Date published: 2026-8-25

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Junctophilin-3 CRISPR/Cas9 KO Plasmid (h): sc-409301

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • Junctophilin-3 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 Junctophilin-3 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

    Junctophilin-3 CRISPR/Cas9 KO Plasmid (h)

    sc-409301
    20 µg
    $397.00

    Overview

    JPH3 encodes junctophilin-3, a membrane-bridging protein that stabilizes junctional membrane complexes by tethering the plasma membrane to the endoplasmic/sarcoplasmic reticulum. In neurons, junctophilin-3 supports localized Ca²⁺ microdomains and excitation–contraction/excitation–secretion coupling by organizing contacts that influence Ca²⁺ signaling, membrane excitability, and synaptic function. These processes intersect with pathways controlling intracellular calcium homeostasis, ER signaling, and activity-dependent responses. Disruption or altered expression of JPH3 has been linked to neurodegenerative phenotypes, including Huntington disease-like 2, making it relevant for studying calcium-dependent vulnerability and neuronal dysfunction.

    Junctophilin-3 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the JPH3 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the JPH3 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 JPH3 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 Junctophilin-3 protein expression.

    This CRISPR knockout system enables efficient generation of JPH3-deficient cell models for investigation of Junctophilin-3 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting JPH3 exon(s) critical for Junctophilin-3 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 JPH3 genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by Junctophilin-3 CRISPR/Cas9 KO Plasmid (h) and Junctophilin-3 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the JPH3 locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by Junctophilin-3 HDR Plasmid (h) and Junctophilin-3 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by JPH3 homology arms to support homology-directed repair at defined JPH3 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.