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Ifnar1fl fl

Manufactured by Jackson ImmunoResearch
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Ifnar1fl/fl is a laboratory reagent used in research applications. It is a mouse genetic strain with the Ifnar1 gene flanked by loxP sites, allowing for conditional knockout of the gene. The core function of Ifnar1fl/fl is to serve as a tool for studying the role of the Ifnar1 gene in biological processes.

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4 protocols using ifnar1fl fl

1

Transgenic Mouse Lines for Research

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C57Bl/6J wild type mice were originally obtained from The Jackson Laboratory, Ifnar1fl/fl [70 (link)], Cre-Alb ERT2 [71 (link)], Stat1–/–[72 (link)], Irf7–/–[63 (link)], Tdo2–/–reporter [30 (link)] mice were bred and maintained on a C57Bl/6J background under specific pathogen-free (SPF) conditions at the Institute for Molecular Biotechnology (IMBA) of the Austrian Academy of Sciences, Vienna, Austria.
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2

Conditional Knockout of IFNAR1 in Mice

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All mouse experiments were approved by the Institutional Animal Care and Use Committee (IACUC) of The University of Pennsylvania. Mice were maintained in a specific pathogen-free facility in accordance with the American Association for Laboratory Animal Science guidelines. All mice were of C57BL/6NJ background, and unless otherwise described are 6-8 weeks of age. Mice of both sexes were utilized for these studies. Rag1−/−, Ifnar1fl/fl, and Col1a2-CreERT2/+ mice were obtained from Jackson Laboratory (Bar Harbor, ME, USA). Ifnar1S526A mice (“SA”) and bone marrow chimeras were generated as previously described [23 (link)]. Fibroblast-specific IFNAR1 knockout mice (Ifnar1Δfib) were established by crossing Ifnar1fl/fl mice with Col1a2-CreERT2/+ mice. The resultant Col1a2-CreERT2/+; Ifnar1fl/fl mice were genotyped by PCR (Figure 3I). The Col1a2-CreERT2/+ was induced by administering tamoxifen (Sigma #T5648, St. Louis, MO, USA) 0.2 mg/g, daily for 5 days. Deletion of IFNAR1 was confirmed by PCR with primers for mouse wildtype IFNAR1 (Forward: 5’-CTGGGAGCCAGGGCATAAC-3’, Reverse 5’-CCAGCCTTTCGGAGTGTGC-3’) (Figure 3I). Littermates were randomly assigned into experimental groups, which were either co-housed or exposed to other groups’ bedding to ensure exposure to all groups’ microbiota.
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3

IFNAR1 Knockdown in Macrophages

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Animal experimental procedures were approved by the Purdue Animal Care and Use Committee and performed in strict compliance with the National Institutes of Health Guide for the Care and Use of Laboratory Animals. C57BL/6, Ifnar1fl/fl, and Cx3cr1CreERT2/CreERT2 mice were purchased from the Jackson Laboratory (Bar Harbor, ME) and bred in our animal facility. Ifnar1fl/fl mice were crossed with Cx3cr1CreERT2/CreERT2 mice to generate Ifnar1fl/+-Cx3cr1CreERT2/+ mice. Ifnar1fl/+-Cx3cr1CreERT2/+ mice were then crossed with Ifnar1fl/+-Cx3cr1CreERT2/+ mice to generate Ifnar1fl/fl-Cx3cr1CreERT2/+ and Cx3cr1CreERT2/+ mice. Ifnar1fl/fl-Cx3cr1CreERT2/+ mice at 7-8 weeks old were subjected to i.p. injection of 75mg/kg Tamoxifen (TAM) for a total of 5 consecutive days to induce IFNAR1 knockdown in MG/macrophages. TAM-treated Ifnar1fl/fl-Cx3cr1CreERT2/+ mice were housed for additional 7-8 weeks to allow peripheral monocyte/macrophages to be replenished and then subjected to ischemic stroke. Cx3cr1CreERT2/+ control mice were subjected to the same procedure of TAM treatment followed by ischemic stroke induction. Mice were housed and bred with controlled humidity, temperature and 12h:12h light-dark cycle in the animal facility with food and water available ad libitum.
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4

Conditional Knockout of IFNAR1 in Mice

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All mouse experiments were approved by the Institutional Animal Care and Use Committee (IACUC) of The University of Pennsylvania. Mice were maintained in a specific pathogen-free facility in accordance with the American Association for Laboratory Animal Science guidelines. All mice were of C57BL/6NJ background, and unless otherwise described are 6-8 weeks of age. Mice of both sexes were utilized for these studies. Rag1−/−, Ifnar1fl/fl, and Col1a2-CreERT2/+ mice were obtained from Jackson Laboratory (Bar Harbor, ME, USA). Ifnar1S526A mice (“SA”) and bone marrow chimeras were generated as previously described [23 (link)]. Fibroblast-specific IFNAR1 knockout mice (Ifnar1Δfib) were established by crossing Ifnar1fl/fl mice with Col1a2-CreERT2/+ mice. The resultant Col1a2-CreERT2/+; Ifnar1fl/fl mice were genotyped by PCR (Figure 3I). The Col1a2-CreERT2/+ was induced by administering tamoxifen (Sigma #T5648, St. Louis, MO, USA) 0.2 mg/g, daily for 5 days. Deletion of IFNAR1 was confirmed by PCR with primers for mouse wildtype IFNAR1 (Forward: 5’-CTGGGAGCCAGGGCATAAC-3’, Reverse 5’-CCAGCCTTTCGGAGTGTGC-3’) (Figure 3I). Littermates were randomly assigned into experimental groups, which were either co-housed or exposed to other groups’ bedding to ensure exposure to all groups’ microbiota.
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