B6 cg tg cd4 cre 1cwi bfluj

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B6.Cg-Tg(Cd4-cre)1Cwi/BfluJ is a transgenic mouse strain that expresses Cre recombinase under the control of the CD4 promoter. This strain can be used to conditionally delete or activate target genes in T cells.

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Cd4-Cre (117 citations) Tg(Cd4-cre)1Cwi/BfluJ (8 citations) CD4-Cre (B6.Cg-Tg(Cd4-cre)1Cwi/BfluJ), (5 citations) B6.Cg-Tg(Cd4-cre)1Cwi/BfluJ (CD4Cre) (4 citations) CD4-Cre B6.Cg-Tg(Cd4-cre)1Cwi/BfluJ mice (2 citations) B6.Cg-Tg(Cd4-cre)1Cwi/BfluJ (Cd4cre) mice (2 citations)

7 protocols using b6 cg tg cd4 cre 1cwi bfluj

Generation and Characterization of Transgenic Mice

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C57BL/6 and BALB/c mice were obtained from Harlan Laboratories (Indianapolis, IN). CD4-cre mice, purchased from Jackson Laboratories [017336; B6.Cg-Tg(Cd4-cre)1Cwi/BfluJ], express the cre recombinase under the control of the CD4 promoter and have been previously described [58 (link),59 (link)]. IKKβ^fl/fl mice, which express a loxP-flanked IKKβ locus and have been previously described [60 (link)], were generously provided by Dr. Michael Karin (University of California San Diego, San Diego, CA). CD4-cre mice were crossed with IKKβ^fl/fl mice in house (CD4-cre x IKKβ^fl/fl mice). CARMA1-KO mice were originally generated on the 129 background [16 (link)], were a gift from Dr. Daniel Littman (New York University, New York, NY) and were backcrossed for 6–10 generations onto the C57BL/6 background at the University of Chicago specific pathogen-free (SPF) barrier facility. MyD88-KO mice are deficient in the adaptor molecule MyD88 in all tissues [61 (link)] and were a gift from Dr. Alexander Chervonsky (University of Chicago, Chicago, IL). All mice were on the C57BL/6 background and bred at the University of Chicago SPF facility in agreement with our Institutional Animal Care and Use Committee (IACUC) and according to the National Institutes of Health guidelines for animal use.

Barnes S.E., Wang Y., Chen L., Molinero L.L., Gajewski T.F., Evaristo C, & Alegre M.L. (2015). T cell-NF-κB activation is required for tumor control in vivo. Journal for Immunotherapy of Cancer, 3, 1.

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Generation and Characterization of Genetically Modified Mice

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C57BL/6J, B6.Cg-Tg(Cd4-cre)1Cwi/BfluJ, C.B6 (Cg)-Rag2^tm1.1Cgn/J (Rag2-KO), and C57BL/6-Il17a^tm1Bcgen/J (Il17a-GFP) were purchased from Jackson Laboratory. B6.SJLPtprc^a/BoyAiTac (CD45.1+) were purchased from Taconic. Stat3^fl/fl mice were from Dr. David Levy (Lee et al., 2002) and bred with CD4-Cre Tg mice. Stat4 KO mice were from Dr. Mark Kaplan (Indiana University). C57BL/6-Mir221Mir222 ^fl/fl mice and miR-221/222-KO (Mir221Mir222 KO) mice were generated as described in Fig.2A and Fig.S2A. C57BL/6-Mir221Mir222^fl/fl mice were bred with CD4-Cre to generate miR-221/222 conditional KO (cKO). Germline Mir221Mir222 KO mice were bred with Rag2-KO to generate Rag2-miR-221/222 double KO mice. Il17a-GFP mice were bred with Mir221Mir222 KO to generate IL17-GFP-miR-221/222-KO.
For some experiments, WT (Mir221Mir222^fl/fl) and miR-221/222 KO mice were cohoused for at least 12 weeks starting at 3-4 weeks old so that microbiota of the gut is shared among them. Cohoused mice were used for the following experiments (Fig.3A-C, Fig.5C-E).
For generation of bone marrow chimera mice Rag2-KO recipient mice were conditioned with 450 Rads prior to injection of 3 million donor BM cells (CD45.1+ and miR-221/222-KO). Mice were then fed Trimethoprim/Sulfamethoxazole antibiotics via drinking water for 5 weeks.

Mikami Y., Philips R.L., Sciumè G., Petermann F., Meylan F., Nagashima H., Yao C., Davis F.P., Brooks S.R., Sun H.W., Takahashi H., Poholek A.C., Shih H.Y., Afzali B., Muljo S.A., Hafner M., Kanno Y, & O’Shea J.J. (2021). MicroRNA-221 and -222 modulate intestinal inflammatory Th17 cell response as negative feedback regulators downstream of Interleukin-23. Immunity, 54(3), 514-525.e6.

