Date published: 2026-8-24

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TOK-1 CRISPR/Cas9 KO Plasmid (h): sc-406452

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • TOK-1 CRISPR/Cas9 Knockout (KO) Plasmid (h) 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 TOK-1 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: TOK-1β Antibody (B-10): sc-271985
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    TOK-1 CRISPR/Cas9 KO Plasmid (h)

    sc-406452
    20 µg
    $397.00

    Overview

    BCCIP (also referred to as TOK-1) encodes a BRCA2 and CDKN1A (p21) interacting protein that supports genome maintenance by coordinating DNA replication stress responses and DNA repair. It has been implicated in homologous recombination-associated processes, replication fork stability, and checkpoint control, linking it to pathways that preserve chromosomal integrity during S phase. Through functional interactions with BRCA2 and p21, BCCIP can influence cell-cycle progression and the fidelity of DNA damage resolution. Dysregulation or reduced activity of BCCIP is frequently explored in the context of genomic instability phenotypes relevant to cancer biology and other disorders associated with impaired DNA repair.

    TOK-1 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the BCCIP gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the BCCIP 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 BCCIP 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 TOK-1 protein expression.

    This CRISPR knockout system enables efficient generation of BCCIP-deficient cell models for investigation of TOK-1 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting BCCIP exon(s) critical for TOK-1 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 BCCIP genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by TOK-1 CRISPR/Cas9 KO Plasmid (h) and TOK-1 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the BCCIP locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by TOK-1 HDR Plasmid (h) and TOK-1 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by BCCIP homology arms to support homology-directed repair at defined BCCIP 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.