P2Y4 Double Nickase Plasmid (m): sc-425395-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- P2Y4 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
- P2Y4 Double Nickase Plasmid (m) and P2Y4 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting P2ry4. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
P2Y4 Double Nickase Plasmid (m) | sc-425395-NIC | 20 µg | $410.00 |
P2ry4 encodes the mouse P2Y4 receptor, a G protein–coupled purinergic receptor activated by extracellular nucleotides that couples predominantly to Gq/11 to stimulate phospholipase C signaling. Downstream calcium mobilization and PKC-dependent pathways link P2Y4 to regulation of epithelial ion transport, mucosal secretion, and smooth muscle contractility, with additional roles in immune cell signaling and tissue homeostasis. Purinergic GPCR signaling intersects with inflammatory cascades, barrier function, and metabolic stress responses, making P2ry4 a relevant target for studying nucleotide-driven communication in airway, gastrointestinal, and vascular biology. Dysregulated P2Y receptor activity has been associated with inflammatory and fibrotic phenotypes in multiple organ systems, supporting mechanistic investigation of P2ry4 in disease-relevant models.
P2Y4 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the P2ry4 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within P2ry4. 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 P2ry4 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 P2ry4-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.