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Genetically Modified Mouse Strains

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C57/BL6J, P2rx7^−/− (B6.129P2-P2rx7tm1Gab/J), Icos^−/− (B6.129P2-Icostm1Mak/J), OT-II (B6.Cg-Tg(TcraTcrb)425Cbn/J), CD45.1 (B6.SJL-Ptprca Pepcb/BoyJ), CD90.1 (B6.PL-Thy1a/CyJ), and Cd4-cre (B6.Cg-Tg(Cd4-cre)1Cwi/BfluJ) mice were from The Jackson Laboratory. The P2rx7^fl/fl mice were from the European Mouse Mutant Archive (EMMA ID 05116; Skarnes et al., 2011 (link)). Cd4-Cre P2rx7^fl/fl mice were generated by crossing the two strains. All mice were bred in the specific pathogen–free facility at the Institute for Research in Biomedicine (IRB), Bellinzona, Switzerland. All animal experiments were performed in accordance with the Swiss Federal Veterinary Office guidelines and authorized by the Cantonal Veterinary.

Faliti C.E., Gualtierotti R., Rottoli E., Gerosa M., Perruzza L., Romagnani A., Pellegrini G., De Ponte Conti B., Rossi R.L., Idzko M., Mazza E.M., Bicciato S., Traggiai E., Meroni P.L, & Grassi F. (2019). P2X7 receptor restrains pathogenic Tfh cell generation in systemic lupus erythematosus. The Journal of Experimental Medicine, 216(2), 317-336.

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Mouse Models for Immunology Research

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5- to 8-wk-old male and female, age-matched mice were used for all experiments. C57BL/6NCrl and B6.SJL-Ptprc^aPepc^b/BoyCrl were purchased from Charles River Laboratories. B6.129S2-Ifnar1^tm1Agt/Mmjax (Strain #:028288, Ifnar1^−/−), B6.129S(Cg)-Stat1^tm1Dlv/J (Strain #:012606, Stat1^−/−), B6.129S7-Ifngr1^tm1Agt/J (Strain #:003288, Ifngr1^−/−), B6.C(Cg)-Cd79a^tm1(cre)Reth/EhobJ (Strain #:020505, Mb1^Cre), B6.Cg-Tg(Cd4-cre)1Cwi/BfluJ (Strain #:022071, Cd4^Cre), B6.Cg-Foxp3tm2Tch/J (Strain #:006772, Foxp3^eGFP), and B6.129P2-Aicda^tm1(cre)Mnz/J (Strain #: 007770, Aicda^Cre/Cre) mice were purchased from The Jackson Laboratory. B6.Cg-Mx1^tm1.1Agsa/J (Mx1^gfp) were kindly provided by A. García-Sastre (Icahn School of Medicine at Mount Sinai) and have been described previously (32 (link)). Ifnlr1^tm1.1Svko (Ifnrl1^fl/fl) and Ifnlr1^tm1.2Svko (Ifnrl1^−/−) mice were kindly provided by Sergei V Kotenko (Rutgers New Jersey Medical School) and have been described previously (35 (link)). Tg(Tcrb51–11.5)AR1251Ayr (TClib^Tg) mice have been described previously (41 (link)). Mice were maintained and bred under specific pathogen-free conditions at the University of Minnesota. All animal experiments were approved by the Institutional Animal Care and Use Committee of the University of Minnesota. All animals were maintained under specific pathogen-free conditions at the University of Minnesota.

Martinez R.J., Breed E.R., Worota Y., Ashby K.M., Vobořil M., Mathes T., Salgado O.C., O’Connor C.H., Kotenko S.V, & Hogquist K.A. (2023). Type III interferon drives thymic B cell activation and regulatory T cell generation. Proceedings of the National Academy of Sciences of the United States of America, 120(9), e2220120120.

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Atg16l1 Conditional Knockout Mice

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Atg16l1^fl/fl mice were generated and provided by the H. Virgin laboratory (Washington University, Saint Louis, MO), as described (Hwang et al., 2012 (link)). Atg16l1^fl/fl mice were crossed to B6.Cg-Tg(Cd4-cre)1Cwi/BfluJ (CD4-Cre mice) and B6.129(Cg)-Foxp3^{tm4(YFP/cre)Ayr}/J (Foxp3^Cre mice, Jackson Laboratory, Bar Harbor, ME) to generate Atg16l1^ΔCD4 and Atg16l1^ΔFoxp3 mice, respectively. All above strains, together with B6.SJL-CD45.1 (CD45.1⁺), B6 Rag1^-/- (Jackson Laboratory), and B6 Foxp3^hCD2 mice (Komatsu et al., 2009 (link)) were bred and maintained under specific pathogen-free conditions. Unless stated otherwise, mice were analyzed at 8–12 weeks (young mice) or > 5 months of age (aged mice). In the gene expression analysis Atg16l1^ΔFoxp3 mice and Foxp3^Cre mice were co-housed and age- and sex- matched. In all other experiments mice used were age- and sex-matched littermates that were kept co-housed throughout the experiments.

