T2R38 Double Nickase Plasmid (m): sc-436483-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- T2R38 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
- T2R38 Double Nickase Plasmid (m) and T2R38 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Tas2r138. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
T2R38 Double Nickase Plasmid (m) | sc-436483-NIC | 20 µg | $410.00 | |||
T2R38 Double Nickase Plasmid (m2) | sc-436483-NIC-2 | 20 µg | $410.00 |
Mouse Tas2r138 encodes the bitter taste receptor T2R38, a GPCR that detects thiourea-related bitter ligands and couples to G protein signaling to modulate intracellular Ca²⁺ dynamics and downstream second-messenger pathways. Beyond gustatory perception, T2R family receptors are expressed in extraoral tissues where they can influence chemosensory responses and cellular signaling programs linked to epithelial and immune function. Tas2r138 variation and altered receptor signaling are often studied in the context of sensory biology and chemoreception, with broader relevance to mechanisms by which GPCR signaling shapes tissue-level responses. As a tractable receptor-encoding locus, Tas2r138 supports pathway-focused studies of GPCR activation, signal transduction, and receptor-dependent transcriptional adaptations.
T2R38 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Tas2r138 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Tas2r138. 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 Tas2r138 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 Tas2r138-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.