AT2/Angiotensin Receptor 2/AGTR2 CRISPR Activation Plasmid (h): sc-418156-ACT

AGTR2 encodes the angiotensin II type 2 receptor (AT2), a seven-transmembrane GPCR in the renin–angiotensin system that counterbalances AT1-driven signaling. Upon angiotensin II binding, AT2 modulates G protein–coupled and β-arrestin–linked pathways and is frequently associated with nitric oxide/cGMP signaling, phosphatase activation, and regulation of MAPK activity, shaping cellular programs that influence differentiation, neurite outgrowth, inflammation, and tissue remodeling. AGTR2 expression and signaling are studied in vascular biology and developmental contexts, and are frequently interrogated in models of hypertension-associated remodeling, cardiovascular injury responses, kidney disease mechanisms, and cancer cell signaling crosstalk. Because receptor output is highly context-dependent, controlled perturbation of endogenous AGTR2 levels is useful for dissecting pathway bias and receptor–ligand dynamics in relevant cell types.

AT2/Angiotensin Receptor 2/AGTR2 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous AGTR2 expression without altering the underlying DNA sequence.

AT2/Angiotensin Receptor 2/AGTR2 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the AGTR2 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 AGTR2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous AT2/Angiotensin Receptor 2/AGTR2 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native AGTR2 locus and enabling the study of AT2/Angiotensin Receptor 2/AGTR2-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of AT2/Angiotensin Receptor 2/AGTR2 pathway restoration in tumor cells with silenced or reduced AGTR2 expression.

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