Villin cre

Manufactured by Jackson ImmunoResearch

Sourced in United States

Villin-Cre is a lab equipment product that serves as a genetic tool for research purposes. It is used to enable cell-specific gene expression or deletion in the intestinal epithelium of mice.

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Villin-Cre mice (54 citations) Villin-Cre transgenic mice (7 citations) Villin-Cre (018963) (2 citations) Villin-Cre animals (2 citations) Villin-Cre transgenic (2 citations) Villin-Cre mouse (2 citations) B6.SJL-Tg(Villin-cre)997Gum/J (2 citations) Villin-Cre recombinase C57/BL6 mice (2 citations)

50 protocols using villin cre

Conditional AhR Knockout Mice

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Ahr^fl/fl (stock no. 006203) and Villin-Cre (stock no. 021504) mice on a C57BL/6 background were purchased from Jackson Laboratory (Bar Harbor, ME) and bred in-house at China Pharmaceutical University. For IEC-specific Ahr disruption, Ahr^fl/fl were crossed with Villin-Cre mice to obtain Ahr^ΔIEC mice. WT mice on a C57BL/6 background were obtained from Beijing Vital River Laboratory Animal Technology Company (Beijing, China). All mice were housed in the specific pathogen-free facility and maintained under a temperature-controlled (22°C–23°C) room with a 12:12-hour light/dark cycle. All animal procedures were performed in compliance with the guidelines of the Institutional Animal Care and Use Committee of China Pharmaceutical University (Nanjing, China).

Qian M., Liu J., Zhao D., Cai P., Pan C., Jia W., Gao Y., Zhang Y., Zhang N., Zhang Y., Zhang Q., Wu D., Shan C., Zhang M., Schnabl B., Yang S., Shen X, & Wang L. (2021). Aryl Hydrocarbon Receptor Deficiency in Intestinal Epithelial Cells Aggravates Alcohol-Related Liver Disease. Cellular and Molecular Gastroenterology and Hepatology, 13(1), 233-256.

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Genetic Mouse Models for Intestinal Research

Cited 1 time

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Animal experiments were approved by the National Animal Experiment Board of Finland. Mice were housed and monitored according to the Federation of European Laboratory Animal Science Associations guidelines and recommendations. The mice were weighed and their health was closely monitored during the experiment. The mouse lines Lef1^fl/fl (25 (link)), Apc^fl/fl (76 (link)), Lgr5-EGFP-IRES-Cre^ERT2 (4 (link)), Rosa26^LSL-TdTomato (Jackson Laboratory, stock no. 021875), Apc^Min/+ (Jackson Laboratory, stock no. 002020), Villin-Cre^ERT2 (Jackson Laboratory, stock no. 020282), and Villin-Cre (Jackson Laboratory, stock no. 021504) have been described previously. Lef1^fl/fl mice with mixed C57BL/6 and 129SV background were used after backcrossing to the C57BL/6 strain for >6 generations. All experiments were performed three times with independent cohorts. Approximately equal numbers of male and female mice of same age were used for all the experiments.

Heino S., Fang S., Lähde M., Högström J., Nassiri S., Campbell A., Flanagan D., Raven A., Hodder M., Nasreddin N., Xue H.H., Delorenzi M., Leedham S., Petrova T.V., Sansom O, & Alitalo K. (2021). Lef1 restricts ectopic crypt formation and tumor cell growth in intestinal adenomas. Science Advances, 7(47), eabj0512.

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Murine Models of Helminth Infection

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Villin-Cre and Rag1^-/- mice were obtained from Jackson Laboratories. Vav-Cre mice were obtained from T. Graf (Centre for Genomic Regulation, Barcelona, Spain). Setd7^-/- and Setd7^f/f mice were described previously [20 (link),47 (link)]. We did not observe any physiological effects from Cre expression during homeostasis or infection. Animals were maintained in a specific-pathogen-free environment and tested negative for pathogens in routine screening. All experiments were carried out at the University of British Columbia following institutional guidelines. We used both males and females that were littermates and age matched (ranging from 7–15 weeks old) for all experiments. Isolation of T. muris eggs was carried out as described previously [24 (link)]. Mice were infected on day 0 with high dose (~200) or low dose (~35) of embryonated eggs by oral gavage, and parasite burdens were assessed microscopically on days 14, 21, 28, or 32 post-infection. Mice were infected with 200 H. polygyrus bakeri L3 larvae by oral gavage and parasite burdens were assessed microscopically on day 28. Liposome-encapsulated verteporfin (VP, Visudyne) was a kind gift by Novartis and was used at 50 mg/kg [42 (link)] by intraperitoneal injection at days -3, 0, 4, 7, 10, 13, 17, 20. Control mice were injected with the same volume of vehicle with the same schedule.

