Date published: 2026-7-14

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Myosin VI CRISPR/Cas9 KO Plasmid (h): sc-401815

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • Myosin VI 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 VI 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 VI Antibody (A-9): sc-393558
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    Myosin VI CRISPR/Cas9 KO Plasmid (h)

    sc-401815
    20 µg
    $397.00

    Overview

    MYO6 encodes human myosin VI, an unconventional actin-based motor that uniquely moves toward the minus end of actin filaments to support intracellular trafficking and membrane dynamics. Myosin VI participates in clathrin-mediated endocytosis, endosomal sorting, Golgi and secretory pathway transport, and organization of actin-rich structures such as microvilli and stereocilia. Through interactions with adaptor proteins and cargo, it contributes to cell migration, adhesion, and mechanosensory processes, linking cytoskeletal remodeling to vesicle transport. Dysregulation of MYO6 has been associated with hearing-related phenotypes and altered epithelial organization, making it relevant for studies of sensory biology and cytoskeleton-driven trafficking defects.

    Myosin VI CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the MYO6 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the MYO6 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 MYO6 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 VI protein expression.

    This CRISPR knockout system enables efficient generation of MYO6-deficient cell models for investigation of Myosin VI signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting MYO6 exon(s) critical for Myosin VI 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 MYO6 genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by Myosin VI CRISPR/Cas9 KO Plasmid (h) and Myosin VI CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the MYO6 locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by Myosin VI HDR Plasmid (h) and Myosin VI HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by MYO6 homology arms to support homology-directed repair at defined MYO6 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.