Phenotypes associated with this allele

• Allele Symbol: Tg(Alb1-cre)1Khk
• Allele Name: transgene insertion 1, Klaus H Kaestner
• Allele ID: MGI:2664969
• Summary: 10 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
cn1	Foxa1^tm1Khk/Foxa1^tm1Khk Foxa2^tm1Khk/Foxa2^tm1Khk Tg(Alb1-cre)1Khk/0	involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL	MGI:5314251
cn2	Akt2^tm1.2Mbb/Akt2^tm1.2Mbb Tg(Alb1-cre)1Khk/0	involves: 129P2/OlaHsd * 129S4/SvJaeSor * C57BL/6 * SJL	MGI:4889114
cn3	Akt2^tm1.2Mbb/Akt2^tm1.2Mbb Lep^ob/Lep^ob Tg(Alb1-cre)1Khk/0	involves: 129P2/OlaHsd * 129S4/SvJaeSor * C57BL/6 * SJL	MGI:4889115
cn4	Jag1^tm1Grid/Jag1^tm1.1Loo Tg(Alb1-cre)1Khk/0	involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL	MGI:3848171
cn5	Jag1^tm1.1Loo/Jag1^+ Notch2^tm1Grid/Notch2^+ Tg(Alb1-cre)1Khk/0	involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL	MGI:3848170
cn6	Jag1^tm1.1Loo/Jag1^tm1.1Loo Tg(Alb1-cre)1Khk/0	involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL	MGI:3848168
cn7	Hhex^tm1Cwb/Hhex^tm2Cwb Tg(Alb1-cre)1Khk/?	involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL	MGI:3721920
cn8	Hhex^tm2Cwb/Hhex^tm2Cwb Tg(Alb1-cre)1Khk/?	involves: 129S1/Sv * C57BL/6 * SJL	MGI:3721919
cn9	Foxm1^tm1Rhc/Foxm1^tm1Rhc Tg(Alb1-cre)1Khk/0	involves: 129X1/SvJ * C57BL/6 * SJL	MGI:3522668
cn10	Hnf4a^tm1Sad/Hnf4a^tm1Sad Tg(Alb1-cre)1Khk/0	involves: C57BL/6 * SJL	MGI:2665532

Genotype
MGI:5314251

cn1

• Allelic Composition: Foxa1^tm1Khk/Foxa1^tm1Khk; Foxa2^tm1Khk/Foxa2^tm1Khk; Tg(Alb1-cre)1Khk/0
• Genetic Background: involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL

• ♀: phenotype observed in females
• ♂: phenotype observed in males
• N: normal phenotype

neoplasm

decreased incidence of tumors by chemical induction ( J:181296 )

• male mutants injected with DEN followed by TCPOBOP (carcinogen treatment) show reduced tumor growth compared to control males that develop severe hepatocellular carcinoma

increased incidence of tumors by chemical induction ( J:181296 )

• 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

increased hepatocellular carcinoma incidence ( J:181296 )

• 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

decreased incidence of tumors by chemical induction ( J:181296 )

• male mutants injected with DEN followed by TCPOBOP (carcinogen treatment) show reduced tumor growth compared to control males that develop severe hepatocellular carcinoma

increased incidence of tumors by chemical induction ( J:181296 )

• 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

increased hepatocellular carcinoma incidence ( J:181296 )

• 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:4889114

cn2

• Allelic Composition: Akt2^tm1.2Mbb/Akt2^tm1.2Mbb; Tg(Alb1-cre)1Khk/0
• Genetic Background: involves: 129P2/OlaHsd * 129S4/SvJaeSor * C57BL/6 * SJL

homeostasis/metabolism

decreased liver triglyceride level ( J:155432 )

• in fed mice fed a Surwit high-fat diet at 1 and 4 months

growth/size/body

growth/size/body region phenotype ( J:155432 )

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

liver/biliary system

decreased liver triglyceride level ( J:155432 )

• in fed mice fed a Surwit high-fat diet at 1 and 4 months

Genotype
MGI:4889115

cn3

• Allelic Composition: Akt2^tm1.2Mbb/Akt2^tm1.2Mbb; Lep^ob/Lep^ob; Tg(Alb1-cre)1Khk/0
• Genetic Background: involves: 129P2/OlaHsd * 129S4/SvJaeSor * C57BL/6 * SJL

homeostasis/metabolism

increased circulating glucose level ( J:155432 )

• fasted mice exhibit increased plasma glucose levels compared with Akt2^tm1Mbb Lep^ob homozygotes

abnormal lipid homeostasis ( J:155432 )

• mice exhibit reduced lipogenesis compared to in Akt2^tm1Mbb Lep^ob homozygotes

decreased liver triglyceride level ( J:155432 )

• mice exhibit decreased liver triglyceride levels compared with Akt2^tm1Mbb Lep^ob homozygotes

growth/size/body

decreased body weight ( J:155432 )

