated males while in DEN-treated controls estrogen treatment prevents liver injury and carcinogenesis

liver/biliary system
• female mutants injected with N,N-diethylnitrosamine (DEN) followed by TCPOBOP two-step strategy (carcinogen treatment) to induce rapid hepatocellular carcinoma formation, develop multiple and large liver tumors unlike control females that are resistant to hepatocellular carcinoma development
• male mutants injected with DEN followed by TCPOBOP show reduced tumor growth compared to control males that develop severe hepatocellular carcinoma




Genotype
MGI:4889115
cn2
Allelic
Composition
Akt2tm1.2Mbb/Akt2tm1.2Mbb
Lepob/Lepob
Tg(Alb1-cre)1Khk/0
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJaeSor * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Akt2tm1.2Mbb mutation (1 available); any Akt2 mutation (53 available)
Lepob mutation (5 available); any Lep mutation (21 available)
Tg(Alb1-cre)1Khk mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• fasted mice exhibit increased plasma glucose levels compared with Akt2tm1Mbb Lepob homozygotes
• mice exhibit reduced lipogenesis compared to in Akt2tm1Mbb Lepob homozygotes
• mice exhibit decreased liver triglyceride levels compared with Akt2tm1Mbb Lepob homozygotes

growth/size/body
• mice exhibit decreased body weight compared with Akt2tm1Mbb Lepob homozygotes
• however, body composition was normal

liver/biliary system
• mice exhibit decreased liver triglyceride levels compared with Akt2tm1Mbb Lepob homozygotes
• mice exhibit decreased liver weight compared with Akt2tm1Mbb Lepob homozygotes




Genotype
MGI:4889114
cn3
Allelic
Composition
Akt2tm1.2Mbb/Akt2tm1.2Mbb
Tg(Alb1-cre)1Khk/0
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJaeSor * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Akt2tm1.2Mbb mutation (1 available); any Akt2 mutation (53 available)
Tg(Alb1-cre)1Khk mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• in fed mice fed a Surwit high-fat diet at 1 and 4 months

growth/size/body
N
• mice exhibit normal body weight and susceptibility to diet-induced obesity

liver/biliary system
• in fed mice fed a Surwit high-fat diet at 1 and 4 months




Genotype
MGI:3721920
cn4
Allelic
Composition
Hhextm1Cwb/Hhextm2Cwb
Tg(Alb1-cre)1Khk/?
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hhextm1Cwb mutation (0 available); any Hhex mutation (17 available)
Hhextm2Cwb mutation (1 available); any Hhex mutation (17 available)
Tg(Alb1-cre)1Khk mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
liver/biliary system
• intrahepatic bile duct morphogenesis is abnormal and results in hepatic cysts
• at E18.5, the portal tracts are often surrounded by many irregular biliary duct-like structures/cysts
• mice exhibit a ductal plate malformation
• in the liver, the portal vein is surrounded by multiple cysts (likely of biliary cell origin) and irregular duct-like structures
• at E18.5, the portal tracts are often surrounded by many irregular biliary duct-like structures/cysts
• cysts present in the parenchymal tissue appear to form in the absence of a branch of the portal vein
• at 8 weeks, 24 of 26 mice have cysts and four of these mice have more than 50 visible cysts
• cysts are seen in all lobes of the liver, multioculated, almost all filled with a clear fluid, range in size from 0.5mm to 8mm, and worsen with age
• hepatic cysts are a result of abnormal morphogenesis of the intrahepatic bile duct

endocrine/exocrine glands
• intrahepatic bile duct morphogenesis is abnormal and results in hepatic cysts

growth/size/body
• at E18.5, the portal tracts are often surrounded by many irregular biliary duct-like structures/cysts
• cysts present in the parenchymal tissue appear to form in the absence of a branch of the portal vein
• at 8 weeks, 24 of 26 mice have cysts and four of these mice have more than 50 visible cysts
• cysts are seen in all lobes of the liver, multioculated, almost all filled with a clear fluid, range in size from 0.5mm to 8mm, and worsen with age
• hepatic cysts are a result of abnormal morphogenesis of the intrahepatic bile duct




Genotype
MGI:3848168
cn5
Allelic
Composition
Jag1tm1.1Loo/Jag1tm1.1Loo
Tg(Alb1-cre)1Khk/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Jag1tm1.1Loo mutation (0 available); any Jag1 mutation (78 available)
Tg(Alb1-cre)1Khk mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
normal phenotype
• no abnormal phenotype was observed including in the bile ducts




