Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
α1A-AR Double Nickase Plasmid (h): sc-401726-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- α1A-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
- α1A-AR Double Nickase Plasmid (h) and α1A-AR Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ADRA1A. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: α1A-AR Antibody (4D8): sc-100291
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
α1A-AR Double Nickase Plasmid (h) | sc-401726-NIC | 20 µg | $410.00 | |||
α1A-AR Double Nickase Plasmid (h2) | sc-401726-NIC-2 | 20 µg | $410.00 |
ADRA1A encodes the human alpha1A-adrenergic receptor (α1A-AR), a G protein-coupled receptor that primarily couples to Gq/11 to stimulate phospholipase C signaling, inositol trisphosphate-dependent Ca2+ mobilization, and protein kinase C activation. Through these pathways, α1A-AR regulates smooth muscle contraction, vascular tone, and neurotransmission, with downstream effects on MAPK/ERK signaling and broader transcriptional responses. ADRA1A expression and signaling balance contribute to adrenergic control of cardiovascular and urogenital physiology, and dysregulation is relevant to conditions involving altered sympathetic signaling and tissue remodeling. As a cell-surface GPCR with well-defined second-messenger outputs, it is commonly used to study receptor desensitization, biased signaling, and cross-talk with other GPCR and growth factor pathways.
α1A-AR Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ADRA1A locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ADRA1A. 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 ADRA1A 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 ADRA1A-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.