Date published: 2026-7-1

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Myosin IIIb CRISPR/Cas9 KO Plasmid (h): sc-414483

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

    Myosin IIIb CRISPR/Cas9 KO Plasmid (h)

    sc-414483
    20 µg
    $397.00

    Overview

    MYO3B encodes myosin IIIb, an actin-dependent motor protein that couples ATP hydrolysis to movement along F-actin and participates in cytoskeletal remodeling. Myosin III family members are implicated in regulating membrane protrusion dynamics and actin bundle organization, processes central to cell polarity, vesicle trafficking, and signal-dependent changes in cell architecture. Through these roles, MYO3B supports actin-driven cellular behaviors such as migration and adhesion that interface with pathways controlling cytoskeletal tension and mechanotransduction. Dysregulation of actin–myosin networks is broadly relevant to disorders involving epithelial integrity and neurosensory cell structure, making MYO3B a useful target for mechanistic studies of cytoskeletal control.

    Myosin IIIb CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the MYO3B gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the MYO3B 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 MYO3B 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 IIIb protein expression.

    This CRISPR knockout system enables efficient generation of MYO3B-deficient cell models for investigation of Myosin IIIb signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting MYO3B exon(s) critical for Myosin IIIb 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 MYO3B genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by Myosin IIIb CRISPR/Cas9 KO Plasmid (h) and Myosin IIIb CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the MYO3B locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by Myosin IIIb HDR Plasmid (h) and Myosin IIIb HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by MYO3B homology arms to support homology-directed repair at defined MYO3B 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.