B6 sjl cd45.1

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B6.SJL (CD45.1) is a laboratory mouse strain that expresses the CD45.1 (Ptprc) allele. This strain is commonly used as a congenic control for studies involving B6 mice and the CD45.1 marker.

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B6.SJL-Ptprca Pepcb/BoyJ (CD45.1) (83 citations) B6.SJL (73 citations) B6 CD45.1 (52 citations) B6.SJL-PtprcaPepcb/BoyJ (B6 CD45.1), (12 citations) CD45.1 (B6.SJL-PtprcaPep3b/BoyJ) (8 citations) CD45.1+ B6 (7 citations) CD45.1 SJL (5 citations) BALB/c CD45.1+(CByJ.SJL(B6)-Ptprca/J) (5 citations) B6·SJL/BoyJ (CD45.1+, (3 citations) C57BL/6 (B6.SJL-Ptprca Pepcb/BoyJ (CD45.1) mice (2 citations)

18 protocols using b6 sjl cd45.1

Generation and Analysis of Mouse Chimeras

Cited 3 times

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Mice were bred at UCLA and Memorial Sloan Kettering Cancer Center in accordance with the guidelines of the institutional Animal Care and Use Committee (IACUC). The following mouse strains were used this study: C57BL/6 (CD45.2) (Jackson Labs, #000664), B6.SJL (CD45.1) (Jackson Labs, #002114), Rag2^−/− (Jackson Labs #008449), Klra8^−/− (Ly49H-deficient), Zbtb32^−/−, and Il12rb2^−/−x Il18ra1^−/− (MSKCC, J.C. Sun). Experiments were conducted using 7–8 week old age- and gender-matched mice in accordance with approved institutional protocols.
Generation of mixed bone marrow chimeric mice was performed as previously described^{18 (link)}. Parabiosis surgery was performed as previously described^{12 (link), 15 (link), 16 (link), 17 (link)}. Intravascular labeling of lymphocytes of experimental mice was performed by injecting (i.v.) 2.5 μg of fluorophore-conjugated CD45 (30-F11) and euthanized 3 minutes later.

Weizman O.E., Song E., Adams N.M., Hildreth A.D., Riggan L., Krishna C., Aguilar O.A., Leslie C.S., Carlyle J.R., Sun J.C, & O’Sullivan T.E. (2019). Mouse cytomegalovirus-experienced ILC1s acquire a memory response dependent on the viral glycoprotein m12. Nature immunology, 20(8), 1004-1011.

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Generating Gpr18 Bone Marrow Chimeras

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For non-competitive chimeras for influenza infections, 5 x 10⁶ whole bone marrow cells from either Gpr18^+/+ or Gpr18^-/- mice were injected into 800 cGy-irradiated B6.Ly5.2 CD45.1⁺ recipients (NCI). For mixed bone marrow chimeras to analyze lineage commitment, 5 x 10⁶ bone marrow cells from either Gpr18^+/+ or Gpr18^-/- mice were mixed with 5 x 10⁶ bone marrow cells from B6.SJL CD45.1⁺ (The Jackson Laboratory) mice and injected into 800 cGy-irradiated B6.Ly5.2 CD45.1⁺ recipients. Bone marrow chimeras used to analyze GPR18-dependent antibody responses were generated by transplanting 2 x 10⁶ bone marrow cells from Gpr18^+/+ or Gpr18^-/- mice (IgH^b) with 2 x 10⁶ bone marrow from IgH^a mice into 800 cGy-irradiated B6.Ly5.2 CD45.1⁺ recipients. Eight weeks post-transplant, mice were analyzed for chimerism in the specified tissues or used for further experiments. Athymic nude mice were pretreated with a 150μg dose of αCD8α antibody (clone 53–6.7) intraperitoneally 3 days prior to 800 cGy irradiation and transplantation to reduce pre-existing host IELs.

Becker A.M., Callahan D.J., Richner J.M., Choi J., DiPersio J.F., Diamond M.S, & Bhattacharya D. (2015). GPR18 Controls Reconstitution of Mouse Small Intestine Intraepithelial Lymphocytes following Bone Marrow Transplantation. PLoS ONE, 10(7), e0133854.

