Cd45.1 congenic mice

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CD45.1 congenic mice are a type of laboratory mouse that express the CD45.1 allele instead of the more common CD45.2 allele. The CD45 protein is a receptor-linked protein tyrosine phosphatase that is essential for the development and activation of T cells and B cells. The CD45.1 congenic mice are a useful tool for distinguishing between different cell populations in immunological studies and experiments.

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17 protocols using cd45.1 congenic mice

Generation and Characterization of Tgfbr Knock-in Mice

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Tgfbr1^M318R and Tgfbr2^G357W knock-in mice were generated as previously described [4]. Homozygousity Tgfbr1^M318R/^M318R is embryonic lethal due to vascular malformations. Heterozygous Tgfbr1^M318R/+ (R1) mice were compared to age- and sex-matched controls homozygous for Tgfbr1^+/+. Heterozygous Tgfbr2^G357W (R2) mice were compared to age- and sex-matched controls homozygous for Tgfbr2^+/+. R1 and WT mice were cohoused to minimize cage effects. Recombination Activating Gene 2 (RAG2) deficient mice were obtained from Taconic Farms. CD45.1 congenic mice were purchased from Jackson and backcrossed >12 generations with 129SvE mice purchased from Taconic Farms. IL-5 transgenic mice [132] and were bred onsite and housed under specific pathogen free conditions. Animals were maintained on a fixed diet of autoclaved water and chow (NIH-31M). All experiments were approved by the NIAID’s ACUC and conducted in accordance with Animal Study Protocol (ASP) LAD11E. Gross photos were taken with a Canon PowerShot ELPH170 IS digital camera with 12X optical zoom.

Laky K., Kinard J.L., Li J.M., Moore I.N., Lack J., Fischer E.R., Kabat J., Latanich R., Zachos N.C., Limkar A.R., Weissler K.A., Thompson R.W., Wynn T.A., Dietz H.C., Guerrerio A.L, & Frischmeyer-Guerrerio P.A. (2023). Epithelial-intrinsic defects in TGFβR signaling drive local allergic inflammation manifesting as eosinophilic esophagitis. Science immunology, 8(79), eabp9940.

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Genetic Manipulation of Murine Dendritic Cells

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C57BL/6 mice were from Joint Ventures Sipper BK Experimental Animal Company (Shanghai, China). OT-II mice (which have transgenic expression of a T-cell antigen receptor specific for chicken ovalbumin amino acids 323–339 (OVA_(323–339)) (amino acids 323–339) (ISQAVHAAHAEINEAGR) (Sigma-Aldrich) in the context of the MHC class II molecule I-Ab), CD45.1⁺ congenic mice, and transgenic CD11c-cre mice were from The Jackson Laboratory. Mice bearing a Mettl3^fl allele (Mettl3^fl mice) were from Chinese Academy of Sciences^{53 (link)}. Mice lacking Mettl3 exon2, exon3, and exon4 specifically in DC, were generated by breeding of mettl3^fl mice with CD11c-Cre mice. All mice were maintained under pathogen-free conditions and were used at 6–8 weeks of age unless indicated otherwise. All animal experiments were carried out according to the National Institute of Health Guide for the Care and Use of Laboratory Animals, with the approval of the Scientific Investigation Board of Second Military Medical University (Shanghai, China).

Wang H., Hu X., Huang M., Liu J., Gu Y., Ma L., Zhou Q, & Cao X. (2019). Mettl3-mediated mRNA m6A methylation promotes dendritic cell activation. Nature Communications, 10, 1898.

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Influenza Infection and Immune Response

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WT C57/BL6 mice were purchased from the Jackson Laboratory; Blimp‐1 control (Prdm1^fl^/fl, where Prdm is PR domain 1), CD4‐Cre transgenic, CD8‐cre transgenic, IRF4 control (Irf4^fl^/fl), and CD45.1 congenic mice were originally from the Jackson Laboratory and bred inhouse. T‐cell‐specific Blimp‐1 cKO mice were generated through breeding CD4‐cre to Prdm1^fl^/fl mice. CD8 T‐cell‐specific IRF4 cKO mice were generated through breeding CD8‐cre to Irf4^fl^/fl mice. IFNAR1‐deficient (Ifnar1^−/−) mice were originally from Dr. U. Deshmukh at the University of Virginia; Vert‐X mice were originally from Dr. C. Karp from Cincinnati Children's Hospital; STAT2‐deficient (Stat2^−/−) mice were originally from Dr. C. Schindler at the Columbia University. All mice were housed in a specific pathogen‐free environment and all animal experiments were performed in accordance with protocols approved by the University of Virginia Animal Care and Use Committee (ACUC) or Indiana University Institutional Animal Care and Use Committee (IACUC). For influenza virus infection, mice were anesthetized first and then intranasally infected with Influenza A/PR8/34 strain (∼150 pfu/mouse in serum‐free IMDM media (Gibco) or PBS) as previously reported 8.

