GPR92 Double Nickase Plasmid (m): sc-436329-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- GPR92 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
- GPR92 Double Nickase Plasmid (m) and GPR92 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Lpar5. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
GPR92 Double Nickase Plasmid (m) | sc-436329-NIC | 20 µg | $410.00 | |||
GPR92 Double Nickase Plasmid (m2) | sc-436329-NIC-2 | 20 µg | $410.00 |
Lpar5 encodes the mouse lysophosphatidic acid receptor GPR92, a class A GPCR that transduces extracellular lipid signals into intracellular second-messenger responses. Upon activation, GPR92 can engage heterotrimeric G proteins to regulate cAMP production, phospholipase C signaling with Ca²⁺ mobilization, and downstream MAPK/ERK pathway activity, shaping cell migration, survival, and inflammatory gene expression programs. LPA–GPR92 signaling has been linked to neuroimmune communication and peripheral inflammatory responses, and dysregulation of GPCR-mediated lipid signaling is relevant to models of pain, immune activation, and tissue remodeling. These features make Lpar5 a useful target for studying lipid mediator biology and GPCR-dependent signaling networks in murine systems.
GPR92 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Lpar5 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Lpar5. 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 Lpar5 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 Lpar5-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.