B6 cg ifnar1tm1.2ees j

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B6(Cg)-Ifnar1tm1.2Ees/J is a genetically modified mouse model that carries a targeted mutation in the Ifnar1 gene, which encodes the alpha subunit of the type I interferon receptor. This model is useful for studying the role of type I interferon signaling in various biological processes.

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13 protocols using b6 cg ifnar1tm1.2ees j

Genetically Modified Mice for Immunological Research

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Mouse experiments performed at Wistar Institute (WI) and were approved by IACUC of the Wistar Institute and experiments performed in Tianjin Medical University were approved by animal safety committee of the University. C57BL/6 mice were obtained from Jackson, S100A9KO and LF-KO mice were described earlier [9 (link)]. Transgenic knock-in mice with Ser526 substitution to Ala526 in IFNAR1 (“SA mice”, C57BL/6-Ifnar1tm1.1Syfu/J; Jackson stock No. 035564) were described previously [12 (link)]. The colonies were maintained at Wistar Institute animal facility. IFNAR1-KO mice were obtained from Jackson Lab (B6(Cg)-Ifnar1^tm1.2Ees/J). All mice were bred in pathogen-free facilities, and age-matched littermates were used as controls. The FloxP-flanking SOCS3 transgenic (SOCS3^fl/fl) mice were obtained from Dr. Zhihong Chen (Fudan University, China)[13 (link)]. Conditional SOCS3 knock out mice (SOCS3-KO) were obtained by cross breeding of SOCS3^fl/fl mice with Lyz2-Cre transgenic mice.

Perego M., Fu S., Cao Y., Kossenkov A., Yao M., Bonner E., Alicea-Tores K., Liu W., Jiang Z., Chen Z., Fuchs S.Y., Zhou J, & Gabrilovich D.I. (2022). Mechanisms regulating transitory suppressive activity of neutrophils in newborns: PMN-MDSC in newborns. Journal of leukocyte biology, 112(5), 955-968.

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Generation of Bone Marrow Chimeras

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All mouse strains—C57BL/6, C57BL/6_Ly5.1 (B6.SJL-Ptprca Peb/BoyJ), IFNAR^−/− [B6(Cg)-Ifnar1tm1.2Ees/J], and OT-I [C57BL/6-Tg(TcraTcrb)1100Mjb/J]—were purchased from The Jackson Laboratory. All mouse colonies were maintained in the animal housing facility at BNITM, Hamburg. All animal experiments were conducted according to the guidelines of the German animal protection law and under approvals 31/17 and 92/18 issued by the state of Hamburg. Bone marrow chimeras were generated as previously described (41 (link)). Briefly, 6- to 10-week-old recipient mice were lethally irradiated (550 rad, 4 h apart, by a cesium source) and reconstituted with 3 × 10⁶ donor bone marrow cells.

Port J.R., Wozniak D.M., Oestereich L., Pallasch E., Becker-Ziaja B., Müller J., Rottstegge M., Olal C., Gómez-Medina S., Oyakhliome J., Ighodalo Y., Omomoh E., Olokor T., Adomeh D.I., Asogun D., Ogbani-Emovon E., Hartmann K., Krasemann S., Nelson E.V., Escudero-Pérez B., McElroy A.K., Günther S, & Muñoz-Fontela C. (2020). Severe Human Lassa Fever Is Characterized by Nonspecific T-Cell Activation and Lymphocyte Homing to Inflamed Tissues. Journal of Virology, 94(21), e01367-20.

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Characterization of Cxcl12-GFP Mice

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C57BL/6J were purchased from Charles River. Cxcl12-GFP mice have been previously described (Sugiyama et al., 2006 (link)). Unless stated otherwise, experiments were performed in female mice, which were infected and analyzed between 10 and 20 wk of age. LepR-Cre (B6.129-Lepr^tm3(cre)Mgmj/J; 032457), Rosa26-CAG-loxp-stop-loxp-tdTomato (B6;129S6-Gt(ROSA)26Sor^{tm14(CAG-tdTomato)Hze}/J; 007908), CD8^−/− (B6.129S2-Cd8a^tm1Mak/J; 002665), and IFNAR^−/− (B6(Cg)-Ifnar1^tm1.2Ees/J) mice were from Jackson Laboratory. Animals were maintained in the animal facility of the University Hospital Zurich and treated in accordance with guidelines of the Swiss Federal Veterinary Office. Experiments and procedures were approved by the Veterinäramt des Kantons Zurich, Switzerland.

Isringhausen S., Mun Y., Kovtonyuk L., Kräutler N.J., Suessbier U., Gomariz A., Spaltro G., Helbling P.M., Wong H.C., Nagasawa T., Manz M.G., Oxenius A, & Nombela-Arrieta C. (2021). Chronic viral infections persistently alter marrow stroma and impair hematopoietic stem cell fitness. The Journal of Experimental Medicine, 218(12), e20192070.

