Cag creert2

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CAG-CreERT2 is a Cre recombinase-based transgenic construct that is expressed under the control of the CAG promoter and is fused to the estrogen receptor (ERT2) ligand-binding domain. This allows for temporal control of Cre-mediated recombination events in transgenic mouse models.

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5 protocols using cag creert2

Diverse Transgenic Mouse Models for Gastric Cancer Research

Cited 4 times

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Mist1-CreERT2 mice (Shi et al., 2009 (link)), Cxcl12-dsRED mice (Ding and Morrison, 2013 (link)), Troy^−/− and Troy-BAC-CreERT2 mice (Fafilek et al., 2013 (link)), H/K-ATPase-Cxcl12 mice (Shibata et al., 2013 (link)), Eef1a1-LSL-Notch1(IC) mice (Buonamici et al., 2009 (link)), Wnt5a^flox mice (Miyoshi et al., 2012 (link)) were described previously. Cxcr4-EGFP mice were kindly provided by Richard J. Miller (Northwestern University Medical School, USA). LSL-Kras^G12D and LSL-Trp53^R172H mice were provided by Dr. Kenneth Olive (Columbia University, USA). Apc^flox mice were obtained from the National Cancer Institute (NCI). Lgr5-DTR-GFP mice were provided by Genentech. Cdh1^flox, R26-mTmG, R26-LacZ, R26-TdTomato, R26-Confetti, R26-EYFP, Cxcl12^flox, Tie2-Cre, Id2-GFP, and Cag-CreERT2 mice were purchased from the Jackson Laboratory. Cre recombinase was activated by oral administration of TAM (1–5mg/0.2mL corn oil, as indicated). All animal studies and procedures were approved by the ethics committees at Columbia University and the Academy of Sciences of the Czech Republic. Human stomach tissue sections were obtained from DGC patients who underwent surgical resection or endoscopic submucosal dissection from 2001 to 2012 at Gifu University Hospital, Gifu, Japan. All study protocols were approved by the ethics committees, and written informed consent was obtained from all patients.

Hayakawa Y., Ariyama H., Stancikova J., Sakitani K., Asfaha S., Renz B.W., Dubeykovskaya Z.A., Shibata W., Wang H., Westphalen C.B., Chen X., Takemoto Y., Kim W., Khurana S.S., Tailor Y., Nagar K., Tomita H., Hara A., Sepulveda A.R., Setlik W., Gershon M.D., Saha S., Ding L., Shen Z., Fox J.G., Friedman R.A., Konieczny S.F., Worthley D.L., Korinek V, & Wang T.C. (2015). Mist1 expressing gastric stem cells maintain the normal and neoplastic gastric epithelium and are supported by a perivascular stem cell niche. Cancer cell, 28(6), 800-814.

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REV-ERBα Deletion in CX3CR1+ Cells

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All mouse experiments were performed according to protocols approved by the Washington University IACUC (Institutional Animal Care and Use Committee, Office of Laboratory Animal Welfare Assurance: D1600245, USDA Registration #43-R-008) and under the supervision of the Department of Comparative Medicine. REV-ERBα global knockout (RKO), 5XFAD, CAG::Cre^ERT2+, CX3CR1::Cre^ERT2+, and MAPT P301S mice with C57/Bl6J background were obtained from The Jackson Laboratory. REV-ERBα floxed mice were kindly provided by Dr. Lazar (University of Pennsylvania, Philadelphia, USA)^{47 (link)}. All mice were housed under 12:12 hr light-dark cycle and free access to water and food. CX3CR1::Cre^ERT2+; Nr1d1^fl/fl mice were given tamoxifen (Sigma, 2 mg/day for 5 days) by oral gavage at 2 months of age to induce REV-ERBα deletion. Unneeded mice were sacrificed by CO₂ euthanasia according to the approved protocol of Washington University IACUC.

Lee J., Dimitry J.M., Song J.H., Son M., Sheehan P.W., King M.W., Travis Tabor G., Goo Y.A., Lazar M.A., Petrucelli L, & Musiek E.S. (2023). Microglial REV-ERBα regulates inflammation and lipid droplet formation to drive tauopathy in male mice. Nature Communications, 14, 5197.

