GPR91 Double Nickase Plasmid (m): sc-429973-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- GPR91 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
- GPR91 Double Nickase Plasmid (m) and GPR91 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Sucnr1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
GPR91 Double Nickase Plasmid (m) | sc-429973-NIC | 20 µg | $410.00 | |||
GPR91 Double Nickase Plasmid (m2) | sc-429973-NIC-2 | 20 µg | $410.00 |
Mouse Sucnr1 encodes GPR91, a succinate-sensing G protein–coupled receptor that links metabolic stress to inflammatory and vascular signaling. Extracellular succinate produced during hypoxia, ischemia, or mitochondrial dysfunction can activate GPR91 to engage downstream pathways including Gαi/Gαq-mediated signaling, MAPK/ERK activation, intracellular Ca²⁺ flux, and modulation of cAMP, influencing cytokine output and paracrine communication. GPR91 activity has been studied in contexts such as renal physiology and injury responses, retinal angiogenic signaling, adipose tissue inflammation, and immune cell activation, making Sucnr1 a useful node for interrogating immunometabolic regulation. These processes are relevant to experimental models of metabolic syndrome, fibrosis, and inflammatory tissue remodeling where succinate accumulation serves as a signaling cue.
GPR91 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Sucnr1 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Sucnr1. 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 Sucnr1 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 Sucnr1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.