Jiang L., Yao S., Huang S., Wright J., Braciale T.J, & Sun J. (2016). Type I IFN signaling facilitates the development of IL‐10‐producing effector CD8+ T cells during murine influenza virus infection. European Journal of Immunology, 46(12), 2778-2788.

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Conditional Knockout Mice for Immunological Studies

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Il4^−/−, and CD45.1 congenic mice were purchased from Jackson Laboratories. CYLD floxed^{61 (link)} and Scinderin floxed mice^{37 (link)} were kindly provided by Dr. Ting, Icahn School of Medicine at Mount Sinai, and Dr. Glogauer, University of Toronto, respectively. The floxed mice were crossed with Foxp3-cre-YFP^{62 (link)} mice to generate the conditional knockout mice in the animal facility at La Jolla Institute for Immunology. For inducible deletion of CYLD in Treg cells, CYLD floxed mice were crossed with mice expressing CreERT2 fusion gene under control of Foxp3 gene. For the induction of Cre recombinase nuclear translocation, 6-week-old mice were injected intraperitoneally with 100 μl of 10 mg/ml tamoxifen (Sigma T5648) once every day for seven days. All mice were maintained according to the animal protocols approved by the Institutional Animal Care and Use Committee of the La Jolla Institute for Immunology. Six to twelve week-old mice were used for most experiments, and aged mice (8 month-old) were used for histological analysis. Both female and male mice were randomly assigned to each group since there was no difference in observed phenotypes between male and female mice. However, only female heterozygote Foxp3^cre/+ mice were used for other experiments.

Lee J.H., Zou L., Yang R., Han J., Wan Q., Zhang X., El Baghdady S., Roman A., Elly C., Jin H.S., Park Y., Croft M, & Liu Y.C. (2020). The deubiquitinase CYLD controls protective immunity against helminth infection by regulation of Treg plasticity. The Journal of allergy and clinical immunology, 148(1), 209-224.e9.

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Generation of Mixed Bone Marrow Chimeras

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C57BL/6, Thy1.1, and CD45.1 congenic mice were obtained from The Jackson Laboratory. IL-21R KO mice (B6N.129-Il21r/J), originally purchased from The Jackson Laboratory, were bred in house under specific pathogen free conditions at the Animal Research Facility at The George Washington University (Washington, DC). Mixed bone marrow chimeric animals (WT: IL-21R KO at a 1:1 ratio) were generated as previously described (19 (link)). Briefly, lethally irradiated Thy1.1 recipients (8Gy/20g of body weight) were injected intravenously with 5x10⁶ magnetically purified hematopoietic progenitor cells from WT (CD45.1) and IL-21R KO (CD45.2) animals (Stemcell). Transferred animals received water supplemented with sulfamethoxazole and trimethoprim (Hi-Tech Pharmacal Co) for 4-5 weeks after injection and experiments were conducted 4-8 weeks post reconstitution. All animal experiments were approved by The George Washington University School of Medicine and Health Sciences Institutional Animal Care and Use Committee.

Moretto M.M., Hwang S., Chen K, & Khan I.A. (2019). Complex and Multilayered role of IL-21 signaling during thymic development. Journal of immunology (Baltimore, Md. : 1950), 203(5), 1242-1251.

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Murine Models for Muscular Dystrophy Research

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C57BL/10 (no. 000476), mdx mice (C57BL/10ScSn-Dmdmdx/J) (no. 001801), and mdx mice in the DBA2/J background (D2-mdx) (no. 013141) were obtained from The Jackson Laboratory. CD45.1 congenic mice (no. 002014) were also obtained from The Jackson Laboratory and crossed with mdx mice at the UCI. B6A/J (no. 012767) and C57BL/6 mice (no. 000664) were bred in vivariums at Children’s National Hospital. VCP (77 (link)) and double homeobox 4 (DUX4) (78 (link)) mice were provided by collaborators at the UCI and Ohio State University, respectively. Animal experiments were approved by the Institutional Animal Care and Use Committee of UCI and performed under Institutional Animal Care and Use Committee guidelines.

Coulis G., Jaime D., Guerrero-Juarez C., Kastenschmidt J.M., Farahat P.K., Nguyen Q., Pervolarakis N., McLinden K., Thurlow L., Movahedi S., Hughes B.S., Duarte J., Sorn A., Montoya E., Mozaffar I., Dragan M., Othy S., Joshi T., Hans C.P., Kimonis V., MacLean A.L., Nie Q., Wallace L.M., Harper S.Q., Mozaffar T., Hogarth M.W., Bhattacharya S., Jaiswal J.K., Golann D.R., Su Q., Kessenbrock K., Stec M., Spencer M.J., Zamudio J.R, & Villalta S.A. (2023). Single-cell and spatial transcriptomics identify a macrophage population associated with skeletal muscle fibrosis. Science Advances, 9(27), eadd9984.

