P2Y9 Double Nickase Plasmid (m): sc-429620-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- P2Y9 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
- P2Y9 Double Nickase Plasmid (m) and P2Y9 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Lpar4. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
P2Y9 Double Nickase Plasmid (m) | sc-429620-NIC | 20 µg | $410.00 |
Mouse Lpar4 encodes the lysophosphatidic acid receptor P2Y9, a GPCR that couples extracellular LPA signals to heterotrimeric G proteins to regulate second-messenger cascades such as phospholipase C activation, intracellular calcium mobilization, and MAPK/ERK signaling. Through these pathways, P2Y9 influences cell migration, cytoskeletal remodeling, proliferation, and survival programs that shape tissue development and inflammatory responses. LPA–LPAR4 signaling also interfaces with Rho-family GTPase activity and can modulate cAMP depending on cellular context, linking receptor activation to broader transcriptional and metabolic changes. Dysregulation of LPA receptor signaling has been associated with fibrosis, immune dysfunction, and tumor-associated phenotypes, making Lpar4 a relevant target for mechanistic studies of microenvironment-driven signaling.
P2Y9 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Lpar4 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Lpar4. 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 Lpar4 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 Lpar4-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.