α2A-AR Double Nickase Plasmid (m): sc-419023-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- α2A-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
- α2A-AR Double Nickase Plasmid (m) and α2A-AR Double Nickase Plasmid (m2) 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 (m) | sc-419023-NIC | 20 µg | $410.00 |
Adra2a encodes the mouse α2A-adrenergic receptor (α2A-AR), a Gi/o-coupled GPCR that modulates neurotransmitter release and sympathetic tone by inhibiting adenylyl cyclase, reducing cAMP, and tuning ion channel activity. α2A-AR signaling influences presynaptic feedback regulation of catecholamine transmission, with downstream effects on PKA-dependent pathways and neuronal excitability. In peripheral tissues, this receptor participates in autonomic regulation of vascular tone and metabolic homeostasis through GPCR-mediated second messenger control. Dysregulated adrenergic signaling involving ADRA2A has been studied in neurobehavioral phenotypes, stress responsivity, and cardiometabolic trait-associated pathways in mouse models.
α2A-AR Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Adra2a locus in mouse 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.