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Rag1 knockout mice

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Rag1 knockout mice are genetically modified mice that lack the recombination-activating gene 1 (Rag1). This gene plays a crucial role in the development of T and B cells, which are essential components of the adaptive immune system. Rag1 knockout mice are commonly used as a model system in immunological research to study the function and development of the immune system.

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Lab products found in correlation

C57bl 6, by Jackson ImmunoResearch (3 mentions) Balb c, by Jackson ImmunoResearch (2 mentions) Plzf cre recombinase mice, by Jackson ImmunoResearch (1 mentions) Rosamt mg reporter mice, by Jackson ImmunoResearch (1 mentions) Batffl flplzf cre, by Jackson ImmunoResearch (1 mentions) R26 creert2 mice, by Jackson ImmunoResearch (1 mentions) Ot 1 mice, by Jackson ImmunoResearch (1 mentions) C57bl 6 mice, by Jackson ImmunoResearch (1 mentions) Batf3 mice, by Jackson ImmunoResearch (1 mentions)

6 protocols using rag1 knockout mice

1

T Cell-Specific DOT1L Deletion in Mice

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Six- to eight-week-old female wild-type C57BL/6, BALB/c, and Rag1 knock out (KO) mice were from the Jackson Laboratory (Bar Harbor, ME, USA). Dot1lflox/flox mice were bred with CD4-Cre mice to generate mice with specific DOT1L deletion in T cells. All mice Dot1lf/f or Dot1l−/− mice were utilized at the age of 6–12 weeks unless specified in the text. Mice were housed under specific pathogen-free conditions and handled according to the guidelines of the University Committee on the Use and Care of Animals at the University of Michigan.
Bian Y., Li W., Kremer D.M., Sajjakulnukit P., Li S., Crespo J., Nwosu Z.C., Zhang L., Czerwonka A., Pawłowska A., Xia H., Li J., Liao P., Yu J., Vatan L., Szeliga W., Wei S., Grove S., Liu J.R., McLean K., Cieslik M., Chinnaiyan A.M., Zgodziński W., Wallner G., Wertel I., Okła K., Kryczek I., Lyssiotis C.A, & Zou W. (2020). Cancer SLC43A2 alters T cell methionine metabolism and histone methylation. Nature, 585(7824), 277-282.
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2

T Cell-Specific DOT1L Deletion in Mice

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Six- to eight-week-old female wild-type C57BL/6, BALB/c, and Rag1 knock out (KO) mice were from the Jackson Laboratory (Bar Harbor, ME, USA). Dot1lflox/flox mice were bred with CD4-Cre mice to generate mice with specific DOT1L deletion in T cells. All mice Dot1lf/f or Dot1l−/− mice were utilized at the age of 6–12 weeks unless specified in the text. Mice were housed under specific pathogen-free conditions and handled according to the guidelines of the University Committee on the Use and Care of Animals at the University of Michigan.
Bian Y., Li W., Kremer D.M., Sajjakulnukit P., Li S., Crespo J., Nwosu Z.C., Zhang L., Czerwonka A., Pawłowska A., Xia H., Li J., Liao P., Yu J., Vatan L., Szeliga W., Wei S., Grove S., Liu J.R., McLean K., Cieslik M., Chinnaiyan A.M., Zgodziński W., Wallner G., Wertel I., Okła K., Kryczek I., Lyssiotis C.A, & Zou W. (2020). Cancer SLC43A2 alters T cell methionine metabolism and histone methylation. Nature, 585(7824), 277-282.
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3

Evaluating Anti-PD-1 Immunotherapy in Mice

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All animal experiments were approved by the Institutional Animal Care and Use Committee (IACUC) of University of California, San Diego (UCSD). Wild type (WT) C57BL/6 were purchased from Jackson Laboratories. Rag-1 knockout mice were obtained from Jackson Laboratories and bred by the UCSD Animal Care Program. The TLR7 agonist, 1V270, was synthesized by our laboratory [23 (link)]. Rat anti–mouse PD-1 (clone J43, BE0033–2), rat anti-mouse CD8 (Clone YTS169.4, BE0117) and rat anti-mouse CD4 (Clone GK1.5, BE0003) monoclonal antibodies were purchased from BioXcell.
Shankara Narayanan J.S., Ray P., Hayashi T., Whisenant T.C., Vicente D., Carson D.A., Miller A.M., Schoenberger S.P, & White R.R. (2019). Irreversible Electroporation Combined with Checkpoint Blockade and TLR7 Stimulation Induces Anti-Tumor Immunity in a Murine Pancreatic Cancer Model. Cancer immunology research, 7(10), 1714-1726.
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4

