Adenosine A3-R Double Nickase Plasmid (m): sc-419016-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Adenosine A3-R 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
- Adenosine A3-R Double Nickase Plasmid (m) and Adenosine A3-R Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Adora3. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Adenosine A3-R Double Nickase Plasmid (m) | sc-419016-NIC | 20 µg | $410.00 |
Mouse Adora3 encodes the adenosine A3 receptor (Adenosine A3-R), a Gi/o-coupled GPCR that senses extracellular adenosine and modulates intracellular cAMP, MAPK/ERK signaling, and PI3K-associated survival pathways. A3-R activation also influences phospholipase C signaling, Ca2+ mobilization, and the balance of pro- and anti-inflammatory mediator release in immune and stromal compartments. In murine systems, Adora3 is commonly studied in the context of hypoxia and tissue stress where adenosine accumulates, shaping leukocyte recruitment, vascular tone, and barrier function. Dysregulated adenosine receptor signaling has been linked to inflammatory disease mechanisms, nociceptive processing, and tumor–immune microenvironment biology, making Adora3 a useful node for pathway dissection.
Adenosine A3-R Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Adora3 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Adora3. 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 Adora3 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 Adora3-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.