Date published: 2026-7-9

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CPI-17 CRISPR/Cas9 KO Plasmid (h): sc-401966

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • CPI-17 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 CPI-17 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: CPI-17 Antibody (F-4): sc-48406
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    CPI-17 CRISPR/Cas9 KO Plasmid (h)

    sc-401966
    20 µg
    $397.00

    Overview

    PPP1R14A encodes CPI-17, a phosphorylation-dependent inhibitor of myosin light chain phosphatase (MLCP) that amplifies contractile signaling by stabilizing myosin regulatory light chain phosphorylation. Upon phosphorylation by kinases such as PKC and Rho-associated pathways, CPI-17 suppresses PP1 catalytic activity within MLCP to regulate smooth muscle tone, cytoskeletal dynamics, and calcium sensitization. This regulatory node integrates GPCR and RhoA/ROCK signaling with actomyosin remodeling and cell motility programs. Dysregulated PPP1R14A/CPI-17 activity has been linked to aberrant smooth muscle contractility and proliferative remodeling contexts, supporting its study in cardiovascular, airway, and gastrointestinal pathophysiology models.

    CPI-17 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the PPP1R14A gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the PPP1R14A 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 PPP1R14A 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 CPI-17 protein expression.

    This CRISPR knockout system enables efficient generation of PPP1R14A-deficient cell models for investigation of CPI-17 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting PPP1R14A exon(s) critical for CPI-17 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 PPP1R14A genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by CPI-17 CRISPR/Cas9 KO Plasmid (h) and CPI-17 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the PPP1R14A locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by CPI-17 HDR Plasmid (h) and CPI-17 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by PPP1R14A homology arms to support homology-directed repair at defined PPP1R14A 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.