beta 1 Adrenergic Receptor/ADRB1/β₁-AR CRISPR Activation Plasmid (h): sc-400660-ACT

ADRB1 encodes the human β1-adrenergic receptor (β1-AR), a G protein–coupled receptor that primarily couples to Gs to stimulate adenylyl cyclase, elevate cAMP, and activate PKA-dependent signaling. This pathway regulates cardiac chronotropy and inotropy, modulates calcium handling, and influences transcriptional responses through downstream effectors such as CREB. β1-AR signaling intersects with GPCR desensitization and trafficking mechanisms, including GRK/β-arrestin–mediated phosphorylation, internalization, and receptor resensitization. Dysregulated ADRB1 expression or signaling is implicated in cardiovascular pathophysiology and provides a mechanistic entry point for studying stress-responsive signaling networks and receptor pharmacology in human cells.

beta 1 Adrenergic Receptor/ADRB1/β1-AR CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous ADRB1 expression without altering the underlying DNA sequence.

beta 1 Adrenergic Receptor/ADRB1/β1-AR CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the ADRB1 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 ADRB1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous beta 1 Adrenergic Receptor/ADRB1/β1-AR expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native ADRB1 locus and enabling the study of beta 1 Adrenergic Receptor/ADRB1/β1-AR-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of beta 1 Adrenergic Receptor/ADRB1/β1-AR pathway restoration in tumor cells with silenced or reduced ADRB1 expression.

For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.