Oudhoff M.J., Antignano F., Chenery A.L., Burrows K., Redpath S.A., Braam M.J., Perona-Wright G, & Zaph C. (2016). Intestinal Epithelial Cell-Intrinsic Deletion of Setd7 Identifies Role for Developmental Pathways in Immunity to Helminth Infection. PLoS Pathogens, 12(9), e1005876.

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Transgenic Mouse Models for Gut Research

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C57BL/6 (WT) and Villin-Cre (C57BL/6 background) were purchased from The Jackson Laboratory. Defa6-Cre mice were obtained from Dr. Richard Blumberg, Brigham and Women’s Hospital, Harvard. Generation and characterization of IL-22-Floxed (Il22Ra1^fl/fl) mice was performed as described (45 (link)). Rorc^−/− and Il22^−/− (both C57BL/6 background) mice were received from Dr. Jay K. Kolls. Il22Ra1^fl/fl mice were bred with Villin-Cre, Lgr5-EGFP-cre^ERT2, or Defa6-cre mice to generate entire gut epithelium ISC-specific and Paneth cell-specific IL-22Ra1 knockout mice. Lgr5-EGFP-cre^ERT2;RosaLSLtdTomato mice were obtained from Dr. Vincent Yang, Stony Brook University. We used 6–8 week aged mice (both genders) for all experiments unless indicated in the figure. All mice were housed in specific pathogen-free conditions at Stony Brook University, Stony Brook, NY. All animal studies were conducted with the approval of Stony Brook University Institutional Animal Care and Use Committee.

Gaudino S.J., Beaupre M., Lin X., Joshi P., Rathi S., McLaughlin P.A., Kempen C., Mehta N., Eskiocak O., Yueh B., Blumberg R.S., van der Velden A.W., Shroyer K.R., Bialkowska A.B., Beyaz S, & Kumar P. (2020). IL-22 receptor signaling in Paneth cells is critical for their maturation, microbiota colonization, Th17-related immune responses, and anti-Salmonella immunity. Mucosal Immunology, 14(2), 389-401.

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Genetically Modified Mouse Models

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Mice were bred under specific pathogen-free conditions in the Animal Facility at Kobe University Graduate School of Medicine. Villin-Cre and Apc^Min/+ mice (strain #004586 and #002020, respectively) were purchased from the Jackson Laboratory (Bar Harbor, ME, USA). LAT1^fl/fl mice were generated as previously described [19 (link)], and LAT1^fl/fl; vil-cre; Apc^Min/+ and LAT1^fl/fl; Apc^Min/+ mice were generated by breeding these strains. All mice were of a C57BL/6J background, and both female and male mice were used in all experiments. All animal experiments were approved by the Institutional Animal Care and Use Committee of Kobe University (approval number: P190307).

Sui Y., Hoshi N., Ohgaki R., Kong L., Yoshida R., Okamoto N., Kinoshita M., Miyazaki H., Ku Y., Tokunaga E., Ito Y., Watanabe D., Ooi M., Shinohara M., Sasaki K., Zen Y., Kotani T., Matozaki T., Tian Z., Kanai Y, & Kodama Y. (2023). LAT1 expression influences Paneth cell number and tumor development in ApcMin/+ mice. Journal of Gastroenterology, 58(5), 444-457.

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Genetically Modified Mouse Models for Research

Cited 2 times

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All animal work was approved by Duke University’s Institutional Animal Care and Use Committee. All mice were maintained in a barrier facility with 12-hour light/dark cycles. Mice were genotyped by PCR and both males and females were analyzed. TRE-Arhgef11^CA were generated in the lab as previously described [7 (link)]. Other animal strains used in this study were Villin-rtTA (Jackson Laboratories,[40 (link)]), VillinCre (Jackson Laboratories [41 (link)]), and Rosa-rtTA3 (Jackson Laboratories).

