DEK CRISPR Activation Plasmid (h): sc-402862-ACT

DEK (human) encodes a conserved chromatin-associated phosphoprotein that binds DNA and RNA to regulate chromatin architecture, transcriptional control, and mRNA splicing. It participates in processes linked to DNA replication stress responses, double-strand break repair, and maintenance of genome stability, supporting cell-cycle progression and proliferation programs. DEK activity intersects with epigenetic regulation and inflammatory transcriptional networks, and altered expression has been associated with oncogenic signaling contexts and dysregulated differentiation. As a nuclear regulator with broad effects on gene expression, DEK is frequently studied for its roles in transformation biology, hematopoietic and epithelial cell models, and stress-adaptive transcriptional states.

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

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

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