Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
DUSP27 CRISPR Activation Plasmid (h): sc-404063-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- DUSP27 CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- DUSP27 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 DUSP27 CRISPR Activation Plasmid (h) and DUSP27 CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the DUPD1 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: DUSP27 Antibody (F-12): sc-515513
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
DUSP27 CRISPR Activation Plasmid (h) | sc-404063-ACT | 20 µg | $397.00 |
DUPD1 encodes the dual specificity phosphatase family member DUSP27, a protein implicated in regulating phosphorylation-dependent signaling by modulating serine/threonine and tyrosine residues on target proteins. DUSP27-associated activity is linked to control of kinase-driven pathways that coordinate cellular differentiation, cytoskeletal organization, and stress-responsive signaling programs. In human tissues, DUSP27 expression has been examined in the context of muscle development and remodeling, where altered phosphatase/kinase balance can influence contractile function and cell-state transitions. Dysregulated DUSP family signaling is broadly relevant to diseases featuring aberrant MAPK-related pathway activity and altered phosphorylation homeostasis, supporting use of DUSP27 perturbation models for mechanistic studies.
DUSP27 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous DUPD1 expression without altering the underlying DNA sequence.
DUSP27 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the DUPD1 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 DUPD1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous DUSP27 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native DUPD1 locus and enabling the study of DUSP27-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of DUSP27 pathway restoration in tumor cells with silenced or reduced DUPD1 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.