GPR35 Double Nickase Plasmid (h): sc-416792-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- GPR35 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
- GPR35 Double Nickase Plasmid (h) and GPR35 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting GPR35. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
GPR35 Double Nickase Plasmid (h) | sc-416792-NIC | 20 µg | $410.00 | |||
GPR35 Double Nickase Plasmid (h2) | sc-416792-NIC-2 | 20 µg | $410.00 |
GPR35 encodes a rhodopsin-like G protein–coupled receptor that is enriched in immune and gastrointestinal tissues and couples predominantly to Gi/o- and β-arrestin–linked signaling. Receptor activation modulates second-messenger pathways that converge on MAPK/ERK signaling, calcium flux, and chemotactic programs, influencing cytokine production and leukocyte trafficking. GPR35 has been studied in the context of mucosal inflammation and barrier regulation, and its expression is reported in multiple tumor microenvironments where it may shape metabolic and inflammatory signaling. These properties make GPR35 a useful target for dissecting GPCR-driven immunoregulation, epithelial responses, and microenvironmental crosstalk in human cell models.
GPR35 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the GPR35 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within GPR35. 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 GPR35 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 GPR35-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.