
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
α2A-AR CRISPR Activation Plasmid (h) | sc-401545-ACT | 20 µg | $397.00 |
ADRA2A encodes the human α2A-AR, a Gi/o-coupled adrenergic receptor that modulates cellular excitability and secretion by inhibiting adenylyl cyclase, reducing cAMP/PKA signaling, and regulating ion channel activity. Receptor activation also influences MAPK/ERK and β-arrestin–linked pathways, shaping neurotransmitter release and synaptic transmission in the central and peripheral nervous systems. In addition to roles in neuroendocrine and autonomic regulation, ADRA2A signaling impacts metabolic and vascular processes through control of catecholamine-responsive circuits. Dysregulated adrenergic receptor signaling has been associated with neuropsychiatric phenotypes and cardiometabolic traits, supporting its use as a mechanistic target in receptor pharmacology and signal transduction studies.
α2A-AR CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous ADRA2A expression without altering the underlying DNA sequence.
α2A-AR CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the ADRA2A locus in human cell lines. The system is built around a catalytically inactive Cas9 (dCas9) carrying two inactivating mutations (D10A and N863A) that eliminate nuclease activity while preserving DNA binding. This dCas9 is fused to VP64, a potent transcriptional activator, and is co-expressed with a blasticidin resistance gene for selection. The second plasmid encodes the MS2-p65-HSF1 fusion protein, a secondary activator complex that works in concert with dCas9-VP64, alongside a hygromycin resistance gene. The third plasmid encodes a target-specific 20 nt sgRNA fused to two MS2 RNA aptamers that recruit the MS2-p65-HSF1 complex to the activation site, accompanied by a puromycin resistance gene. The three plasmids are delivered at a 1:1:1 mass ratio for balanced expression of all system components.
Once assembled at the target locus, the SAM complex binds within approximately 200 bp upstream of the ADRA2A transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous α2A-AR expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native ADRA2A locus and enabling the study of α2A-AR-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of α2A-AR pathway restoration in tumor cells with silenced or reduced ADRA2A expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.