P2X3 Double Nickase Plasmid (m): sc-432763-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- P2X3 Double Nickase Plasmid (m) 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
- P2X3 Double Nickase Plasmid (m) and P2X3 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting P2rx3. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: P2X3 Antibody (B-5): sc-390572
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
P2X3 Double Nickase Plasmid (m) | sc-432763-NIC | 20 µg | $410.00 |
P2rx3 encodes the P2X3 receptor, an ATP-gated trimeric cation channel enriched in peripheral sensory neurons where it mediates fast depolarizing currents in response to extracellular nucleotides. P2X3 activity regulates Ca2+ and Na+ influx, shaping nociceptive neurotransmission and neurogenic inflammation, and it interfaces with purinergic signaling networks that influence excitability, synaptic transmission, and sensory neuron plasticity. In mouse models, altered P2rx3 function has been linked to mechanisms underlying inflammatory and neuropathic pain states as well as visceral sensory pathways relevant to bladder and airway reflexes. This target is broadly used to dissect ATP-driven signaling in dorsal root ganglia, trigeminal neurons, and related sensory circuits.
P2X3 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the P2rx3 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within P2rx3. 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 P2rx3 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 P2rx3-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.