TRPV4 Double Nickase Plasmid (h): sc-401432-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TRPV4 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
- TRPV4 Double Nickase Plasmid (h) and TRPV4 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting TRPV4. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TRPV4 Double Nickase Plasmid (h) | sc-401432-NIC | 20 µg | $410.00 | |||
TRPV4 Double Nickase Plasmid (h2) | sc-401432-NIC-2 | 20 µg | $410.00 |
TRPV4 encodes a Ca2+-permeable, nonselective cation channel of the transient receptor potential vanilloid family that functions as a polymodal sensor for mechanical forces, osmotic stress, and temperature. Channel activation drives calcium-dependent signaling that influences cytoskeletal remodeling, cell volume regulation, and transcriptional programs, intersecting with pathways such as MAPK/ERK, NFAT, and inflammatory mediator release. TRPV4 activity contributes to epithelial and endothelial barrier responses, chondrocyte and osteoclast biology, and mechanotransduction in sensory and vascular tissues. Altered TRPV4 function has been linked to heritable neuropathies and skeletal dysplasias, and it is frequently studied in the context of edema, pain signaling, and inflammatory tissue remodeling.
TRPV4 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the TRPV4 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within TRPV4. 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 TRPV4 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 TRPV4-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.