
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
DEK Lentiviral Activation Particles (h) | sc-402862-LAC | 200 µl | $455.00 |
DEK encodes a conserved chromatin-associated phosphoprotein that modulates higher-order chromatin architecture, influences nucleosome topology, and participates in transcriptional control, RNA processing, and DNA replication. It is recruited to sites of DNA damage and contributes to genome stability through effects on repair pathway choice, replication stress responses, and cell-cycle progression. Through these activities, DEK interfaces with pathways governing chromatin remodeling, DNA damage signaling, and inflammatory transcriptional programs. Altered DEK expression and dysregulated chromatin function have been associated with proliferative and stress-adaptation phenotypes relevant to oncology and immune-mediated disease models.
DEK Lentiviral Activation Particles (h) address this need by packaging the complete synergistic activation mediator (SAM) transcriptional activation system into transduction-ready, high-titer lentiviral particles, enabling efficient DEK upregulation across a broader range of human cell types.
DEK Lentiviral Activation Particles (h) deliver all functional components of the synergistic activation mediator (SAM) system via lentiviral transduction. The system comprises three particle preparations co-transduced into target cells: one encoding catalytically inactive dCas9 (D10A and N863A mutations) fused to the VP64 transactivation domain with a blasticidin resistance gene; one encoding the MS2-p65-HSF1 fusion protein with a hygromycin resistance gene; and one encoding a target-specific 20 nt sgRNA fused to two MS2 RNA aptamers with a puromycin resistance gene. Following lentiviral transduction and genomic integration of the expression cassettes, the SAM components are stably expressed and assemble at the target locus within the proximal promoter region upstream of the DEK transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous DEK expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native DEK genomic locus and regulatory architecture.
The lentiviral format offers several practical advantages: stable genomic integration supports heritable activation across cell divisions; high-titer particle preparations eliminate the need for in-house viral production; and compatibility with primary, non-dividing, and transfection-resistant cell types expands experimental accessibility. Successful transduction can be confirmed and enriched through triple antibiotic selection using puromycin, hygromycin, and blasticidin.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.