Generation of Batf Conditional Knockout Mice

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Batffl/fl mice were kindly provided by E.J. Taparowsky (Betz et al., 2010 (link)). PLZF-Cre recombinase mice (stock #:024529) were purchased from the Jackson Laboratory and crossed to one another to generate age-matched Batffl/flPLZF-Cre− (WT) and Batffl/flPLZF-Cre+ (Batf innate lymphoid cell-conditional knockout, cKO) mice. Batf knockout mice (stock #: 013758) and Rag1 knockout mice (stock #:129S7) were purchased from Jackson Laboratory. Rag1−/−Batf−/− mice were generated by crossing Rag1−/− with Batf−/− mice. R26-CreERT2 mice (stock #: 008463) and RosamT/mG reporter mice (stock #: 007576) were purchased from the Jackson laboratory. Batffl/fl was crossed with ERT2CreRosamTmG to generate Batffl/flERT2CreRosamTmG mice. Mice were bred and maintained in a closed breeding facility, and mouse handling conformed to the requirements of the Institutional Animal Care and Use Guidelines of the Medical College of Wisconsin.
Wu X., Khatun A., Kasmani M.Y., Chen Y., Zheng S., Atkinson S., Nguyen C., Burns R., Taparowsky E.J., Salzman N.H., Hand T.W, & Cui W. (2022). Group 3 innate lymphoid cells require BATF to regulate gut homeostasis in mice. The Journal of Experimental Medicine, 219(11), e20211861.
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5

Generation of CD11c-specific SOCS1 knockout mice

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To generate mice in which SOCS1 was specifically deleted in CD11c+ cells, CD11c-Cre-GFP transgenic mice (19 (link)) were obtained from The Jackson Laboratory (Stock#007567, Bar Harbor, ME) and bred with SOCS1fl/fl mice (15 (link)) (generously provided by Dr. Yoshimura, Keio University). Five to ten week old sex-matched Cre-SOCS1f/f and CD11c-Cre+ SOCS1f/f littermates were used for all experiments. C57BL/6 mice, OT-1 mice bearing a TCR specific for the SIINFEKL epitope of ovalbumin on a Rag1-/- background, and Rag1-/- knockout mice were purchased from The Jackson Laboratory (Bar Harbor, ME). Animal protocols were approved by the Earle A. Chiles Research Institute IACUC (Animal Welfare Assurance No. A3913-01).
Alice A.F., Kramer G., Bambina S., Baird J.R., Bahjat K.S., Gough M.J, & Crittenden M.R. (2017). Amplifying IFNγ signaling in DC by CD11c-specific loss of SOCS1 increases innate immunity to infection while decreasing adaptive immunity. Journal of immunology (Baltimore, Md. : 1950), 200(1), 177-185.
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6

Behavioral and Biochemical Analyses of Mice

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Adult C57BL/6J mice (males and females, 8-10 weeks) were used for all behavioral and biochemical studies. STING "goldenticket" knockout mice (Stock No: 017537), Ifnar1 global knockout mice (Stock No: 028288), Rag1 knockout mice (Stock No: 002216), Ifnar1 conditional knockout mice (Ifnar1 fx/fx ; Stock No: 028256) and Batf3 -/-mice (Stock No: 013755) were purchased from the Jackson Laboratory and maintained on a C57BL/6J background. Nav1.8-Cre mice, also maintained on a C57BL/6J background, were a gift from Rohini Kuner (University of Heidelberg). Behavioral testing was performed comparing STING gt/gt and Ifnar1 -/-mice with wildtype littermate controls. These mice were maintained at an AAALAC-approved Duke University facility with two to five mice housed in each cage maintained in a 12h light-dark cycle with ad libitum access to food and water. Animals were randomly assigned to different experimental groups. Our previous studies using similar types of behavioral and biochemical analyses 27, (link)45, (link)46 (link)
Wang K., Donnelly C.R., Jiang C., Liao Y., Tao X., Bang S., Lee M.K., Hilton M.J., & Ji R. (2021). STING suppresses cancer pain via immune and neuronal modulation.
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