HGF Double Nickase Plasmid (h): sc-400433-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- HGF 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
- HGF Double Nickase Plasmid (h) and HGF Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting HGF. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: HGFα Antibody (H-10): sc-374422
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
HGF Double Nickase Plasmid (h) | sc-400433-NIC | 20 µg | $410.00 | |||
HGF Double Nickase Plasmid (h2) | sc-400433-NIC-2 | 20 µg | $410.00 |
Hepatocyte growth factor (HGF) encodes a secreted pleiotropic cytokine that functions as the high-affinity ligand for the MET receptor tyrosine kinase. HGF–MET signaling activates PI3K–AKT, RAS–MAPK, STAT, and focal adhesion–dependent pathways to regulate cell survival, proliferation, motility, morphogenesis, and epithelial–mesenchymal interactions. In tissue injury contexts, HGF contributes to regenerative programs and stromal–epithelial crosstalk that shape extracellular matrix remodeling and angiogenic responses. Dysregulated HGF expression or aberrant MET pathway activity is linked to oncogenic invasion and metastasis biology, fibrotic remodeling, and inflammation-associated pathologies, making HGF a frequent target in mechanistic studies of microenvironment signaling.
HGF Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the HGF locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within HGF. 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 HGF 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 HGF-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.