MYEOV2 CRISPR Activation Plasmid (h): sc-409378-ACT

COPS9 (also known as MYEOV2) encodes a component associated with the COP9 signalosome, a conserved regulator of cullin-RING ubiquitin ligases that tunes protein turnover through deneddylation and ubiquitin–proteasome pathways. Through control of ubiquitin-dependent degradation, COPS9/MYEOV2-linked processes influence cell-cycle progression, DNA damage responses, and signal transduction programs including MAPK and NF-κB-associated networks. Dysregulation of COP9 signalosome activity has been connected to aberrant proteostasis and transcriptional rewiring observed in multiple cancer contexts, supporting investigation of COPS9/MYEOV2 in proliferation and stress-adaptation phenotypes. These functions make it a relevant target for mechanistic studies of ubiquitin-mediated regulation and pathway crosstalk in human cells.

MYEOV2 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous COPS9 expression without altering the underlying DNA sequence.

MYEOV2 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the COPS9 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 COPS9 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous MYEOV2 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native COPS9 locus and enabling the study of MYEOV2-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of MYEOV2 pathway restoration in tumor cells with silenced or reduced COPS9 expression.

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