Corin CRISPR Activation Plasmid (h): sc-404362-ACT

Human CORIN encodes corin, a type II transmembrane serine protease expressed prominently in cardiomyocytes where it proteolytically activates pro-atrial natriuretic peptide and pro-brain natriuretic peptide into mature natriuretic hormones. Through this natriuretic peptide processing axis, corin influences cGMP-dependent signaling, sodium and water homeostasis, vascular tone, and cardiac remodeling responses to hemodynamic stress. CORIN activity interfaces with extracellular proteolysis and membrane-anchored protease regulation, impacting downstream transcriptional programs that shape hypertrophic and fibrotic pathways. Genetic and expression alterations in CORIN have been associated with dysregulated natriuretic peptide signaling and cardiovascular phenotypes, supporting its relevance in mechanistic studies of cardiac function and blood pressure regulation.

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

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

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