Date published: 2026-9-10

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NOK CRISPR/Cas9 KO Plasmid (m): sc-433993

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • NOK 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 NOK 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
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    NOK CRISPR/Cas9 KO Plasmid (m)

    sc-433993
    20 µg
    $397.00

    Overview

    Serine/threonine/tyrosine kinase 1 (Styk1), also known as NOK, encodes a receptor-like protein kinase implicated in regulating growth factor–responsive signaling and epithelial cell behavior. In mouse systems, NOK has been linked to modulation of MAPK/ERK and PI3K/AKT pathway outputs that influence proliferation, survival, and cellular transformation phenotypes. Altered STYK1/NOK activity has been associated with oncogenic signaling contexts, making it relevant for mechanistic studies of tumor biology and kinase-driven network rewiring. These features position Styk1 as a useful node for dissecting receptor kinase cross-talk, downstream phosphorylation events, and stress-adaptive signaling programs.

    NOK CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Styk1 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Styk1 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 Styk1 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 NOK protein expression.

    This CRISPR knockout system enables efficient generation of Styk1-deficient cell models for investigation of NOK signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting Styk1 exon(s) critical for NOK 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 Styk1 genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by NOK CRISPR/Cas9 KO Plasmid (m) and NOK CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Styk1 locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by NOK HDR Plasmid (m) and NOK HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Styk1 homology arms to support homology-directed repair at defined Styk1 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.