Date published: 2026-7-3

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Na+ CP type IIIα CRISPR/Cas9 KO Plasmid (m): sc-422820

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • Na+ CP type IIIα 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 Na+ CP type IIIα 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

    Na+ CP type IIIα CRISPR/Cas9 KO Plasmid (m)

    sc-422820
    20 µg
    $397.00

    Overview

    Scn3a encodes the mouse voltage-gated sodium channel Na+ CP type IIIα, a pore-forming α subunit that drives rapid inward Na+ currents underlying action potential initiation and propagation in excitable cells. By shaping spike threshold, firing frequency, and recovery from inactivation, Na+ CP type IIIα influences neuronal network excitability and activity-dependent signaling programs linked to synaptic transmission. SCN3A activity intersects with membrane excitability pathways that couple ionic flux to calcium-dependent transcription, axonal conduction, and neurodevelopmental patterning. Genetic and functional perturbation of SCN3A has been associated with altered excitability phenotypes and is studied in the context of epilepsy-related mechanisms, neurodevelopmental disorders, and circuit dysfunction.

    Na+ CP type IIIα CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Scn3a gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Scn3a 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 Scn3a 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 Na+ CP type IIIα protein expression.

    This CRISPR knockout system enables efficient generation of Scn3a-deficient cell models for investigation of Na+ CP type IIIα signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting Scn3a exon(s) critical for Na+ CP type IIIα 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 Scn3a genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by Na+ CP type IIIα CRISPR/Cas9 KO Plasmid (m) and Na+ CP type IIIα CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Scn3a locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by Na+ CP type IIIα HDR Plasmid (m) and Na+ CP type IIIα HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Scn3a homology arms to support homology-directed repair at defined Scn3a 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.