P2Y7 Double Nickase Plasmid (h): sc-403664-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- P2Y7 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
- P2Y7 Double Nickase Plasmid (h) and P2Y7 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting LTB4R. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
P2Y7 Double Nickase Plasmid (h) | sc-403664-NIC | 20 µg | $410.00 | |||
P2Y7 Double Nickase Plasmid (h2) | sc-403664-NIC-2 | 20 µg | $410.00 |
LTB4R encodes leukotriene B4 receptor 1 (BLT1), a G protein–coupled receptor that transduces leukotriene B4 signals to activate PLCβ/Ca2+ flux, MAPK cascades, and PI3K-dependent chemotactic programs in myeloid and other immune cells. BLT1 signaling coordinates leukocyte adhesion, migration, and degranulation, linking lipid mediator sensing to inflammatory network regulation. Dysregulated LTB4R activity has been associated with chronic inflammatory phenotypes and immune-driven tissue injury in multiple disease contexts, supporting its use as a target for mechanistic studies of leukotriene pathways. In biomedical research, perturbation of LTB4R enables interrogation of GPCR-driven trafficking, cytokine release, and crosstalk with eicosanoid metabolism and innate immune signaling.
P2Y7 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the LTB4R locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within LTB4R. 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 LTB4R 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 LTB4R-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.