PDGF-C Double Nickase Plasmid (h): sc-401977-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- PDGF-C 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
- PDGF-C Double Nickase Plasmid (h) and PDGF-C Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting PDGFC. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
PDGF-C Double Nickase Plasmid (h) | sc-401977-NIC | 20 µg | $410.00 | |||
PDGF-C Double Nickase Plasmid (h2) | sc-401977-NIC-2 | 20 µg | $410.00 |
Human PDGFC encodes platelet-derived growth factor C (PDGF-C), a secreted growth factor that signals primarily through PDGFRα-containing receptor complexes to regulate mesenchymal cell behavior. Following proteolytic activation, PDGF-C promotes downstream MAPK/ERK and PI3K/AKT signaling to influence cell proliferation, migration, and extracellular matrix remodeling during development and tissue homeostasis. Dysregulated PDGF-C activity has been associated with fibrotic remodeling and tumor–stroma interactions, making PDGFC a useful node for studying growth factor–driven microenvironmental programs. PDGF-C also intersects with angiogenic and wound-healing processes, supporting mechanistic investigations of stromal activation and vascular remodeling.
PDGF-C Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the PDGFC locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within PDGFC. 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 PDGFC 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 PDGFC-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.