DUSP5 CRISPR Activation Plasmid (h): sc-401837-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- DUSP5 CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- DUSP5 CRISPR Activation Plasmid (h) consists of three plasmids at a 1:1:1 mass ratio: a plasmid encoding the deactivated Cas9 (dCas9) nuclease (D10A and N863A) fused to the transactivation domain VP64, and a blasticidin resistance gene; a plasmid encoding the MS2-p65-HSF1 fusion protein, and a hygromycin resistance gene; a plasmid encoding a target-specific 20 nt guide RNA fused to two MS2 RNA aptamers, and a puromycin resistance gene
- The resulting SAM complex binds to a site-specific region approximately 200-250 nt upstream of the transcriptional start site and provides robust recruitment of transcription factors for highly efficient gene activation
- gRNAs encoded by DUSP5 CRISPR Activation Plasmid (h) and DUSP5 CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the DUSP5 transcriptional start site. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: DUSP5 Antibody (H-9): sc-393801
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
DUSP5 CRISPR Activation Plasmid (h) | sc-401837-ACT | 20 µg | $397.00 |
Dual specificity protein phosphatase 5 (DUSP5) is a nuclear MAPK phosphatase that dephosphorylates ERK1/2 and functions as a negative-feedback regulator of mitogen-activated signaling. By limiting ERK-driven transcriptional programs, DUSP5 influences cell-cycle progression, differentiation, and stress-response signaling downstream of receptor tyrosine kinases and RAS–RAF–MEK pathways. Altered DUSP5 expression or activity has been associated with dysregulated MAPK/ERK output in diverse biological contexts, including inflammation and tumor biology. As a pathway “brake,” DUSP5 is frequently examined as a modulator of signal amplitude and duration in stimulus-dependent gene expression.
DUSP5 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous DUSP5 expression without altering the underlying DNA sequence.
DUSP5 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the DUSP5 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 DUSP5 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous DUSP5 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native DUSP5 locus and enabling the study of DUSP5-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of DUSP5 pathway restoration in tumor cells with silenced or reduced DUSP5 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.