DSC1 CRISPR Activation Plasmid (h): sc-402944-ACT

Human DSC1 encodes desmocollin-1, a calcium-dependent cadherin family adhesion protein localized to desmosomes in stratified epithelia. DSC1 supports strong intercellular junctions by engaging desmosomal cadherin interactions and coupling to plakoglobin, plakophilins, and desmoplakin to anchor intermediate filaments, thereby contributing to epidermal barrier integrity and tissue mechanics. Its expression is tightly linked to keratinocyte differentiation programs and epithelial morphogenesis, and altered DSC1 regulation is studied in the context of compromised cell–cell adhesion, epithelial dysplasia, and tumor biology. Because desmosome remodeling interfaces with cytoskeletal dynamics and stress signaling, DSC1 is frequently investigated in pathways governing epithelial cohesion, differentiation, and migration.

DSC1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous DSC1 expression without altering the underlying DNA sequence.

DSC1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the DSC1 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 DSC1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous DSC1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native DSC1 locus and enabling the study of DSC1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of DSC1 pathway restoration in tumor cells with silenced or reduced DSC1 expression.

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