AVP Receptor V2 Double Nickase Plasmid (h): sc-403177-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- AVP Receptor V2 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
- AVP Receptor V2 Double Nickase Plasmid (h) and AVP Receptor V2 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting AVPR2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
AVP Receptor V2 Double Nickase Plasmid (h) | sc-403177-NIC | 20 µg | $410.00 | |||
AVP Receptor V2 Double Nickase Plasmid (h2) | sc-403177-NIC-2 | 20 µg | $410.00 |
AVPR2 encodes the vasopressin V2 receptor (AVP receptor V2), a G protein–coupled receptor predominantly coupled to Gs that elevates intracellular cAMP upon arginine vasopressin binding. This signaling activates PKA-dependent pathways that regulate membrane trafficking and water reabsorption programs, including control of aquaporin-2 localization in epithelial systems. AVPR2 function integrates endocrine osmoregulation with cellular second-messenger signaling and receptor desensitization/internalization processes. Dysregulation or loss-of-function variants in AVPR2 are associated with impaired vasopressin responsiveness and are widely studied in disorders of water balance and GPCR signaling defects.
AVP Receptor V2 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the AVPR2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within AVPR2. 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 AVPR2 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 AVPR2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.