B6 fvb 129 tg alb1 cre 1dlr j

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B6.FVB(129)-Tg(Alb1-cre)1Dlr/J is a transgenic mouse strain. It carries the Cre recombinase gene under the control of the albumin promoter. This allows for Cre-mediated recombination in hepatocytes.

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B6 cg tg vil1 cre 997gum j, by Jackson ImmunoResearch (2 mentions) Villin cre, by Jackson ImmunoResearch (2 mentions) B6.129 ctnnb1tm2kem knwj, by Jackson ImmunoResearch (1 mentions)

4 protocols using b6 fvb 129 tg alb1 cre 1dlr j

Genetic Manipulation of Glucocorticoid Receptor

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B6.Cg-Nr3c1^tma1.1jda/J (strain #021021) or GR^Flox/Flox, B6.Cg.Tg(Vil1-cre)997Gum/J (strain #004586) or Villin^Cre, and B6.FVB(129)-Tg(Alb1-cre)1Dlr/J (strain #016832) or Alb^Cre mice were purchased from Jackson Laboratories (Sacramento, CA). GR^Flox/Flox mice are floxed mutant mice that possess loxP sites flanking exon 3 of the Nr3c1 gene. Villin^Cre mice express Cre recombinase in villus and crypt epithelial cells of the intestine. Alb^Cre mice express Cre recombinase in hepatocytes in the liver. GR^Flox/Flox-Alb^Cre (GR^ΔHC) lack GR gene exclusively in the hepatocytes, whereas and GR^Flox/Flox-Villin^Cre (GR^ΔIEC) mice lack GR gene exclusively in the intestinal epithelium, including all types of cells in the intestinal epithelium. All animal experiments were performed according to the protocols approved by the University of Tennessee Health Science Center Institutional Animal Care and Use Committee. Animals were housed in an institutional animal care facility with 12:2-h light-dark cycles. All mice had free access to regular laboratory chow and water until the start of experiments. During the experiments, they were fed a liquid diet as described below.

Shukla P.K., Meena A.S., Pierre J.F, & Rao R. (2021). Central role of intestinal epithelial glucocorticoid receptor in alcohol‐ and corticosterone‐induced gut permeability and systemic response. The FASEB Journal, 36(1), e22061.

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Conditional Knockout Mice for Hepatocyte and Intestinal GR

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B6.Cg‐Nr3c1^tma1.1jda/J (strain #021021) or GR^Flox/Flox, B6.Cg. Tg(Vil1‐cre)997Gum/J (strain #004586) or Villin^Cre, and B6.FVB(129)‐Tg(Alb1‐cre)1Dlr/J (strain #016832) or Alb^Cre mice were purchased from Jackson Laboratories (Sacramento, CA). GR^Flox/Flox mice are floxed mutant mice that possess loxP sites flanking exon 3 of the Nr3c1 gene. Villin^Cre mice express Cre recombinase in villus and crypt epithelial cells of the intestine. Alb^Cre mice express Cre recombinase in hepatocytes in the liver. GR^Flox/Flox‐Alb^Cre (GR^ΔHC) lack the GR gene exclusively in the hepatocytes, whereas and GR^Flox/Flox‐Villin^Cre (GR^ΔIEC) mice lack the GR gene exclusively in the intestinal epithelium, including all types of cells in the intestinal epithelium. All animal experiments were performed according to the protocols approved by the University of Tennessee Health Science Center Institutional Animal Care and Use Committee. Animals were housed in an institutional animal care facility with 12:2‐h light–dark cycles. All mice had free access to regular laboratory chow and water until the start of experiments. During the experiments, they were fed a liquid diet as described below.

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Generation and Validation of Hepatocyte-Specific Xdh Knockout Mice

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Xdh floxed (FLX) mice were generated by Taconic. Balb/C blastocysts were injected with C57BL/6NTac embryonic stem cells containing a vector targeting the Xdh locus (Fig. 1B) and transferred to pseudopregnant females. First-generation chimeric offspring were bred with C57BL/6 Flp deleter mice to remove the Neo selection gene and generate C57BL/6Ntac mice containing the Xdh FLX allele. For all experiments, mice homozygous for the FLX Xdh allele (Xdh^{floxed/floxed}) were bred with Xdh^{floxed/floxed} mice heterozygous for Alb-1cre (B6.FVB(129)-Tg (alb1-cre)1Dlr/J; The Jackson Laboratory) to generate Xdh^{floxed/floxed}Alb-1^Cre/Wt (hepatocyte-specific Xdh knockout [HXO]) and Xdh^{floxed/floxed}Alb-1^Wt/Wt (littermate FLX controls). Genotyping was confirmed with PCR. For Xdh FLX, primers flanking the loxP sites in intron 1 (5′-GTATGGTCTGTAGTATGTCCACTGC-3′ and 5′-CCTTTCAAGACACGCATTCC-3′) and intron 2 (5′-TTGGGTGATCCTAGGCTCC-3′ and 5′-CTTCTTCTGGTCTCTCTGGACC-3′) were used. For Alb-1-cre, primers flanking the Cre transgene (5′-CCAGGCTAAGTGCCTTCTCTACA-3′ and 5′-AATGCTTCTGTCCGTTTGCCGGT-3′) were used.

Harmon D.B., Mandler W.K., Sipula I.J., Dedousis N., Lewis S.E., Eckels J.T., Du J., Wang Y., Huckestein B.R., Pagano P.J., Cifuentes-Pagano E., Homanics G.E., Van’t Erve T.J., Stefanovic-Racic M., Jurczak M.J., O’Doherty R.M, & Kelley E.E. (2019). Hepatocyte-Specific Ablation or Whole-Body Inhibition of Xanthine Oxidoreductase in Mice Corrects Obesity-Induced Systemic Hyperuricemia Without Improving Metabolic Abnormalities. Diabetes, 68(6), 1221-1229.

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Pkhd1 Mouse Model of Polycystic Kidney Disease

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We used the Pkhd1^del4/del4 mouse (a kind gift from S. Somlo, Yale University, New Haven, CT), an orthologue model of the human CHF (19 (link)). Pkhd1^del4/del4 mice were generated on a mixed C57BL6/129Sv background, harboring an inactivating deletion in the exon 4 of the Pkhd1 gene (orthologous of the human PKHD1), while WT littermates of the same genetic background served as controls. To generate Pkhd1/β-catenin liver specific double KO mice we crossed Pkhd1^del4/del4 mice with AlbCre mice (B6.FVB(129)-Tg(Alb1-cre)1Dlr/J) and β-catenin^fl/fl (B6.129-Ctnnb1^tm2Kem/KnwJ) that were obtained from Jackson Laboratories (Bar Harbor, ME, USA). All mice were maintained at the Yale Animal Resources Center and used according to a protocol approved by the Yale University Institutional Animal Care and Use Committee (IACUC) and the Office of Animal Research Support (OARS) of Yale University. After mouse sacrifice, liver tissue was harvested, fixed in formalin, and embedded in paraffin.

Fabris L., Milani C., Fiorotto R., Mariotti V., Kaffe E., Seller B., Sonzogni A., Strazzabosco M, & Cadamuro M. (2022). Dysregulation of the Scribble/YAP/β-catenin axis sustains the fibroinflammatory response in a PKHD1−/− mouse model of Congenital Hepatic Fibrosis. FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 36(6), e22364.

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