cadherin-24 CRISPR Activation Plasmid (h): sc-401990-ACT

CDH24 encodes cadherin-24, a calcium-dependent cell–cell adhesion protein that contributes to the organization and stability of epithelial contacts through cadherin-mediated adherens junctions. By supporting homophilic interactions at the plasma membrane and coupling to cytoskeletal networks via catenin-associated complexes, cadherin-24 can influence tissue architecture, polarity, and contact-dependent signaling. Altered cadherin expression patterns are frequently linked to changes in cellular cohesion and migratory behavior, making CDH24 a useful target for studying adhesion remodeling in development and disease-associated phenotypes. CDH24 dysregulation has been investigated in contexts where epithelial integrity and junctional signaling are perturbed, providing a functional entry point for mechanistic studies of cell adhesion pathways.

cadherin-24 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous CDH24 expression without altering the underlying DNA sequence.

cadherin-24 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the CDH24 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 CDH24 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous cadherin-24 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native CDH24 locus and enabling the study of cadherin-24-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of cadherin-24 pathway restoration in tumor cells with silenced or reduced CDH24 expression.

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