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 (m): sc-419021-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- α1A-AR 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
- α1A-AR Double Nickase Plasmid (m) and α1A-AR Double Nickase Plasmid (m2) 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 (m) | sc-419021-NIC | 20 µg | $410.00 |
Adra1a encodes the mouse α1A-adrenergic receptor (α1A-AR), a G protein–coupled receptor that primarily couples to Gq/11 to stimulate phospholipase C signaling, inositol phosphate production, intracellular Ca2+ mobilization, and PKC activation. Through these pathways, α1A-AR regulates smooth muscle tone, vascular reactivity, and sympathetic neurotransmission, and can engage downstream MAPK/ERK signaling to influence cellular proliferation and stress responses. In the nervous system and peripheral organs, Adra1a activity integrates catecholamine cues with ion channel function and contractile machinery. Dysregulated adrenergic signaling involving α1A-AR has been implicated in cardiovascular and autonomic phenotypes as well as context-dependent roles in neurophysiology, making Adra1a a useful target for dissecting GPCR-driven signaling networks.
α1A-AR Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Adra1a locus in mouse 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.