AVP Double Nickase Plasmid (h): sc-403139-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- AVP 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 Double Nickase Plasmid (h) and AVP Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting AVP. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
AVP Double Nickase Plasmid (h) | sc-403139-NIC | 20 µg | $410.00 | |||
AVP Double Nickase Plasmid (h2) | sc-403139-NIC-2 | 20 µg | $410.00 |
Arginine vasopressin (AVP) encodes a neurohypophyseal peptide hormone synthesized as prepropressophysin in hypothalamic magnocellular neurons and processed to AVP, neurophysin II, and copeptin. AVP signals primarily through AVPR1A/AVPR1B (Gq/PLCβ–IP3/Ca2+ and PKC pathways) and AVPR2 (Gs/cAMP–PKA) to regulate renal water reabsorption via aquaporin-2 trafficking, vascular tone, and pituitary ACTH release in stress-responsive circuits. Through these pathways, AVP contributes to systemic osmoregulation, hemodynamic control, and neuroendocrine integration. Dysregulation of AVP production or receptor signaling is implicated in disorders of water balance and sodium homeostasis, and altered AVP-axis activity is also studied in stress-related phenotypes and certain tumor contexts.
AVP Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the AVP locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within AVP. 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 AVP 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 AVP-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.