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C57BL/6 Mice Sourcing and Maintenance

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Male, 6- to 8-week-old, CD45.2 wild-type C57BL/6 mice were purchased from Hunan Slack King Laboratory Animal Co., Ltd. (Changsha, China). CD45.1 congenic mice were purchased from the Jackson Laboratory. All animals were maintained under specific pathogen-free (SPF) conditions in the Animal Care Center of Tongji Medical College.

Wang Q., Pan W., Liu Y., Luo J., Zhu D., Lu Y., Feng X., Yang X., Dittmer U., Lu M., Yang D, & Liu J. (2018). Hepatitis B Virus-Specific CD8+ T Cells Maintain Functional Exhaustion after Antigen Reexposure in an Acute Activation Immune Environment. Frontiers in Immunology, 9, 219.

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Mouse Models for Muscular Dystrophy Research

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C57BL/10 (#:000476), mdx mice (C57BL/10ScSn-Dmdmdx/J) (#:001801) and mdx mice in the DBA2/J background (D2-mdx) (#:013141) were obtained from The Jackson Laboratory. CD45.1 congenic mice (#:002014) were also obtained from The Jackson Laboratory and crossed with mdx mice at the University of California Irvine (UCI). B6A/J (#:012767) and C57BL/6 mice (#:000664) were bred in vivariums at Children’s National Hospital. VCP (53 (link)) and DUX4 (54 ) mice were provided by collaborators at UCI and Ohio State University, respectively. Animal experiments were approved by the Institutional Animal Care and Use Committee of UCI.

Coulis G., Jaime D., Guerrero-Juarez C., Kastenschmidt J.M., Farahat P.K., Nguyen Q., Pervolarakis N., McLinden K., Thurlow L., Movahedi S., Duarte J., Sorn A., Montoya E., Mozaffar I., Dragan M., Othy S., Joshi T., Hans C.P., Kimonis V., MacLean A.L., Nie Q., Wallace L.M., Harper S.Q., Mozaffar T., Hogarth M.W., Bhattacharya S., Jaiswal J.K., Golann D.R., Su Q., Kessenbrock K., Stec M., Spencer M.J., Zamudio J.R, & Villalta S.A. (2023). Single-cell and spatial transcriptomics identify a macrophage population associated with skeletal muscle fibrosis. bioRxiv.

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Transgenic Mouse Models for Stat5 and Bcl6

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Mice with deletion of the entire Stat5A/5B locus (Stat5^−/−) and mice with the entire Stat5A/5B locus gene flanked with loxP sites (Stat5^fl/fl) were used^{69 (link)}. The Stat5^fl/+ mice were bred with Stat5^+/− mice to generate Stat5^fl/− mice. CD8Cre transgenic mice, Ig^HEL (C57BL/6, MD4), sHEL (C57BL/6, ML5) transgenic mice, BM1 mice, Rag1-deficient mice, CD45.1 congenic mice, CXCR5-deficient mice, PD-1-deficient mice, Lag3-deficiect mice and CD40-deficient mice were obtained from the Jackson Laboratory. Bcl6^fl/flCD4Cre mice were also used^{70 (link)}. Mice were housed in the SPF animal facility at the Medical College of Wisconsin, the animal experiments were performed using protocols approved by the Institutional Animal Care and Use Committee.

Chen Y., Yu M., Zheng Y., Fu G., Xin G., Zhu W., Luo L., Burns R., Li Q.Z., Dent A.L., Zhu N., Cui W., Malherbe L., Wen R, & Wang D. (2019). CXCR5+PD-1+ follicular helper CD8 T cells control B cell tolerance. Nature Communications, 10, 4415.

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Establishment of Tumor Models in Mice

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Female C57BL/6, BALB/c mice(6-8 weeks of age) were purchased from the Chinese Academy of Medical Sciences (Beijing, China). OT-1 TCR-transgenic mice, Pmel transgenic mice, and CD45.1⁺ congenic mice were purchased from Jackson Laboratory. The mice were housed and maintained in laminar flow cabinets under specific, pathogen-free conditions. The mice were cared for and used in accordance with army medical university ethical guidelines. To establish tumor models, C57BL/6 mice were injected s.c. with MC38-OVA or B16 cells.
OVA-derived peptide(H-2Kb, SIINFEKL), control H-2Kb RAHYNIVTF peptides, and gp100 peptide were purchased from Sigma-Aldrich. All Abs used for flow cytometry were obtained from Biolegend. ROS inhibitor (apocynin) was purchased from MCE.

Fan X., Peng H., Wang X., Sun Y., Dong Y., Zhou J., Chen J, & Huang S. (2024). Tumor-associated CD8+T cell tolerance induced by erythroid progenitor cells. Frontiers in Immunology, 15, 1381919.

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