TRPC6 Double Nickase Plasmid (h): sc-401205-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TRPC6 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
- TRPC6 Double Nickase Plasmid (h) and TRPC6 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting TRPC6. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: TRPC6 Antibody (B-10): sc-515837
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TRPC6 Double Nickase Plasmid (h) | sc-401205-NIC | 20 µg | $410.00 | |||
TRPC6 Double Nickase Plasmid (h2) | sc-401205-NIC-2 | 20 µg | $410.00 |
TRPC6 encodes a nonselective, calcium-permeable TRP channel that is activated downstream of Gq/PLC signaling and diacylglycerol, linking receptor stimulation to membrane depolarization and intracellular Ca2+ dynamics. TRPC6-mediated Ca2+ influx regulates cytoskeletal remodeling, contractility, and transcriptional programs through pathways that include calcineurin–NFAT and other calcium-sensitive effectors, with prominent roles in podocytes and vascular smooth muscle cells. Dysregulated TRPC6 activity and altered channel expression are associated with proteinuric kidney disease, including familial and sporadic focal segmental glomerulosclerosis, and have been studied in contexts of renal fibrosis and vascular remodeling.
TRPC6 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the TRPC6 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within TRPC6. 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 TRPC6 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 TRPC6-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.