Date published: 2026-7-11

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FXYD3 CRISPR/Cas9 KO Plasmid (h): sc-406431

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • FXYD3 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 FXYD3 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: FXYD3 Antibody (A-8): sc-271808
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    FXYD3 CRISPR/Cas9 KO Plasmid (h)

    sc-406431
    20 µg
    $397.00

    Overview

    FXYD3 (dysadherin) is a member of the FXYD family of small single-pass membrane proteins that modulate Na⁺/K⁺-ATPase activity, thereby influencing ion homeostasis, membrane potential, and epithelial transport physiology. Through regulation of pump kinetics and downstream effects on cell volume and signaling, FXYD3 can impact processes including proliferation, stress responses, and cell–cell adhesion dynamics. Altered FXYD3 expression has been reported across multiple cancer contexts and is frequently studied for links to tumor cell motility, invasiveness, and epithelial state changes. As a surface-associated regulator, it is also relevant to investigations of membrane protein networks and Na⁺/K⁺-ATPase–coupled pathways.

    FXYD3 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the FXYD3 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the FXYD3 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 FXYD3 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 FXYD3 protein expression.

    This CRISPR knockout system enables efficient generation of FXYD3-deficient cell models for investigation of FXYD3 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting FXYD3 exon(s) critical for FXYD3 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 FXYD3 genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by FXYD3 CRISPR/Cas9 KO Plasmid (h) and FXYD3 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the FXYD3 locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by FXYD3 HDR Plasmid (h) and FXYD3 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by FXYD3 homology arms to support homology-directed repair at defined FXYD3 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.