Date published: 2026-7-10

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IRF-5 CRISPR/Cas9 KO Plasmid (m): sc-424184

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • IRF-5 CRISPR/Cas9 Knockout (KO) Plasmid (m) is a pool of plasmids, each encoding Cas9 nuclease and a target-specific 20 nt guide RNA (gRNA) designed for maximum knockout efficiency using sequences derived from the GeCKO v2 library
  • gRNA sequences direct Cas9 to induce site-specific double-strand breaks (DSBs) in the IRF-5 genomic locus, resulting in gene knockout through non-homologous end joining (NHEJ)
  • The puromycin resistance and RFP genes are flanked by LoxP sites, enabling removal of selection markers via Cre recombinase (Cre Vector: sc-418923) after establishing stable knockout cell lines
  • Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: IRF-5 Antibody (10T1): sc-56714
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    IRF-5 CRISPR/Cas9 KO Plasmid (m)

    sc-424184
    20 µg
    $397.00

    Overview

    Mouse Irf5 encodes interferon regulatory factor 5 (IRF-5), a transcription factor that integrates innate immune sensing with downstream inflammatory gene programs. IRF-5 is activated downstream of endosomal Toll-like receptors and MyD88-dependent signaling, promoting expression of type I interferon and pro-inflammatory cytokine networks through coordinated regulation of interferon-stimulated genes. In macrophages, dendritic cells, and B cells, IRF-5 contributes to polarization and effector responses, shaping cytokine balance and antigen-driven immunity. Dysregulated IRF-5 activity has been linked to autoimmune and inflammatory phenotypes, making Irf5 a useful node for dissecting pathways relevant to systemic immune dysregulation in mouse models.

    IRF-5 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Irf5 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Irf5 together with the Streptococcus pyogenes Cas9 nuclease. The plasmids also encode GFP, allowing fluorescent identification and enrichment of successfully transfected cells by fluorescence microscopy or flow cytometry.

    The multi-guide design increases the likelihood of generating insertions or deletions (indels) that disrupt the Irf5 open reading frame following Cas9-mediated double-strand break formation. DNA breaks introduced by the CRISPR/Cas9 system are repaired through endogenous non-homologous end joining (NHEJ) pathways, frequently resulting in frameshift mutations that abolish IRF-5 protein expression.

    This CRISPR knockout system enables efficient generation of Irf5-deficient cell models for investigation of IRF-5 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting Irf5 exon(s) critical for IRF-5 function
    • Co-expression of SpCas9 and sgRNA from a single plasmid for simplified delivery
    • GFP reporter for identification of transfected cells
    • Pool of plasmids targeting multiple Irf5 genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by IRF-5 CRISPR/Cas9 KO Plasmid (m) and IRF-5 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Irf5 locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by IRF-5 HDR Plasmid (m) and IRF-5 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Irf5 homology arms to support homology-directed repair at defined Irf5 target sites corresponding to the CRISPR/Cas9 KO designs. HDR donor availability may vary. See Related Products for availability.

    For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.