Date published: 2026-7-11

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TRAF1 CRISPR/Cas9 KO Plasmid (m): sc-423492

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • TRAF1 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 TRAF1 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: TRAF1 Antibody (H-3): sc-6253
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    TRAF1 CRISPR/Cas9 KO Plasmid (m)

    sc-423492
    20 µg
    $397.00

    Overview

    Traf1 encodes tumor necrosis factor receptor–associated factor 1 (TRAF1), an adaptor protein that couples members of the TNF receptor superfamily to downstream signaling complexes. In immune and inflammatory contexts, TRAF1 modulates canonical and noncanonical NF-κB signaling, influences MAPK pathway outputs, and helps shape apoptosis and survival decisions through interactions with proteins such as TRAF2 and cIAPs. These activities contribute to regulation of cytokine responses, lymphocyte activation, and innate immune signaling, making Traf1 a useful node for dissecting signal integration in immune cells. Dysregulated TRAF1-associated pathways have been implicated in inflammatory disease mechanisms and immune-oncology–relevant microenvironmental signaling, supporting its broad utility in pathway-focused research models.

    TRAF1 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Traf1 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Traf1 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 Traf1 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 TRAF1 protein expression.

    This CRISPR knockout system enables efficient generation of Traf1-deficient cell models for investigation of TRAF1 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting Traf1 exon(s) critical for TRAF1 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 Traf1 genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by TRAF1 CRISPR/Cas9 KO Plasmid (m) and TRAF1 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Traf1 locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by TRAF1 HDR Plasmid (m) and TRAF1 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Traf1 homology arms to support homology-directed repair at defined Traf1 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.