T1R3 Double Nickase Plasmid (h): sc-401808-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- T1R3 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
- T1R3 Double Nickase Plasmid (h) and T1R3 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting TAS1R3. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
T1R3 Double Nickase Plasmid (h) | sc-401808-NIC | 20 µg | $410.00 | |||
T1R3 Double Nickase Plasmid (h2) | sc-401808-NIC-2 | 20 µg | $410.00 |
TAS1R3 encodes the human taste receptor type 1 member 3 (T1R3), a class C GPCR that heterodimerizes with TAS1R1 or TAS1R2 to form umami and sweet nutrient-sensing receptors. Upon ligand binding, T1R3-containing receptors couple to G proteins and stimulate PLCβ2–IP3 signaling, intracellular Ca²⁺ mobilization, and downstream MAPK and secretory programs. Beyond oral taste buds, TAS1R3 expression in gastrointestinal and metabolic tissues links it to enteroendocrine signaling and nutrient-responsive regulation of hormone release and epithelial function. Dysregulated sweet/umami sensing pathways involving T1R3 have been investigated in contexts such as metabolic dysfunction, inflammation, and altered chemosensory signaling in cancer-associated microenvironments.
T1R3 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the TAS1R3 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within TAS1R3. 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 TAS1R3 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 TAS1R3-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.