
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
DUSP8 CRISPR Activation Plasmid (h) | sc-404385-ACT | 20 µg | $397.00 |
Dual specificity protein phosphatase 8 (DUSP8) is a MAP kinase phosphatase that dephosphorylates activated MAPKs, with prominent regulatory roles in stress-responsive signaling through the JNK and p38 MAPK pathways. By tuning the amplitude and duration of MAPK phosphorylation, DUSP8 influences transcriptional programs controlling proliferation, apoptosis, differentiation, and inflammatory responses. DUSP8-mediated feedback regulation is relevant to contexts where MAPK signaling is rewired, including cancer biology and neuroinflammatory or neurodegenerative processes, and it is commonly interrogated as a node linking extracellular stress cues to nuclear gene expression.
DUSP8 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous DUSP8 expression without altering the underlying DNA sequence.
DUSP8 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the DUSP8 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 DUSP8 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous DUSP8 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native DUSP8 locus and enabling the study of DUSP8-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of DUSP8 pathway restoration in tumor cells with silenced or reduced DUSP8 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.