α1B-AR CRISPR Activation Plasmid (h): sc-403295-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- α1B-AR CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- α1B-AR CRISPR Activation Plasmid (h) consists of three plasmids at a 1:1:1 mass ratio: a plasmid encoding the deactivated Cas9 (dCas9) nuclease (D10A and N863A) fused to the transactivation domain VP64, and a blasticidin resistance gene; a plasmid encoding the MS2-p65-HSF1 fusion protein, and a hygromycin resistance gene; a plasmid encoding a target-specific 20 nt guide RNA fused to two MS2 RNA aptamers, and a puromycin resistance gene
- The resulting SAM complex binds to a site-specific region approximately 200-250 nt upstream of the transcriptional start site and provides robust recruitment of transcription factors for highly efficient gene activation
- gRNAs encoded by α1B-AR CRISPR Activation Plasmid (h) and α1B-AR CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the ADRA1B transcriptional start site. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
α1B-AR CRISPR Activation Plasmid (h) | sc-403295-ACT | 20 µg | $397.00 |
ADRA1B encodes the human α1B-AR (alpha-1B adrenergic receptor), a catecholamine-responsive GPCR that couples primarily to Gq/11 proteins to activate phospholipase C, inositol phosphate signaling, intracellular Ca2+ mobilization, and protein kinase C-dependent pathways. Receptor activation can also engage MAPK/ERK signaling and regulate cytoskeletal dynamics, secretion, and contractile responses in adrenergically innervated tissues. α1B-AR contributes to control of vascular tone and smooth muscle reactivity, and it influences neuronal excitability and stress-responsive signaling. Dysregulated adrenergic signaling involving ADRA1B is studied in the context of cardiovascular physiology, neuropsychiatric phenotypes, and altered proliferative signaling in model systems.
α1B-AR CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous ADRA1B expression without altering the underlying DNA sequence.
α1B-AR CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the ADRA1B 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 ADRA1B transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous α1B-AR expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native ADRA1B locus and enabling the study of α1B-AR-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of α1B-AR pathway restoration in tumor cells with silenced or reduced ADRA1B expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.