Date published: 2026-8-27

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Met Double Nickase Plasmid (m): sc-421635-NIC

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • Met Double Nickase Plasmid (m) consists of a pair of plasmids each encoding a D10A mutated Cas9 nuclease and a target-specific 20 nt guide RNA (gRNA) designed to knockout gene expression with greater specificity than its CRISPR/Cas9 KO counterpart
  • Paired gRNA sequences are offset by approximately 20 bp to allow for specific Cas9-mediated double nicking of the genomic DNA, which mimics a DSB
  • One plasmid in the pair contains a puromycin-resistance gene for selection; the other plasmid in the pair contains a GFP marker to visually confirm transfection
  • Met Double Nickase Plasmid (m) and Met Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Met. One or both designs may be available
  • Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: Met Antibody (B-2): sc-8057
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    Met Double Nickase Plasmid (m)

    sc-421635-NIC
    20 µg
    $410.00

    Mouse Met encodes the receptor tyrosine kinase MET, the cognate receptor for hepatocyte growth factor (HGF), and a central regulator of epithelial–mesenchymal signaling. Upon ligand binding, MET autophosphorylation initiates downstream cascades including PI3K–AKT, RAS–MAPK, STAT, and SRC/FAK pathways, coordinating proliferation, survival, migration, and morphogenesis. MET signaling contributes to developmental programs such as organogenesis and tissue regeneration, and its dysregulation is widely studied in invasive growth and oncogenic pathway remodeling. In murine systems, Met function is frequently interrogated in models of tumor progression, stromal interactions, and wound-repair biology.

    Met Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Met locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Met. When directed to adjacent sites on opposite DNA strands, the two nickases generate offset single-strand nicks that together produce a staggered double-strand break, requiring coordinated on-target activity from both guides. The resulting DNA break is resolved by endogenous cellular repair pathways, most commonly through non-homologous end joining (NHEJ), leading to insertions or deletions that disrupt Met function. By requiring dual sgRNA engagement at the target locus, the double nicking approach enhances editing specificity and provides a complementary CRISPR strategy for applications where additional control over targeting precision is desired.

    To support efficient identification of edited cells, one plasmid encodes GFP for fluorescent visualization of transfected populations, while the companion plasmid carries a puromycin resistance gene for antibiotic selection. Together, these features support efficient enrichment of co-transfected populations and simplify the validation of Met-disrupted clones.

    For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.