Date published: 2026-8-31

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TRPC2 CRISPR/Cas9 KO Plasmid (m): sc-423513

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • TRPC2 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 TRPC2 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

    TRPC2 CRISPR/Cas9 KO Plasmid (m)

    sc-423513
    20 µg
    $397.00

    Overview

    Trpc2 encodes TRPC2, a member of the transient receptor potential canonical (TRPC) family of cation channels that regulates receptor-operated Ca2+ influx downstream of phospholipase C signaling. In mouse, TRPC2 is prominently linked to sensory signal transduction in the vomeronasal system, where calcium entry shapes neuronal excitability and downstream MAPK/CaM-dependent pathways that influence immediate early gene programs. Through these calcium-dependent processes, Trpc2 contributes to pheromone-evoked behaviors and neuroendocrine coupling, making it relevant to studies of chemosensation, neural circuit function, and behavior-associated phenotypes. Disruption of Trpc2 is commonly used to interrogate how TRP channel-mediated calcium dynamics coordinate sensory processing and organismal responses.

    TRPC2 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Trpc2 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Trpc2 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 Trpc2 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 TRPC2 protein expression.

    This CRISPR knockout system enables efficient generation of Trpc2-deficient cell models for investigation of TRPC2 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting Trpc2 exon(s) critical for TRPC2 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 Trpc2 genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by TRPC2 CRISPR/Cas9 KO Plasmid (m) and TRPC2 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Trpc2 locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by TRPC2 HDR Plasmid (m) and TRPC2 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Trpc2 homology arms to support homology-directed repair at defined Trpc2 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.