Date published: 2026-8-25

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Myf-6 CRISPR/Cas9 KO Plasmid (m): sc-421777

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • Myf-6 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 Myf-6 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

    Myf-6 CRISPR/Cas9 KO Plasmid (m)

    sc-421777
    20 µg
    $397.00

    Overview

    Myf6 (Myf-6; also known as MRF4) encodes a basic helix-loop-helix transcription factor within the myogenic regulatory factor network that orchestrates skeletal muscle lineage specification and terminal differentiation. Myf-6 participates in myoblast maturation, myotube maintenance, and muscle fiber gene expression through cooperative and partially redundant interactions with MYOD1, MYF5, and MYOG, influencing transcriptional programs linked to sarcomere assembly and metabolic remodeling. In mouse, Myf6 is widely used to study developmental and adult myogenesis, neuromuscular adaptation, and fiber-type regulation, as well as mechanisms of muscle weakness and degeneration in genetic and injury-based models. Perturbation of Myf6-regulated transcription provides a tractable entry point for dissecting myogenic gene regulatory circuits and chromatin-dependent control of muscle identity.

    Myf-6 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Myf6 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Myf6 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 Myf6 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 Myf-6 protein expression.

    This CRISPR knockout system enables efficient generation of Myf6-deficient cell models for investigation of Myf-6 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting Myf6 exon(s) critical for Myf-6 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 Myf6 genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by Myf-6 CRISPR/Cas9 KO Plasmid (m) and Myf-6 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Myf6 locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by Myf-6 HDR Plasmid (m) and Myf-6 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Myf6 homology arms to support homology-directed repair at defined Myf6 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.