B6 sjl ptprca boyaitac

Manufactured by Taconic Biosciences

The B6.SJL-Ptprca/BoyAiTac is a laboratory mouse strain. It carries the Ptprca (CD45.1) allele, which can be used as a marker in various immunological studies.

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7 protocols using b6 sjl ptprca boyaitac

Establishing Congenic Wild-Type and Knockout Mouse Strains

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Wild-type mice were obtained from both the Jackson Laboratory (C57BL/6J and B6.SJL-Ptprc^aPepc^b/BoyJ) and Taconic Biosciences (B6NTac and B6.SJL-Ptprc^a/BoyAiTac). B6 mice were bred for dual congenic expression using a dam or sire from opposing place of purchase to eliminate any strain drift between the two wild-type strains. IL-12p40−/− (B6.129S1-Il12bt^m1Jm/J) and IL-12p35−/− (B6.129S1-Il12at^m1Jm/J) were sourced from the Jackson Laboratory. IL-12p40−/− mice were backcrossed to wild-type mice (B6.SJL-PtprcaPepcb/BoyJ) to generate CD45.1 congenic IL-12p40−/− mice. SMARTA TCR transgenic mice were obtained from Jackson Laboratories (B6.Cg-Ptprca Pepcb Tg(TcrLCMV)1Aox/PpmJ). For all experiments, both female and male mice between 4 and 35 weeks of age were used. Animals were bred and maintained under specific pathogen free (SPF) conditions at the University of Maryland, Baltimore. Experiments were performed with animals at least four weeks of age for bone marrow isolation and six weeks of age for all other experiments and approved by the University of Maryland, Baltimore Institutional Animal Care and Use Committee.

Gerber A.N., Abdi K, & Singh N.J. (2021). The subunits of IL-12, originating from two distinct cells, can functionally synergize to protect against pathogen dissemination in vivo. Cell reports, 37(2), 109816.

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Generation of Mixed Bone Marrow Chimeras

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C57BL/6J (wild type WT) and B6.SJL-Ptprc^a/BoyAiTac (CD45.1) 6-8 week old mice were purchased from Taconic. IL21R knockout (IL-21R KO) and CD4 knockout (CD4 KO) mice, purchased from The Jackson Laboratory (B6N.129-Il21r^tm1Kopf/J) were bred in house. Mice were housed under specific pathogen free conditions at the Animal Research Facility at The George Washington University (Washington, DC). All animal experiments were approved by the George Washington School of Medicine and Health Sciences Institutional Animal Care and Use Committee.
For some experiments, WT/IL-21R KO mixed bone marrow chimera animals were generated. Bone marrow was extracted from IL-21R KO (CD45.2) and B6.SJL (CD45.1) mice as previously described (11 (link)) and 5×10⁶ total cells (at a 1: 1 ratio for WT: IL-21R KO) were injected i.v. into lethally irradiated recipients (8Gy/20g of body weight). Recipient animals received sulfamethoxazole and trimethoprim (Hi-Tech Pharmacal) supplemented water for 5 weeks post-transfer. Experiments were performed 8 weeks post-reconstitution.
For BrdU experiments, mice were injected with bromodeoxyuridine (BrdU) (1mg/mouse) intraperitoneally starting at day 7 p.i. and every other day thereafter until the end of the experiment.

Moretto M.M, & Khan I.A. (2015). IL-21 is important for induction of KLRG1+ effector CD8 T cells during acute intracellular infection. Journal of immunology (Baltimore, Md. : 1950), 196(1), 375-384.

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Dietary Modulation of Immune Cell Function

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C57BL/6J, LysMCre (B6.129P2-Lyz2^tm1cre1fo/J), MHCII^f/f (B6.129X1-H2-Ab1^tm1Koni/J), CD11c-DTR (B6.FVB-Tg(Itgax-DTR/EGFP)57Lan/J) and OT-II (B6.Cg-Tg(TcraTcrb)425Cbn/J) mice were purchased from the Jackson Laboratory. MHCIIKO (B6.129-H2-Ab1^tm1Gru N12) and wild type (B6.SJL-Ptprc^a/BoyAiTac) male mice were purchased from Taconic. CD11c-mCherry mice were kindly provided by Dr. Kamal Khanna (University of Connecticut). Macrophage-specific MHCII KO mice (MMKO) were generated by breeding LysM-Cre with MHCII^f/f mice. Cre-negative MHCII^f/f littermates were used as control. Male mice were ad libitum fed a normal diet (4.5% fat; PMI Nutrition International) or fed a HFD consisting of 60% fat (Research Diets) beginning 6 weeks of age. All mice procedures were approved by the University Committee on Use and Care of Animals (UCUCA) at the University of Michigan and were conducted in compliance with the Institute of Laboratory Animal Research Guide for the Care and Use of Laboratory Animals.

