Met Double Nickase Plasmid (h): sc-400101-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Met Double Nickase Plasmid (h) 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 (h) and Met Double Nickase Plasmid (h2) 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 (D-4): sc-514148
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Met Double Nickase Plasmid (h) | sc-400101-NIC | 20 µg | $410.00 | |||
Met Double Nickase Plasmid (h2) | sc-400101-NIC-2 | 20 µg | $410.00 |
MET encodes the hepatocyte growth factor receptor (Met), a receptor tyrosine kinase that initiates signaling programs controlling cell proliferation, survival, motility, and morphogenesis. Upon HGF binding and receptor autophosphorylation, Met engages pathways including PI3K–AKT, RAS–MAPK/ERK, STAT, and SRC-family signaling, coordinating epithelial–mesenchymal dynamics and tissue remodeling. Dysregulated MET signaling is implicated in oncogenic processes such as invasive growth, metastasis-associated phenotypes, and resistance to pathway-targeted perturbations, making it a key node for mechanistic studies. MET is also relevant to developmental and regenerative biology where HGF–MET signaling guides organogenesis and wound repair responses.
Met Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the MET locus in human 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.