Adenosine A2B-R Double Nickase Plasmid (h): sc-401402-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Adenosine A2B-R 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
- Adenosine A2B-R Double Nickase Plasmid (h) and Adenosine A2B-R Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ADORA2B. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Adenosine A2B-R Double Nickase Plasmid (h) | sc-401402-NIC | 20 µg | $410.00 | |||
Adenosine A2B-R Double Nickase Plasmid (h2) | sc-401402-NIC-2 | 20 µg | $410.00 |
ADORA2B encodes the human adenosine A2B receptor (A2B-R), a low-affinity G protein–coupled receptor that senses elevated extracellular adenosine in metabolically stressed tissues. A2B-R primarily couples to Gs to increase cAMP/PKA signaling and can also engage Gq/PLC pathways, shaping transcriptional programs via CREB and other downstream effectors. This receptor modulates vascular tone and permeability, inflammatory mediator release, immune cell trafficking, and fibroblast activation, linking purinergic signaling to tissue remodeling. Dysregulated ADORA2B activity has been implicated in hypoxia- and inflammation-associated processes relevant to airway disease, ischemic injury, fibrosis, and tumor microenvironment biology.
Adenosine A2B-R Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ADORA2B locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ADORA2B. 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 ADORA2B 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 ADORA2B-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.