Date published: 2026-8-15

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FHOD3 CRISPR/Cas9 KO Plasmid (m): sc-432529

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • FHOD3 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 FHOD3 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: FHOD3 Antibody (G-5): sc-374601
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    FHOD3 CRISPR/Cas9 KO Plasmid (m)

    sc-432529
    20 µg
    $397.00

    Overview

    Fhod3 encodes FHOD3, a diaphanous-related formin that nucleates and elongates linear actin filaments, supporting actin cytoskeleton remodeling and contractile organization. In mouse striated muscle, FHOD3 is enriched at sarcomeric structures and contributes to myofibril assembly, stress fiber formation, and maintenance of cellular architecture through Rho GTPase–regulated actin dynamics. These processes intersect with pathways controlling mechanotransduction, cell shape, and intracellular force transmission, making FHOD3 a useful node for studying cytoskeletal homeostasis. Dysregulated actin organization and sarcomere integrity are linked to cardiomyopathy and muscle dysfunction phenotypes, positioning Fhod3 as a relevant target for modeling structural heart and muscle disease mechanisms in vitro.

    FHOD3 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Fhod3 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Fhod3 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 Fhod3 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 FHOD3 protein expression.

    This CRISPR knockout system enables efficient generation of Fhod3-deficient cell models for investigation of FHOD3 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting Fhod3 exon(s) critical for FHOD3 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 Fhod3 genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by FHOD3 CRISPR/Cas9 KO Plasmid (m) and FHOD3 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Fhod3 locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by FHOD3 HDR Plasmid (m) and FHOD3 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Fhod3 homology arms to support homology-directed repair at defined Fhod3 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.