Date published: 2026-8-5

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CCK CRISPR/Cas9 KO Plasmid (m): sc-419503

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

    CCK CRISPR/Cas9 KO Plasmid (m)

    sc-419503
    20 µg
    $397.00

    Overview

    Mouse Cck encodes cholecystokinin (CCK), a secreted neuropeptide and gastrointestinal hormone that regulates satiety, digestive enzyme secretion, gallbladder contraction, and gut motility through activation of the CCKAR and CCKBR G protein–coupled receptors. In the nervous system, CCK functions as a neuromodulator that influences synaptic transmission, interneuron signaling, and stress-responsive circuits, with downstream coupling to phospholipase C/Ca²⁺ signaling and MAPK pathways. Cck expression links nutrient sensing to enteroendocrine and neuronal responses, supporting coordinated metabolic and behavioral outputs. Dysregulated CCK signaling has been implicated in studies of feeding behavior, obesity susceptibility, anxiety-like phenotypes, and gastrointestinal functional alterations, making Cck a useful target for pathway-focused mechanistic research.

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

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

    Key Features

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

    Design Variants

    CRISPRs +/- HDRs

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