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Generation of STAT3-deficient OT-II Mice

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C57BL/6 mice were purchased from Orient (Gyeonggido, Republic of Korea). OT-II, B6.SJL (CD45.1) and Tcrb⁻^/⁻ mice were purchased from Jackson Laboratory (Bar Harbor, ME, USA). STAT3^flox/floxCD4-Cre mice were kindly provided by Drs. C. Dong (MD Anderson Cancer Center, Houston, TX, USA) and S. Akira (Osaka University, Osaka, Japan) and were crossed with OT-II to generate T cell-specific STAT3-deficient OT-II mice. All mice were maintained in the specific pathogen free facility at the vivarium of Seoul National University. All animal experiments were performed using a protocol approved by Institutional Animal Care and Use Committee Seoul National University (SNU-140602-2-2).

Choi G, & Chung Y. (2016). Blockade of STAT3 in T Cells Inhibits Germinal Center Reactions against Intranasal Allergens. Biomolecules & Therapeutics, 24(3), 244-251.

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Conditional Ctcf Knockout Mice

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Mice carrying a conditional Ctcf allele (Ctcf^flox) were described in our previous study.^{27 (link)} The Ctcf^flox mice were crossed with Rosa26-CreER mice^{28 (link)} (CreER; kindly provided by Weonsang Simon Ro, Institute of Gastroenterology, Yonsei University College of Medicine) to generate a tamoxifen (TMX) -inducible systemic Ctcf-cKO strain (CTCF-cKO). For Cre-mediated recombination, mice were intraperitoneally injected with tamoxifen (Sigma-Aldrich; St Louis, MO, USA) dissolved in corn oil (Sigma-Aldrich) for 4–5 consecutive days (2 mg day⁻¹). Wild-type (WT) C57BL/6 (CD45.2) and B6.SJL (CD45.1) mice were purchased from The Jackson Laboratory (Bar Harbor, ME, USA). All animals were bred in specific pathogen-free facilities at Yonsei University College of Medicine. Age- and sex-matched CreER littermate mice were used as WT controls throughout the study. All animal studies were approved by the Department of Laboratory Animal Resources Committee of the Yonsei University College of Medicine.

Kim T.G., Kim S., Jung S., Kim M., Yang B., Lee M.G, & Kim H.P. (2017). CCCTC-binding factor is essential to the maintenance and quiescence of hematopoietic stem cells in mice. Experimental & Molecular Medicine, 49(8), e371-.

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Mice Strains for Immunology Research

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Mice were bred at UCLA in accordance with the guidelines of the institutional Animal Care and Use Committee (IACUC). The following mouse strains were used this study: C57BL/6 (CD45.2) (Jackson Labs, #000664), B6.SJL (CD45.1) (Jackson Labs, #002114), Klra8^−/− (Ly49H-deficient), Il12b^tm1.1Lky/J (Il12p40^YFP), Xcr1-Cre (Hemmi et al., 2016 (link)), Rosa26^LsL-DTA, Tmem173^−/−, and Stat4^−/−. Experiments were conducted using 6–8 week old age- and gender-matched mice in accordance with approved institutional protocols.

Riggan L., Hildreth A.D., Rolot M., Wong Y.Y., Satyadi W., Sun R., Huerta C, & O’Sullivan T.E. (2020). CRISPR-Cas9 Ribonucleoprotein-Mediated Genomic Editing in Mature Primary Innate Immune Cells. Cell reports, 31(7), 107651.

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Generating Necdin Null Mice from Fetal Liver

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The generation of Necdin null mice (C57BL/6, CD45.2) was described previously [42 (link)]. Fetal liver cells were isolated from E14.5 embryos as previously described [21 (link)]. Wild type C57BL/6 (CD45.2) and B6.SJL (CD45.1) mice were purchased from Jackson Laboratories. All mice were maintained in the Indiana University School of Medicine Animal Facility according to IACUC-approved protocols, and kept in Thorensten units with filtered germ-free air.

Yao C., Kobayashi M., Chen S., Nabinger S.C., Gao R., Liu S.Z., Asai T, & Liu Y. (2017). Necdin modulates leukemia-initiating cell quiescence and chemotherapy response. Oncotarget, 8(50), 87607-87622.

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Murine Immune Tolerance Models

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C57BL/6 (B6), B6.129S2-Ighm^tm1Cgn/J (B6.μMT), B6.IFNαR1^−/−, B6(Cg)-IFNαR₁^tm1.1Ees/J (B6.IFNαR₁^flox/flox), B6.129P2(Cg)-Ighg₁^{tm1(IRES-cre)Cgn}/J (GC^Cre) and B6.SJL^Ptprc^{< b >} /BoyJ (B6.SJL- CD45.1⁺) mice were purchased from the Jackson Laboratory and bred in house. B6.Sle1b and B6.HKIR mice were described previously (Morel et al., 2000 (link); Notidis et al., 2002 (link)). Female mice of various ages (8–10 weeks, 3 months, and 6 months old) were used for all experiments. All animals were housed at Penn State Hershey Medical Center in specific pathogen-free animal facility. All procedures were performed in accordance with the guidelines approved by our Institutional Animal Care and Use Committee.

