GPR41 Double Nickase Plasmid (h): sc-402190-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- GPR41 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
- GPR41 Double Nickase Plasmid (h) and GPR41 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting FFAR3. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
GPR41 Double Nickase Plasmid (h) | sc-402190-NIC | 20 µg | $410.00 | |||
GPR41 Double Nickase Plasmid (h2) | sc-402190-NIC-2 | 20 µg | $410.00 |
Human FFAR3 encodes the G protein-coupled receptor GPR41, a short-chain fatty acid sensor activated by microbial metabolites such as propionate and butyrate. Upon ligand engagement, GPR41 primarily couples to Gi/o signaling to reduce cAMP and modulate downstream pathways including MAPK/ERK, influencing cellular energy balance, hormone secretion, and immune cell function. FFAR3 activity is implicated in gut–host communication and metabolic regulation, with research links to obesity, insulin sensitivity, and inflammatory processes. Its expression in enteroendocrine and peripheral tissues also supports investigation of neuroendocrine signaling and tissue-specific responses to microbiome-derived cues.
GPR41 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the FFAR3 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within FFAR3. 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 FFAR3 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 FFAR3-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.