• mice exhibit decreased body weight compared with Akt2^tm1Mbb Lep^ob homozygotes

• however, body composition was normal

liver/biliary system

decreased liver triglyceride level ( J:155432 )

• mice exhibit decreased liver triglyceride levels compared with Akt2^tm1Mbb Lep^ob homozygotes

decreased liver weight ( J:155432 )

• mice exhibit decreased liver weight compared with Akt2^tm1Mbb Lep^ob homozygotes

Genotype
MGI:3848171

cn4

• Allelic Composition: Jag1^tm1Grid/Jag1^tm1.1Loo; Tg(Alb1-cre)1Khk/0
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL

liver/biliary system

bile duct proliferation ( J:149131 )

• 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

dilated bile duct ( J:149131 )

• 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

abnormal bile secretion ( J:149131 )

• bile stasis is identified within the lumina of several proliferating ducts

endocrine/exocrine glands

bile duct proliferation ( J:149131 )

• 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

dilated bile duct ( J:149131 )

• 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:3848170

cn5

• Allelic Composition: Jag1^tm1.1Loo/Jag1⁺; Notch2^tm1Grid/Notch2⁺; Tg(Alb1-cre)1Khk/0
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL

normal phenotype

no abnormal phenotype detected ( J:149131 )

• no abnormal phenotype was observed including in the bile ducts

Genotype
MGI:3848168

cn6

• Allelic Composition: Jag1^tm1.1Loo/Jag1^tm1.1Loo; Tg(Alb1-cre)1Khk/0
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL

normal phenotype

no abnormal phenotype detected ( J:149131 )

• no abnormal phenotype was observed including in the bile ducts

Genotype
MGI:3721920

cn7

• Allelic Composition: Hhex^tm1Cwb/Hhex^tm2Cwb; Tg(Alb1-cre)1Khk/?
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL

liver/biliary system

abnormal bile duct development ( J:124126 )

• intrahepatic bile duct morphogenesis is abnormal and results in hepatic cysts

abnormal liver morphology ( J:124126 )

• 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

liver cyst ( J:124126 )

• 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

abnormal bile duct development ( J:124126 )

• intrahepatic bile duct morphogenesis is abnormal and results in hepatic cysts

growth/size/body

liver cyst ( J:124126 )

• hepatic cysts are a result of abnormal morphogenesis of the intrahepatic bile duct

• 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

Genotype
MGI:3721919

cn8

• Allelic Composition: Hhex^tm2Cwb/Hhex^tm2Cwb; Tg(Alb1-cre)1Khk/?
• Genetic Background: involves: 129S1/Sv * C57BL/6 * SJL

liver/biliary system

liver cyst ( J:124126 )

• by 43 weeks, mice have developed severe cystic disease

growth/size/body

liver cyst ( J:124126 )

• by 43 weeks, mice have developed severe cystic disease

Genotype
MGI:3522668

cn9

• Allelic Composition: Foxm1^tm1Rhc/Foxm1^tm1Rhc; Tg(Alb1-cre)1Khk/0
• Genetic Background: involves: 129X1/SvJ * C57BL/6 * SJL

mortality/aging

lethality throughout fetal growth and development, incomplete penetrance ( J:94883 )

• 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

abnormal cell cycle ( J:94883 )

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

liver/biliary system

abnormal liver sinusoid morphology ( J:94883 )

• disruption in the organization of liver sinusoids; variable penetrance

abnormal intrahepatic bile duct morphology ( J:94883 )

• abnormal development of the intrahepatic bile ducts

abnormal hepatoblast morphology ( J:94883 )

• presence of abnormal hepatoblast cells with enlarged polyploid nuclei

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

decreased hepatoblast number ( J:94883 )

• 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

abnormal hepatic cord morphology ( J:94883 )

• disruption in the organization of hepatic cords; variable penetrance

cardiovascular system

abnormal liver sinusoid morphology ( J:94883 )

• disruption in the organization of liver sinusoids; variable penetrance

abnormal hepatic vein morphology ( J:94883 )

• reduction in the number of large hepatic veins; variable penetrance

endocrine/exocrine glands

abnormal intrahepatic bile duct morphology ( J:94883 )

• abnormal development of the intrahepatic bile ducts

Genotype
MGI:2665532

cn10

• Allelic Composition: Hnf4a^tm1Sad/Hnf4a^tm1Sad; Tg(Alb1-cre)1Khk/0
• Genetic Background: involves: C57BL/6 * SJL

liver/biliary system

abnormal liver morphology ( J:84076 )

• presence of large red lesions at 18.5 dpc

decreased liver glycogen level ( J:84076 )

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

abnormal liver development ( J:84076 )

abnormal hepatocyte morphology ( J:84076 )

• hepatocytes were small, round, and loosely associated with each other at 18.5 dpc

dissociated hepatocytes ( J:84076 )

• parenchyma was discontinuous and contained large holes that trapped numerous blood cells

homeostasis/metabolism

decreased liver glycogen level ( J:84076 )

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