GPR52 Double Nickase Plasmid (h): sc-411266-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- GPR52 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
- GPR52 Double Nickase Plasmid (h) and GPR52 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting GPR52. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
GPR52 Double Nickase Plasmid (h) | sc-411266-NIC | 20 µg | $410.00 | |||
GPR52 Double Nickase Plasmid (h2) | sc-411266-NIC-2 | 20 µg | $410.00 |
GPR52 encodes an orphan class A G protein–coupled receptor that signals predominantly through Gs to elevate intracellular cAMP and engage PKA/CREB-dependent transcriptional programs. It is enriched in brain regions linked to basal ganglia circuitry, where it modulates neuronal excitability and synaptic signaling downstream of GPCR second-messenger pathways. Through effects on cAMP homeostasis and network activity, GPR52 is frequently studied in the context of neurobiology and pathway cross-talk with dopaminergic signaling. Altered GPCR signaling dynamics involving GPR52 have been investigated in relation to neuropsychiatric and neurodegeneration-associated phenotypes in experimental models.
GPR52 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the GPR52 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within GPR52. 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 GPR52 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 GPR52-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.