α2A-AR Double Nickase Plasmid (h): sc-401545-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- α2A-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
- α2A-AR Double Nickase Plasmid (h) and α2A-AR Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ADRA2A. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
α2A-AR Double Nickase Plasmid (h) | sc-401545-NIC | 20 µg | $410.00 | |||
α2A-AR Double Nickase Plasmid (h2) | sc-401545-NIC-2 | 20 µg | $410.00 |
ADRA2A encodes the human α2A-adrenergic receptor (α2A-AR), a Gi/o-coupled GPCR that modulates neurotransmitter release and sympathetic tone by inhibiting adenylyl cyclase, lowering intracellular cAMP, and regulating Ca2+ and K+ channel activity. α2A-AR signaling integrates with MAPK/ERK and PLC-linked pathways to shape synaptic transmission, vascular reactivity, and endocrine secretory responses in a cell-type-dependent manner. Dysregulation of ADRA2A expression or receptor signaling has been studied in the context of neuropsychiatric phenotypes, autonomic and cardiovascular physiology, and metabolic traits including insulin secretion dynamics.
α2A-AR Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ADRA2A locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ADRA2A. 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 ADRA2A 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 ADRA2A-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.