Domeier P.P., Chodisetti S.B., Schell S.L., Kawasawa Y.I., Fasnacht M.J., Soni C, & Rahman Z.S. (2018). B-Cell-Intrinsic Type 1 Interferon Signaling Is Crucial for Loss of Tolerance and the Development of Autoreactive B Cells. Cell reports, 24(2), 406-418.

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Mice Strain Characterization for Immunological Studies

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Mice were bred at UCLA in accordance with the guidelines of the institutional Animal Care and Use Committee (IACUC). The following mouse strains were used this study: C57BL/6 (CD45.2) (Jackson Labs, #000664), B6.SJL (CD45.1) (Jackson Labs, #002114), B6(C)-Cgas^{tm1d(EUCOMM)Hmgu}/J (cGAS^−/−) (Jackson Labs, #026554), B6.129S1-Il12b^tm1Jm/J (Il12b^−/−) (Jackson Labs, #002693), B6.129-Il12b^tm1.1Lky/J C57BL/6J-Sting1^gt/J (Il12b^YFP×Sting^Gt), Xcr1^+/DTRvenus,^{29 (link)}Il12b^tm1.1Lky/J (Il12b^YFP) (Jackson Labs, #006412), Tmem173^gt (Sting^Gt) (Jackson Labs, #017537), B6;129S1-Il12rb2^tm1Jm/J (Il12rb2^−/−) (Jackson Labs, #003248), and C57BL/6J-Stat4^em3Adiuj/J (Stat4^−/−) (Jackson Labs, #028526). Experiments were conducted using 6–10-week-old age-and gender-matched mice in accordance with approved institutional protocols.

Hildreth A.D., Padilla E.T., Tafti R.Y., Legala A.R, & O’Sullivan T.E. (2023). Sterile liver injury induces a protective tissue-resident cDC1-ILC1 circuit through cDC1-intrinsic cGAS-STING-dependent IL-12 production. Cell reports, 42(2), 112141.

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Mouse Maintenance Protocol for Research

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C57BL/6 (CD45.2) and B6.SJL (CD45.1) mice were purchased from the Jackson Lab (Bar Harbor, ME, USA) or Harlan Laboratories, Inc. (Indianapolis, IN, USA) and maintained in house. Both male and female mice were used for the experiments. All laboratory mice were maintained in the animal facility at University of Cincinnati or University of Chicago. All experiments on mice in our research protocol were approved by Institutional Animal Care and Use Committee (IACUC) of University of Cincinnati or University of Chicago. All methods were performed in accordance with the relevant guidelines and regulations. The maintenance, monitoring, and end-point treatment of mice were conducted as described previously^{46 (link),56 (link),57 (link)}. Randomization, allocation concealment, and blind outcome assessment were conducted throughout all the experiments.

Jiang X., Hu C., Ferchen K., Nie J., Cui X., Chen C.H., Cheng L., Zuo Z., Seibel W., He C., Tang Y., Skibbe J.R., Wunderlich M., Reinhold W.C., Dong L., Shen C., Arnovitz S., Ulrich B., Lu J., Weng H., Su R., Huang H., Wang Y., Li C., Qin X., Mulloy J.C., Zheng Y., Diao J., Jin J., Li C., Liu P.P., He C., Chen Y, & Chen J. (2017). Targeted inhibition of STAT/TET1 axis as a therapeutic strategy for acute myeloid leukemia. Nature Communications, 8, 2099.

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Immune Cell Phenotyping in Mice

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Mice were bred at UCLA in accordance with the guidelines of the Institutional Animal Care and Use Committee (IACUC). The following mouse strains were used this study: C57BL/6 (CD45.2) (Jackson Labs, #000664), B6.SJL (CD45.1) (Jackson Labs, #002114), Klra8^–/– (Ly49H-deficient). Experiments were conducted using 6–8 week old age- and gender-matched mice in accordance with approved institutional protocols.

Riggan L., Ma F., Li J.H., Fernandez E., Nathanson D.A., Pellegrini M, & O’Sullivan T.E. (2022). The transcription factor Fli1 restricts the formation of memory precursor NK cells during viral infection. Nature immunology, 23(4), 556-567.

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