cadherin-22 CRISPR Activation Plasmid (h): sc-401942-ACT

CDH22 encodes cadherin-22, a calcium-dependent cell–cell adhesion receptor within the cadherin superfamily that supports tissue architecture through homophilic interactions and coupling to catenins and the actin cytoskeleton. By modulating adherens junction assembly and contact-dependent signaling, cadherin-22 can influence epithelial and neuronal organization, cell polarity, and migratory behavior. Altered cadherin expression patterns are frequently linked to dysregulated adhesion, invasion-associated phenotypes, and remodeling of the tumor microenvironment, making CDH22 a relevant target for mechanistic studies of cell–cell communication. CDH22 expression has also been investigated in lineage specification and differentiation contexts where cadherin-mediated adhesion intersects with developmental programs.

cadherin-22 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous CDH22 expression without altering the underlying DNA sequence.

cadherin-22 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the CDH22 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 CDH22 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous cadherin-22 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native CDH22 locus and enabling the study of cadherin-22-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of cadherin-22 pathway restoration in tumor cells with silenced or reduced CDH22 expression.

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