Date published: 2026-7-6

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Csk CRISPR/Cas9 KO Plasmid (m): sc-419846

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • Csk 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 Csk 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: Csk Antibody (E-3): sc-166560
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    Csk CRISPR/Cas9 KO Plasmid (m)

    sc-419846
    20 µg
    $397.00

    Overview

    Csk (C-terminal Src kinase) is a cytosolic tyrosine kinase that phosphorylates the C-terminal regulatory tyrosine of Src family kinases, enforcing an autoinhibited conformation and restraining downstream signaling. By tuning Src-dependent pathways, Csk influences receptor-proximal signaling, focal adhesion dynamics, cytoskeletal remodeling, and immune receptor signaling thresholds in multiple cell types. In mouse models, altered Csk activity perturbs lymphocyte activation and tolerance, and impacts processes linked to inflammation and oncogenic signaling through aberrant Src kinase activation. Consequently, Csk is widely studied as a central negative regulator connecting growth factor and immune signaling to cell adhesion, migration, and proliferation programs.

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

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

    Key Features

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

    Design Variants

    CRISPRs +/- HDRs

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