GPR55 Double Nickase Plasmid (m): sc-432690-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- GPR55 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
- GPR55 Double Nickase Plasmid (m) and GPR55 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Gpr55. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
GPR55 Double Nickase Plasmid (m) | sc-432690-NIC | 20 µg | $410.00 | |||
GPR55 Double Nickase Plasmid (m2) | sc-432690-NIC-2 | 20 µg | $410.00 |
Mouse Gpr55 encodes GPR55, an orphan class A GPCR that responds to bioactive lipids and couples to multiple downstream effectors, including RhoA/ROCK, ERK/MAPK, and PLC-mediated Ca²⁺ signaling. GPR55 activity influences cytoskeletal remodeling, cell migration, and proliferation, and it can modulate inflammatory signaling through crosstalk with endocannabinoid-related pathways. In the immune system and nervous tissue, GPR55 has been implicated in shaping cytokine responses, neuroinflammation, and neuronal excitability. Dysregulated GPR55 signaling has been associated in experimental models with inflammatory disorders, pain-related phenotypes, bone remodeling changes, and altered metabolic homeostasis, supporting its use in mechanistic studies of GPCR-driven signaling networks.
GPR55 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Gpr55 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Gpr55. 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 Gpr55 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 Gpr55-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.