Kabat A.M., Harrison O.J., Riffelmacher T., Moghaddam A.E., Pearson C.F., Laing A., Abeler-Dörner L., Forman S.P., Grencis R.K., Sattentau Q., Simon A.K., Pott J, & Maloy K.J. (2016). The autophagy gene Atg16l1 differentially regulates Treg and TH2 cells to control intestinal inflammation. eLife, 5, e12444.

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Conditional IF1 Knockout Mouse Model

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Mouse experiments were carried out after approval of the institutional review board (Ethical Committee of the UAM, CEI-101-1891-A325; CM PROEX 233/19) in compliance with animal policies and ethical guidelines of the European Community. Mice were housed in the Animal Facility of the CBMSO with a 12-h light/12-h dark cycle and temperatures of 18–23°C with 40–60% humidity.
Conditional IF1 knockout mice (Atp5if1-KO) in T lymphocytes (CD4⁺ IF1-KO) were obtained by breeding the IF1-floxed mice²⁵ (link) with the B6.Cg-Tg(Cd4-cre)1Cwi/BfluJ (The Jackson Laboratory) mouse line. The latter expresses the Cre recombinase in CD4⁺ and CD8⁺ T lymphocytes. Mice were maintained on C57BL/6J background. Two-Three month-old male and female mice were used except in ageing experiments and otherwise indicated. Wild-type and IF1-floxed alleles were distinguished with 5′-TGCCTGACATTGGTATTGGG-3′ and 5′-GTGCAGCTTGTGGGAGTCAG-3′ primers.²⁵ (link) The transgene encoding the Cre recombinase was detected with 5′-CAATTTACTGACCGTACAC-3′ and 5′-TAATCGCCATCTTCC AGCAG-3′ primers. No influence of gender is reported.

Romero-Carramiñana I., Dominguez-Zorita S., Esparza-Moltó P.B, & Cuezva J.M. (2024). Ablation of Atp5if1 impairs metabolic reprogramming and proliferation of T lymphocytes and compromises mouse survival. iScience, 27(6), 109863.

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Conditional Knockout Mice Generation

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Founder mice utilized in this study were purchased from The Jackson Laboratory (Bar Harbor, Maine) and included the following strains: C57BL/6J (Cat #000664), B6.129S7-Rag1tm1Mom/J (RAG1 Knockout (KO), Cat # 002216), B6.Cg-Tg(TcraTcrb)425Cbn/J (OT-II, Cat # 004194), B6.129S2-Cd4tm1Mak/J (CD4 KO, Cat# 002663), B6.129S7-Il1r1^tm1Imx/J (IL-1R KO, Cat# 003245), B6.129P2-Lyz2tm1(cre)Ifo/J (Lyz2-Cre, Cat # 004781), B6.Cg-Tg(Cd4-cre)1Cwi/BfluJ (CD4-Cre, Cat # 022071) and B6.129P2(SJL)-Myd88tm1Defr/J (MyD88^Flox/Flox, Cat # 008888). While CD4-Cre.MyD88^Flox/Flox conditional KO mice were generated by crossing CD4-Cre mice with MyD88^Flox/Flox mice (resulting in Cre-mediated excision of MyD88 in CD4+ as well as CD8+ T-cells), Lyz2-Cre.MyD88^Flox/Flox conditional KO mice were produced by crossing Lyz2-Cre mice with MyD88 ^Flox/Flox mice—resulting in excision of MyD88 in cells of myeloid lineage. For each strain, F1 WT/Cre-WT/FL mice were crossed to produce WT/Cre-FL/FL mice. Backcrossing of F1 WT/Cre-FL/FL mice to WT/WT-FL/FL mice yielded additional WT/Cre-FL/FL experimental mice. All mice were genotyped prior to breeding/experimental use. Mice were provided with food and water ad libitum and housed in specific pathogen free mouse facilities under IACUC-approved protocols (University of Pittsburgh, Pittsburgh, PA).

Reay D.P., Tabib T., Wang Y., Oriss T.B., Young N.A., Lafyatis R.A., Jarjour W.N., Clemens P.R, & Ascherman D.P. (2023). Antigen-driven T cell-macrophage interactions mediate the interface between innate and adaptive immunity in histidyl-tRNA synthetase-induced myositis. Frontiers in Immunology, 14, 1238221.

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