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Transgenic Cas9 and Ifnar1 Knockout Mice

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All animal work was conducted in accordance with protocols approved by the Lawrence Livermore National Laboratory (LLNL) Institution Animal Care and Use Committee. Cas9^tg/tg mice (Rosa26-Cas9 knockin on the C57BL/6J genetic background, B6J.129(Cg)-Gt(ROSA)26Sor^{tm1.1(CAG-cas9∗,-EGFP)Fezh/J}; The Jackson Laboratory, Farmington, CT; catalog number 026179) and Ifnar1^−/− mice (global Ifnar1 KO on the C57BL/6J genetic background, B6(Cg)-Ifnar1^tm1.2Ees/J; The Jackson Laboratory, Farmington, CT; catalog number 028288) were bred separately at LLNL and also mated to generate a double-homozygous mutant Cas9^tg/tg; Ifnar1^−/− mouse strain. All experiments were performed with 6- to 10-week-old mice.

Collette N., Dhungel P., Lund S.J., Schwedler J.L., Saada E.A., Light Y.K., Sinha A., Schoeniger J.S, & Negrete O.A. (2021). Immunocompromised Cas9 transgenic mice for rapid in vivo assessment of host factors involved in highly pathogenic virus infection. Molecular Therapy. Methods & Clinical Development, 23, 286-295.

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Genetic Manipulation of Murine Infections

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All mice were specific pathogen-free, maintained under a 12-hr light-dark cycle (7AM to 7PM), and given a standard chow diet (Harlan irradiated laboratory animal diet) ad libitum. Within each experiment mice of all genotypes were age-matched at 6-10 weeks old at the beginning of infections. Whenever possible we used comparable numbers of each sex across all genotypes in an experiment. Mice work was not subjected to randomization or data blinding. C57BL/6J (B6), B6.129S-Il1rn^tm1Dih/J (Il1rn^−/−, Jax #004754)⁵⁸, B6(Cg)-Ifnar1^tm1.2Ees/J (Ifnar^−/−, Jax #028288) and B6.129S6-^Ch25htm1Rus/J (Ch25h^−/−, JAx #016263)^{71 (link)} were originally purchased from Jackson Laboratories and subsequently bred at UC Berkeley. B6J.C3-Sst1^{C3HeB/FeJKrmn} mice (referred to as B6.Sst1^S throughout) were from the colony of I. Kramnik at Boston University and then transferred to UC Berkeley. Sting^gt/gt mice were previously described^{72 (link)}. All animals used in experiments were bred in-house unless otherwise noted in the figure legends. All animal experiments complied with the regulatory standards of, and were approved by, the University of California Berkeley Institutional Animal Care and Use Committee.

Ji D.X., Yamashiro L.H., Chen K.J., Mukaida N., Kramnik I., Darwin K.H, & Vance R.E. (2019). Type I interferon-driven susceptibility to Mycobacterium tuberculosis is mediated by interleukin-1 receptor antagonist IL-1Ra. Nature microbiology, 4(12), 2128-2135.

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Pristane-Induced Lupus Mouse Model

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Mice were bred and maintained under specific pathogen-free conditions. Female, 10–12-week-old C57BL/6 (B6), B6.129S2-Ighm^tm1Cgn/J (μMT), B6.129P2-Il10^tm1Cgn/J (IL-10−/−), B6.129X1-Elane^tm1Sds/J (Elastase−/−), and B6.129S4-C3^tm1Crr/J (C3−/−), B6.129S7-Itgb2 ^tm1Bay/J (CD18−/−), B6(Cg)-Ifnar1^tm1.2Ees/J (IFNAR−/−), B6N.129S2-Casp1^tm1Flv/J (Casp1−/−), and B6.129P2-Nos2^tm1Lau/J (Nos2−/−) mice were from Jackson Laboratory (Bar Harbor, ME). C57BL/6J-Ticam1 ^Lps2/J (Trif ^Lps2; TRIF−/−) and B6.129P2(SJL)-MyD88^tm1.1Defr/J (MyD88−/−) mice were bred at the University of Florida. To induce lupus, 0.5 mL of pristane (Sigma-Aldrich, St. Louis, MO) was administered i.p. Controls were left untreated. Peritoneal exudate cells were collected by lavage. In some experiments, bronchoalveolar lavage (BAL) was performed. After euthanizing the mice, a small incision was cut in the trachea and the alveolar spaces were lavaged with 1 ml of PBS. Cells collected by BAL were resuspended in RPMI1640 + 10% fetal bovine serum and incubated at 37° C for 1-hr before treating with IL-10 (1 ng/ml). After 15-min incubation, the cells were fixed, permeabilized, and surface-stained with anti-CD11b antibodies and intracellularly-stained with anti-phospho-Stat3 antibodies as below. These studies were approved by the Institutional Animal Care and Use Committee.

Zhuang H., Han S., Lee P.Y., Khaybullin R., Shumyak S., Lu L., Chatha A., Afaneh A., Zhang Y., Xie C., Nacionales D., Moldawer L., Qi X., Yang L.J, & Reeves W.H. (2017). Pathogenesis of diffuse alveolar hemorrhage in murine lupus. Arthritis & rheumatology (Hoboken, N.J.), 69(6), 1280-1293.

