GPR40 Double Nickase Plasmid (h): sc-401434-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- GPR40 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
- GPR40 Double Nickase Plasmid (h) and GPR40 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting FFAR1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
GPR40 Double Nickase Plasmid (h) | sc-401434-NIC | 20 µg | $410.00 | |||
GPR40 Double Nickase Plasmid (h2) | sc-401434-NIC-2 | 20 µg | $410.00 |
FFAR1 encodes GPR40, a lipid-sensing class A GPCR highly responsive to medium- and long-chain free fatty acids. Upon activation, GPR40 couples primarily to Gαq/11 to stimulate phospholipase C signaling, elevate intracellular Ca2+, and engage PKC-dependent pathways that modulate stimulus–secretion coupling and broader metabolic signaling networks. In human tissues, FFAR1 activity is tightly linked to nutrient-driven regulation of endocrine and metabolic homeostasis, with research connections to β-cell function, insulin secretory dynamics, and lipid-induced signaling adaptation. Dysregulated fatty-acid sensing and downstream Ca2+-dependent signaling have been studied in the context of metabolic disease mechanisms, including type 2 diabetes and obesity-associated insulin resistance, as well as inflammation-linked metabolic remodeling.
GPR40 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the FFAR1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within FFAR1. 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 FFAR1 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 FFAR1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.