Date published: 2026-7-10

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Myc CRISPR/Cas9 KO Plasmid (m): sc-421770

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • Myc 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 Myc 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: Myc Antibody (9E10): sc-40
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    Myc CRISPR/Cas9 KO Plasmid (m)

    sc-421770
    20 µg
    $397.00

    Overview

    Myc encodes the MYC transcription factor, a central regulator of cell growth, biomass accumulation, and cell cycle progression in mouse cells. MYC binds E-box elements to control broad gene expression programs that coordinate ribosome biogenesis, nucleotide and amino acid metabolism, and mitochondrial function, while integrating signals from pathways such as MAPK/ERK, PI3K–AKT–mTOR, and WNT/β-catenin. Tight control of Myc is required for normal development and tissue homeostasis, and its dysregulation is strongly linked to oncogenic transformation and altered differentiation states. Because MYC influences apoptosis, DNA replication stress responses, and chromatin accessibility, it is widely studied in cancer biology, stem cell programs, and metabolic remodeling.

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

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

    Key Features

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

    Design Variants

    CRISPRs +/- HDRs

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