GPR22 Double Nickase Plasmid (h): sc-418054-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- GPR22 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
- GPR22 Double Nickase Plasmid (h) and GPR22 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting GPR22. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
GPR22 Double Nickase Plasmid (h) | sc-418054-NIC | 20 µg | $410.00 |
GPR22 encodes an orphan G protein-coupled receptor (GPCR) that is predicted to regulate signal transduction at the plasma membrane through heterotrimeric G proteins and downstream second-messenger pathways such as cAMP/PKA and MAPK. Although its endogenous ligand remains unclear, GPR22 expression has been linked to modulation of cellular stress responses and metabolic homeostasis, consistent with broader GPCR roles in controlling transcriptional programs, ion flux, and kinase signaling. In human tissues, altered GPR22 expression has been reported in cardiovascular and metabolic contexts, and the receptor has been investigated for potential contributions to hypertrophy- and remodeling-associated phenotypes. These features make GPR22 a useful target for mechanistic studies of GPCR biology, pathway wiring, and genotype-to-phenotype relationships in relevant cell models.
GPR22 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the GPR22 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within GPR22. 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 GPR22 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 GPR22-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.