beta 2 Adrenergic Receptor/ADRB2/β2-AR Double Nickase Plasmid (h): sc-400291-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- beta 2 Adrenergic Receptor/ADRB2/β2-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
- beta 2 Adrenergic Receptor/ADRB2/β2-AR Double Nickase Plasmid (h) and beta 2 Adrenergic Receptor/ADRB2/β2-AR Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ADRB2. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: beta 2 Adrenergic Receptor/ADRB2/β2-AR Antibody (E-3): sc-271322
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
beta 2 Adrenergic Receptor/ADRB2/β2-AR Double Nickase Plasmid (h) | sc-400291-NIC | 20 µg | $410.00 | |||
beta 2 Adrenergic Receptor/ADRB2/β2-AR Double Nickase Plasmid (h2) | sc-400291-NIC-2 | 20 µg | $410.00 |
ADRB2 encodes the human β2-adrenergic receptor (β2-AR), a G protein–coupled receptor that senses catecholamines and couples primarily to Gs to elevate cAMP and activate PKA-dependent signaling. Through regulation of adenylate cyclase activity, receptor desensitization via GRKs and β-arrestins, and downstream transcriptional programs, ADRB2 influences smooth muscle tone, cardiac and skeletal muscle metabolism, and immune cell signaling. β2-AR also engages receptor internalization and trafficking processes that shape signal duration and bias, integrating with MAPK and calcium-linked pathways in a context-dependent manner. Dysregulated ADRB2 signaling or expression has been studied in asthma and airway hyperresponsiveness, cardiovascular physiology, metabolic phenotypes, and stress-associated neuroimmune modulation, making it a widely used node for pathway and pharmacology research.
beta 2 Adrenergic Receptor/ADRB2/β2-AR Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ADRB2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ADRB2. 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 ADRB2 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 ADRB2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.