Date published: 2026-7-13

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γ-catenin CRISPR/Cas9 KO Plasmid (m): sc-421210

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • γ-catenin 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 γ-catenin 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: γ-catenin Antibody (A-6): sc-514115
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    γ-catenin CRISPR/Cas9 KO Plasmid (m)

    sc-421210
    20 µg
    $397.00

    Overview

    Jup encodes γ-catenin (plakoglobin), an armadillo family protein that functions at adherens junctions and desmosomes to couple cadherins to the cytoskeleton and stabilize cell–cell adhesion. In mouse tissues, γ-catenin supports epithelial and cardiac tissue integrity and participates in junctional remodeling during development and wound responses. It can also influence Wnt/β-catenin-related transcriptional programs through interactions with TCF/LEF complexes, linking adhesive state to gene regulation. Dysregulated γ-catenin or desmosomal architecture is associated with altered barrier function, inflammation, and cardiomyopathy-related phenotypes, making Jup a useful node for studying junctional signaling and tissue homeostasis.

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

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

    Key Features

    • sgRNAs targeting Jup exon(s) critical for γ-catenin 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 Jup genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

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