CysLT1 Receptor Double Nickase Plasmid (h): sc-416516-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CysLT1 Receptor 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
- CysLT1 Receptor Double Nickase Plasmid (h) and CysLT1 Receptor Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CYSLTR1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CysLT1 Receptor Double Nickase Plasmid (h) | sc-416516-NIC | 20 µg | $410.00 | |||
CysLT1 Receptor Double Nickase Plasmid (h2) | sc-416516-NIC-2 | 20 µg | $410.00 |
CYSLTR1 encodes the human cysteinyl leukotriene receptor 1 (CysLT1 receptor), a class A GPCR that binds LTC4, LTD4, and LTE4 to initiate Gαq/PLCβ signaling, intracellular Ca2+ mobilization, and downstream MAPK activation. Receptor engagement promotes inflammatory cell activation, smooth muscle contraction, and modulation of vascular permeability, linking CYSLTR1 to leukotriene-driven innate and adaptive immune responses. CYSLTR1 activity integrates with arachidonic acid metabolism and eicosanoid signaling networks and can influence cytokine production and chemotaxis. Dysregulated CysLT1 receptor signaling has been associated with chronic inflammatory phenotypes, airway hyperresponsiveness, and tumor-associated inflammation, making it a useful target for mechanistic studies of leukotriene pathways.
CysLT1 Receptor Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CYSLTR1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CYSLTR1. 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 CYSLTR1 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 CYSLTR1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.