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Conditional Genetic Manipulation in Mice

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All animal experiments were approved by the Animal Care and Use Committee of the School of Basic Medical Science of Shandong University (No. LL-201502043 and ECSBMSSDU2019-2-008). Lgr5-EGFP-ires-Cre^ERT2, CAG-Cre^ERT2, and Rosa26-LSL-Cas9-tdTomato mice were from the Jackson Laboratory (stock number 008875 and 004682) or GemPharmatech co. Ltd (stock numbers T002249). pVillin-Cre mice were provided by Dr. Baichun Jiang. Cul4b transgenic mice were generated as described previously [26 (link)]. Mice were housed in SPF facilities. The wildtype or Cul4b knockout mice from 8 to16 weeks were used for most experiments. For Cre induction, mice with the genotyping of Lgr5-EGFP-ires-Cre^ERT2 and CAG-Cre^ERT2 were intraperitoneally injected with 100 μl tamoxifen at the concentration of 2 mg/ml for 5 consecutive days.

Fan Y., Huo X., Guo B., Zhang X., Yang Y., Lian J., Meng X., Shao Y., Zou Y., Guo H., Wang H., Sun G., Dou H., Wang J., Shao C., Gong Y, & Hu H. (2022). Cullin 4b-RING ubiquitin ligase targets IRGM1 to regulate Wnt signaling and intestinal homeostasis. Cell Death and Differentiation, 29(9), 1673-1688.

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Genetic Manipulation of Mouse Kidney

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All animal studies and experimental procedures were performed according to the German animal care and ethics legislation and were approved by the local government authority, the Committee on Research Animal Care, Regierungspräsidium Freiburg (G-18/144). The study is compliant with all relevant ethical regulations regarding animal research. The Kansl2-floxed, Kansl3-floxed, and Nphs2-Cre mouse strains have been previously described (26 (link), 27 (link)). The Cag-Cre-ERT2 and Gt(ROSA)26Sor^{tm4(ACTB-tdTomato,-EGFP)Luo/J} (referred to as mT/mG) mice were purchased from The Jackson Laboratory (Bar Harbor, ME, USA). All mice were maintained on a C57BL/6 background and kept under a 14-hour light and 10-hour dark cycle, and water and standard chow were available ad libitum. Genotyping was undertaken through standard PCR using the primers listed in table S5.

Tsang T.H., Wiese M., Helmstädter M., Stehle T., Seyfferth J., Shvedunova M., Holz H., Walz G, & Akhtar A. (2023). Transcriptional regulation by the NSL complex enables diversification of IFT functions in ciliated versus nonciliated cells. Science Advances, 9(34), eadh5598.

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Conditional Knockout Mice for Circadian Research

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Bmal1^fl/fl, CAG-Cre^ERT2, TH-Cre, Aldh1l1-Cre^ERT2, Cx3cr1-Cre^ERT2, and Nestin-Cre mice were all originally obtained from The Jackson Laboratory and were crossed in our colony. CaMK2a-iCre;Bmal1^fl/fl were previously described (22 (link), 34 (link)), and fixed/frozen tissue were prepared in house. All mice were maintained on a C57BL/6J background. All Cre^ERT2 lines were treated with tamoxifen (MilliporeSigma) at 2 months of age. Mice were given daily i.p. injections of tamoxifen in corn oil at a dose of 2 mg/day for 5 consecutive days. Both Cre⁺ and Cre^– mice were treated with tamoxifen. In all cases, Cre⁺ mice were hemizygous for Cre. Male and female mice were used in all experiments, as we have not observed sex differences in any of the measured endpoints.

Kanan M.K., Sheehan P.W., Haines J.N., Gomez P.G., Dhuler A., Nadarajah C.J., Wargel Z.M., Freeberg B.M., Nelvagal H.R., Izumo M., Takahashi J.S., Cooper J.D., Davis A.A, & Musiek E.S. (2024). Neuronal deletion of the circadian clock gene Bmal1 induces cell-autonomous dopaminergic neurodegeneration. JCI Insight, 9(2), e162771.

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