GPR4 Double Nickase Plasmid (h): sc-403659-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- GPR4 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
- GPR4 Double Nickase Plasmid (h) and GPR4 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting GPR4. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
GPR4 Double Nickase Plasmid (h) | sc-403659-NIC | 20 µg | $410.00 | |||
GPR4 Double Nickase Plasmid (h2) | sc-403659-NIC-2 | 20 µg | $410.00 |
GPR4 encodes a proton-sensing G protein–coupled receptor that functions as an extracellular pH sensor, coupling acidic microenvironment cues to intracellular second messenger signaling. Upon activation, GPR4 can engage Gs and G13 pathways to modulate cAMP production and Rho-dependent cytoskeletal dynamics, influencing endothelial barrier function, leukocyte trafficking, and inflammatory gene expression. This pH-responsive signaling integrates with vascular and immune regulatory processes that are frequently perturbed in hypoxia- and acidosis-associated tissue settings. Dysregulated GPR4 activity has been investigated in relation to inflammation and vascular dysfunction, providing a mechanistic link between microenvironmental acidity and disease-relevant cellular phenotypes.
GPR4 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the GPR4 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within GPR4. 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 GPR4 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 GPR4-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.