Date published: 2026-9-1

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Myosin Va CRISPR/Cas9 KO Plasmid (h): sc-402108

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • Myosin Va 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 Myosin Va 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: Myosin Va Antibody (G-4): sc-365986
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    Myosin Va CRISPR/Cas9 KO Plasmid (h)

    sc-402108
    20 µg
    $397.00

    Overview

    MYO5A encodes myosin Va, an actin-based motor protein that powers long-range transport of membrane-bound organelles and protein complexes along the cortical actin network. Myosin Va cooperates with Rab GTPases and adaptor proteins to regulate vesicle trafficking, endocytic recycling, secretory granule dynamics, and polarized delivery of cargos in neurons, melanocytes, and immune cells. These processes contribute to synaptic function, melanosome distribution, and cellular polarization, linking MYO5A activity to neurological and pigmentation phenotypes when disrupted. In human cell models, altered myosin Va–dependent transport can influence compartmentalized signaling and cytoskeletal organization relevant to disease-associated cellular dysfunction.

    Myosin Va CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the MYO5A gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the MYO5A 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 MYO5A 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 Myosin Va protein expression.

    This CRISPR knockout system enables efficient generation of MYO5A-deficient cell models for investigation of Myosin Va signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting MYO5A exon(s) critical for Myosin Va 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 MYO5A genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by Myosin Va CRISPR/Cas9 KO Plasmid (h) and Myosin Va CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the MYO5A locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by Myosin Va HDR Plasmid (h) and Myosin Va HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by MYO5A homology arms to support homology-directed repair at defined MYO5A 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.