Date published: 2026-8-27

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myogenin CRISPR/Cas9 KO Plasmid (h): sc-400176

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • myogenin 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 myogenin 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: myogenin Antibody (5FD): sc-52903
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    myogenin CRISPR/Cas9 KO Plasmid (h)

    sc-400176
    20 µg
    $397.00

    Overview

    MYOG encodes myogenin, a basic helix-loop-helix transcription factor that drives terminal skeletal muscle differentiation by coordinating myoblast cell-cycle exit and activation of muscle structural gene programs. Myogenin functions within the core myogenic regulatory factor network alongside MYOD1 and MYF5, and integrates developmental cues from signaling pathways such as WNT, NOTCH, and TGF-β/SMAD to shape lineage commitment and maturation. It binds E-box motifs to regulate transcriptional programs linked to myofibrillogenesis, metabolic remodeling, and neuromuscular development. Dysregulated MYOG expression and myogenic transcriptional circuitry are used as molecular readouts in studies of muscle wasting, impaired regeneration, and neuromuscular disease mechanisms.

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

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

    Key Features

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

    Design Variants

    CRISPRs +/- HDRs

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