α1B-AR Double Nickase Plasmid (h): sc-403295-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- α1B-AR 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
- α1B-AR Double Nickase Plasmid (h) and α1B-AR Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ADRA1B. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
α1B-AR Double Nickase Plasmid (h) | sc-403295-NIC | 20 µg | $410.00 | |||
α1B-AR Double Nickase Plasmid (h2) | sc-403295-NIC-2 | 20 µg | $410.00 |
ADRA1B encodes the human α1B-adrenergic receptor (α1B-AR), a G protein–coupled receptor that preferentially couples to Gq/11 to stimulate phospholipase C signaling, inositol phosphate production, intracellular Ca2+ mobilization, and protein kinase C activation. Through these pathways, α1B-AR influences vascular smooth muscle tone, neurotransmission, and broader sympathetic regulation of cell excitability and contractility, with downstream engagement of MAPK/ERK and other stress-responsive signaling networks. Altered adrenergic receptor signaling has been implicated in cardiovascular and neuropsychiatric biology, making ADRA1B a useful locus for mechanistic studies of GPCR signaling, receptor desensitization/internalization, and pathway-biased responses in relevant cellular models.
α1B-AR Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ADRA1B locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ADRA1B. 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 ADRA1B 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 ADRA1B-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.