Genotype
MGI:3848170
cn6
Allelic
Composition
Jag1tm1.1Loo/Jag1+
Notch2tm1Grid/Notch2+
Tg(Alb1-cre)1Khk/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Jag1tm1.1Loo mutation (0 available); any Jag1 mutation (78 available)
Notch2tm1Grid mutation (1 available); any Notch2 mutation (99 available)
Tg(Alb1-cre)1Khk mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
normal phenotype
• no abnormal phenotype was observed including in the bile ducts




Genotype
MGI:3848171
cn7
Allelic
Composition
Jag1tm1Grid/Jag1tm1.1Loo
Tg(Alb1-cre)1Khk/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Jag1tm1.1Loo mutation (0 available); any Jag1 mutation (78 available)
Jag1tm1Grid mutation (1 available); any Jag1 mutation (78 available)
Tg(Alb1-cre)1Khk mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
liver/biliary system
• diffuse bile duct proliferation is observed around small and large bile ducts by 4 weeks of age
• by 12 weeks of age, 50% of mice have bile duct proliferation with these ducts appearring small and slit-like
• at 8 weeks of age, some mice have dilated bile tracts and expanded portal tracts
• cytokeratin staining also shows irregular, dilated ducts surrounding the periphery of many portal tracts
• bile stasis is identified within the lumina of several proliferating ducts

endocrine/exocrine glands
• diffuse bile duct proliferation is observed around small and large bile ducts by 4 weeks of age
• by 12 weeks of age, 50% of mice have bile duct proliferation with these ducts appearring small and slit-like
• at 8 weeks of age, some mice have dilated bile tracts and expanded portal tracts
• cytokeratin staining also shows irregular, dilated ducts surrounding the periphery of many portal tracts




Genotype
MGI:3721919
cn8
Allelic
Composition
Hhextm2Cwb/Hhextm2Cwb
Tg(Alb1-cre)1Khk/?
Genetic
Background
involves: 129S1/Sv * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hhextm2Cwb mutation (1 available); any Hhex mutation (17 available)
Tg(Alb1-cre)1Khk mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
liver/biliary system
• by 43 weeks, mice have developed severe cystic disease

growth/size/body
• by 43 weeks, mice have developed severe cystic disease




Genotype
MGI:3522668
cn9
Allelic
Composition
Foxm1tm1Rhc/Foxm1tm1Rhc
Tg(Alb1-cre)1Khk/0
Genetic
Background
involves: 129X1/SvJ * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Foxm1tm1Rhc mutation (1 available); any Foxm1 mutation (28 available)
Tg(Alb1-cre)1Khk mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• 40% were dead by E14.5 and 70% were dead by E15.5; some animals survived until birth; heterogeneity of cre recombinase activity is suggested to result in these variable phenotypes

cellular
• decrease in BrdU incorporation without increase in apoptosis suggesting a block in mitosis

liver/biliary system
• disruption in the organization of liver sinusoids; variable penetrance
• abnormal development of the intrahepatic bile ducts
• presence of abnormal hepatoblast cells with enlarged polyploid nuclei
• decrease in BrdU incorporation without increase in apoptosis suggesting a block in mitosis
• reduced numbers of hepatoblasts; 50% reduction in the number of hepatoblasts compared to controls, but no decrease in overall size of liver suggesting a hypertrophy of remaining hepatoblasts
• disruption in the organization of hepatic cords; variable penetrance

cardiovascular system
• disruption in the organization of liver sinusoids; variable penetrance
• reduction in the number of large hepatic veins; variable penetrance

endocrine/exocrine glands
• abnormal development of the intrahepatic bile ducts




Genotype
MGI:2665532
cn10
Allelic
Composition
Hnf4atm1Sad/Hnf4atm1Sad
Tg(Alb1-cre)1Khk/0
Genetic
Background
involves: C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hnf4atm1Sad mutation (0 available); any Hnf4a mutation (28 available)
Tg(Alb1-cre)1Khk mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
liver/biliary system
• presence of large red lesions at 18.5 dpc
• hepatic glycogen stores were 5 times lower than those of wild-type
• hepatocytes were small, round, and loosely associated with each other at 18.5 dpc
• parenchyma was discontinuous and contained large holes that trapped numerous blood cells

homeostasis/metabolism
• hepatic glycogen stores were 5 times lower than those of wild-type





Contributing Projects:
Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO)
Citing These Resources
Funding Information
Warranty Disclaimer, Privacy Notice, Licensing, & Copyright
Send questions and comments to User Support.
last database update
12/10/2024
MGI 6.24
The Jackson Laboratory