Cho K.W., Morris D.L., DelProposto J.L., Geletka L., Zamarron B., Martinez-Santibanez G., Meyer K.A., Singer K., O'Rourke R.W, & Lumeng C.N. (2014). An MHC Class II Dependent Activation Loop Between Adipose Tissue Macrophages and CD4+ T cells Controls Obesity-Induced Inflammation. Cell reports, 9(2), 605-617.

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WT and Knockout Mouse Strains

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Wild-type (WT) mice were obtained from both Jackson Laboratories (C57BL/6J and B6.SJL-PtprcaPepcb/BoyJ) and Taconic Biosciences (B6NTac and B6.SJL-Ptprca/BoyAiTac). B6 mice were bred for dual congenic expression using a dam or sire from opposing place of purchase to eliminate any strain drift between the two WT strains. Wild-type B10.Q/Ai mice were originally obtained from Ron Schwartz, Institute of Allergy and Infection Diseases, NIH, Bethesda, MD. Wild-type B10.A-H2a H2-T18a/SgSnJ mice were obtained from Jackson laboratories. B10.A mice were bred for dual-congenic expression using a dam or sire from opposing genotypes. TCR-αβ KO mice were obtained from the Jackson Laboratories (B6.129S2-Tcratm1Mom/J). CD3ε knockout mice were obtained from NIAID/Taconic mouse contract (B10.A-Cd45a(Ly5a)/NAi N5). Animals were bred and maintained in modified specific pathogen-free facilities at the University of Maryland Baltimore Experiments were performed with animals at least 6 weeks of age and approved by University of Maryland Baltimore Institutional Animal Care and Use Committee.

Fioretti S., Matson C.A., Rosenberg K.M, & Singh N.J. (2022). Host B cells escape CAR-T immunotherapy by reversible downregulation of CD19. Cancer Immunology, Immunotherapy : CII, 72(1), 257-264.

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Establishing Congenic Wild-Type and Knockout Mouse Strains

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Generation and Characterization of Mouse Models

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Cbx3/HP1γ floxed mice were generated and provided by Dr. Prim B. Singh (49 (link)). These mice were backcrossed to C57BL/6 for twelve generations; they bred and developed normally before and after Cre-mediated deletion. The Cbx3/HP1γ transgenic line was generated by inserting a 1 kb fragment of mouse Cbx3/HP1γ cDNA, derived from activated CD8⁺ T cells, into EcoR1/Sma1 cloning sites of the VA-hCD2 vector provided by Dr. Dimitris Kioussis (50 (link)). The purified Cbx3/HP1γ-VA-hCD2 DNA construct was injected into C57BL/6 pronuclei by Dr. Lina Du at the fee-based Dana-Farber/Harvard Cancer Center (DF/HCC) Transgenic Mouse Core. Two founder transgenic lines were produced. The Lef1 floxed mice were generated as described and provided by Dr. Hai-Hui Xue (12 (link)). The following mouse lines were purchased from The Jackson Laboratory: Il21r knock out (B6.129-Il21r^tm1Kopf/J) (51 (link)), CD8α-Cre transgenic (C57BL/6-Tg(Cd8a-cre)1Itan/J) (52 (link)), ROSA26 (B6;129-Gt(ROSA)26Sor^tm2Sho/J) (53 (link)), Prf1 knock out (C57BL/6-Prf1^tm1Sdz/J) (54 (link)), and Ifng knock out (B6.129S7-Ifng^tm1Ts/J) (55 (link)). The B6.SJL line (B6.SJL-Ptprc^a/BoyAiTac) was purchased from Taconic.

Le P.T., Ha N., Tran N.K., Newman A.G., Esselen K.M., Dalrymple J.L., Schmelz E.M., Bhandoola A., Xue H.H., Singh P.B, & Thai T.H. (2021). Targeting Cbx3/HP1γ Induces LEF-1 and IL-21R to Promote Tumor-Infiltrating CD8 T-Cell Persistence. Frontiers in Immunology, 12, 738958.

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Subcutaneous Tumor Model and Vaccination in Mice

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6-8 week old C57BL6/N mice were purchased from Envigo or Taconic Biosciences. 6–8 week old B6.SJL-Ptprc^a/BoyAiTac (known as CD45.1 mice) and B6.129S6-Rag2^tm1Fwa N12 Mice (known as Rag2 KO) were purchased from Taconic Biosciences. Mice were shaved before subcutaneous engraftment of the indicated number of RMA/S cells in 100 uL PBS. Tumor volumes were calculated using caliper measurements and the standard modified ellipsoid formula: tumor volume = (LxW² x 0.52 every 2–3 days. Animals were euthanized when tumor volume exceeded 2000 mm³ or if ulceration was noted. Vaccination of animals was performed by subcutaneous injection of 10 × 10⁶ irradiated (20 Gy) MCA205-ΔTap2 cells expressing libraries of minigenes.

Gejman R.S., Chang A.Y., Jones H.F., DiKun K., Hakimi A.A., Schietinger A, & Scheinberg D.A. (2018). Rejection of immunogenic tumor clones is limited by clonal fraction. eLife, 7, e41090.

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