hDcp2 CRISPR Activation Plasmid (h): sc-418511-ACT

Human DCP2 encodes hDcp2, an mRNA decapping enzyme that removes the 5′ cap to initiate 5′→3′ mRNA decay, shaping transcript turnover and proteome dynamics. hDcp2 functions within cytoplasmic mRNA processing bodies and interfaces with decapping cofactors and exonucleases to regulate RNA surveillance, stress-responsive gene expression, and quality-control pathways such as nonsense-mediated decay. By modulating stability of specific mRNA subsets, DCP2 influences cell-cycle control, differentiation programs, and inflammatory signaling outputs. Dysregulated mRNA decay and processing-body dynamics linked to altered decapping activity are relevant to mechanisms studied in cancer biology, neurobiology, and viral host–RNA interactions.

hDcp2 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous DCP2 expression without altering the underlying DNA sequence.

hDcp2 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the DCP2 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 DCP2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous hDcp2 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native DCP2 locus and enabling the study of hDcp2-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of hDcp2 pathway restoration in tumor cells with silenced or reduced DCP2 expression.

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