Renin Receptor CRISPR Activation Plasmid (h): sc-402411-ACT

ATP6AP2 encodes the human renin receptor (also known as (pro)renin receptor), a multifunctional membrane protein that participates in the renin–angiotensin system by binding renin and prorenin and modulating downstream signaling independent of angiotensin generation. Beyond hormone signaling, ATP6AP2 associates with the vacuolar H+-ATPase complex and contributes to endosomal/lysosomal acidification, receptor trafficking, and cellular homeostasis, with reported links to Wnt/β-catenin pathway regulation. Through these roles, the renin receptor influences processes such as cell growth, stress responses, and tissue remodeling. Dysregulated ATP6AP2 expression or function has been associated with cardio-renal and metabolic phenotypes and has also been investigated in contexts including fibrosis, hypertension-related signaling, and tumor biology.

Renin Receptor CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous ATP6AP2 expression without altering the underlying DNA sequence.

Renin Receptor CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the ATP6AP2 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 ATP6AP2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Renin Receptor expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native ATP6AP2 locus and enabling the study of Renin Receptor-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Renin Receptor pathway restoration in tumor cells with silenced or reduced ATP6AP2 expression.

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