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Genetic Manipulation of Murine Infections

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Standardized Mouse Housing and Handling

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Mice were housed under specific-pathogen-free conditions at the Genentech animal facility. Mice were maintained in accordance with the Guide for the Care and Use of Laboratory Animals (National Research Council, 2011). Genentech is an AAALAC-accredited facility and all animal activities in this research study were conducted under protocols approved by the Genentech Institutional Animal Care and Use Committee (IACUC). Mice were housed in individually ventilated cages within animal rooms maintained under a 14 h–10 h light–dark cycle. Animal rooms were temperature and humidity controlled between 68 and 79 °F (20.0 to 26.1 °C) and from 30% to 70%, respectively, with 10 to 15 room air exchanges per hour. Male mice (aged 8–12 weeks) that appeared healthy and free of obvious abnormalities were used for the study. B6.Cg-Foxn1nu/J (000819), C57BL/6-Tg (CAG-EGFP)1Osb/J (003291) and C57BL/6J (000664) and B6(Cg)-Ifnar1 tm1.2Ees/J (028288) mice were purchased from Jackson Laboratories. B6.129S6-Rag2^tm1Fwa N12 (RAGN12), C.Cg/AnNTac-Foxn1^nu NE9 (BALBNU-M) and BALB/cAnNTac (BALB-M) mice were purchased from Taconic Biosciences.
CD4.cre.tg Rosa26.LSL.tdTomato.cki OT-I.TCR.tg (OT-I^−/− and OT-I^+/+), DPT-IRES-Cre.ERT2. ki.B6N.1C9-1-H4-1_Rosa26.LSL.YFP.cki.B6J_Rosa26.LSL.DTR.cki and E8I.CD8A.IRES.GFP.Cre.tg Rosa26.LSL.tdTomato.cki mice were bred in house.

Ortiz-Muñoz G., Brown M., Carbone C.B., Pechuan-Jorge X., Rouilly V., Lindberg H., Ritter A.T., Raghupathi G., Sun Q., Nicotra T., Mantri S.R., Yang A., Doerr J., Nagarkar D., Darmanis S., Haley B., Mariathasan S., Wang Y., Gomez-Roca C., de Andrea C.E., Spigel D., Wu T., Delamarre L., Schöneberg J., Modrusan Z., Price R., Turley S.J., Mellman I, & Moussion C. (2023). In situ tumour arrays reveal early environmental control of cancer immunity. Nature, 618(7966), 827-833.

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Traumatic Brain Injury in Mice

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All studies were conducted on adult, 2–5 months old, male C57BL/6J (#000664) or global IFNAR1-deficient mice (#028288; B6(Cg)-Ifnar1^tm1.2Ees/J, Ifnar1 null allele) purchased from Jackson Laboratory. The average age across all studies on day of craniectomy was 2.5 months old. Within each experiment, all groups were age matched. Average weight on day of craniectomy was 26.0 ± 3.6 g. Mice were housed in the Animal Care Facility at the University of Iowa (Iowa City, IA) under a 12-h light-dark cycle with ad libitum access to food and water. After craniectomy and fluid percussion injury (FPI) or non-surgical control, all mice remained singly caged. All procedures performed in this study were in accord with protocols approved by the Institutional Animal Care and Use Committee at the University of Iowa.

Todd B.P., Luo Z., Gilkes N., Chimenti M.S., Peterson Z., Mix M.R., Harty J.T., Nickl-Jockschat T., Ferguson P.J., Bassuk A.G, & Newell E.A. (2023). Selective neuroimmune modulation by type I interferon drives neuropathology and neurologic dysfunction following traumatic brain injury. Acta Neuropathologica Communications, 11, 134.

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Mouse Model Generation for IFNAR1 and RAG2 Knockouts

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6 – 8 week old female C57BL/6 and BALB/c mice were purchased from Charles River Laboratories (Hollister, CA, United States). IFNAR1 knockout mice (B6(Cg)-Ifnar1^tm1.2Ees/J) from Jackson Laboratories (Bar Harbor, ME, United States) and BALB/c mice (CRL) were backcrossed at least 10 times to generate BALB/c-Ifnar1^tm1.2Ees mice. RAG2 knockout (129S6/SvEvTac-Rag2^tm1Fwa) mice were purchased from Taconic. All experimental studies were conducted under protocols approved by the Institutional Animal Care and Use Committee of Amgen (IACUC). Animals were housed at Association for Assessment and Accreditation of Laboratory Animal Care (AAALAC) International-accredited facilities (at Amgen) in ventilated micro-isolator housing on corncob bedding. All mice were maintained in pathogen-free conditions in a temperature-controlled environment with 12/12 hour light/dark cycles and received sterile pellet food and reverse osmosis-purified water ad libitum.

Noe P., Wang J.H., Chung K., Cheng Z., Field J.J., Shen X., Cortesio C.L., Pastuskovas C.V., Phee H., Tarbell K.V., Egen J.G, & Casbon A.J. (2023). Therapeutically targeting type I interferon directly to XCR1+ dendritic cells reveals the role of cDC1s in anti-drug antibodies. Frontiers in Immunology, 14, 1272055.

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