Hinnant T., Ning W, & Lechler T. (2023). Compartment specific responses to contractility in the small intestinal epithelium. bioRxiv.

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Genetic Mouse Models for Intestinal Research

Cited 1 time

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APC^Min/+ (Moser et al. 1990 (link); Su et al. 1992 (link)), Villin-Cre (Madison et al. 2002 (link)), Catnb^flox (Brault et al. 2001 (link)), and Rosa26-LacZ mice (Soriano 1999 (link)) were from the Jackson Laboratory. Catnb^lox(ex3) mice were described previously (Harada et al. 1999 (link)). Lgr5-EGFP-IRES-creER^T2 mice (Barker et al. 2007 (link)) were kindly provided by Dr. Hans Clevers. APC^flox (APC^Δ14) mice (Colnot et al. 2004 (link)) were kindly provided by Dr. Christine Perret. Taz^flox mice (Xin et al. 2013 (link)) were kindly provided by Dr. Eric N. Olson.
Yap^flox (Zhang et al. 2010 (link)) and Sav1^flox (Cai et al. 2010 (link)) mice were described previously. Mice with Yap, Sav1, Taz, or β-catenin specifically deleted in the intestinal epithelium were generated by breeding Yap^flox, Sav1^flox, Taz^flox, or Catnb^flox mice with VilCre mice. Mice with APC or Sav1 inactivation or stabilized β-catenin specifically in the intestinal stem cells were generated by breeding APC^flox, Sav1^flox, or Catnb^lox(ex3) mice with Lgr5-EGFP-IRES-creER^T2 mice. Five daily intraperitoneal injections of 100 mg/kg tamoxifen (Sigma) dissolved in corn oil were performed in mice at 6 wk of age. Animal protocols were approved by the Institutional Animal Care and Use Committee of the Johns Hopkins University.

Cai J., Maitra A., Anders R.A., Taketo M.M, & Pan D. (2015). β-Catenin destruction complex-independent regulation of Hippo–YAP signaling by APC in intestinal tumorigenesis. Genes & Development, 29(14), 1493-1506.

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Genetic Manipulation of Cmklr1 in Mice

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Villin-cre (#004586) transgenic mice were purchased from The Jackson Laboratory. Rarres2^−/−, Ccrl2^−/−, and Cmklr1^−/− mice were generated by Cyagen as previously described (20 (link), 46 (link)). Cmklr1-floxed (Cmklr1^fl/fl) mice were generated by Shanghai Model Organisms Center, Inc. by inserting the sequence of flox at axon 3 of murine Cmklr1 gene (MGI#109603). The genotyping primers and the length of PCR production are listed in SI Appendix, Table S1. Cmklr1^fl/fl:Villin-cre (Cmklr1^ΔIEC) were generated by crossing Cmklr1^fl/fl mice with Villin-cre transgenic mice. Age and sex-matched littermates were used for all experiments. All mice used were on a C57BL/6J background and housed under specific pathogen-free conditions. All studies were approved by the Animal Care and Use Committee of the Fudan University Shanghai Medical College.

Lin Y., Cai Q., Luo Y., Li B., Chen Y., Yang X., Xuan Y., Yang H, & He R. (2022). Epithelial chemerin–CMKLR1 signaling restricts microbiota-driven colonic neutrophilia and tumorigenesis by up-regulating lactoperoxidase. Proceedings of the National Academy of Sciences of the United States of America, 119(29), e2205574119.

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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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Animal Welfare-Approved Mouse Breeding

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Adult C57BL/6 male mice were purchased from the Multidisciplinary Centre for Biological Investigation, Campinas-SP, Brazil. Rorc-Cre, Villin-Cre, and HIF-1alfa^{floxed/floxed} mice were from The Jackson Laboratories. All strains were maintained in a C57BL/6 background and kept in regular filter-top cages with free access to sterile water and food. Animal procedures were approved by the Ethics Committee on Animal Use of the University of Campinas (protocol #5495–1/2020).

Fachi J.L., Pral L.P., dos Santos J.A., Codo A.C., de Oliveira S., Felipe J.S., Zambom F.F., Câmara N.O., Vieira P.M., Colonna M, & Vinolo M.A. (2021). Hypoxia enhances ILC3 responses through HIF-1α-dependent mechanism. Mucosal Immunology, 14(4), 828-841.

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