SENP3 CRISPR Activation Plasmid (h): sc-403747-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SENP3 CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- SENP3 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 SENP3 CRISPR Activation Plasmid (h) and SENP3 CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the SENP3 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: SENP3 Antibody (E-7): sc-137219
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SENP3 CRISPR Activation Plasmid (h) | sc-403747-ACT | 20 µg | $397.00 |
Human SENP3 encodes a SUMO-specific protease that preferentially removes SUMO2/3 modifications, thereby reshaping the SUMOylation landscape that regulates protein stability, localization, and macromolecular complex assembly. SENP3 activity is linked to nucleolar homeostasis and ribosome biogenesis, and it modulates transcriptional programs and stress-responsive signaling through dynamic deSUMOylation of nuclear substrates. By influencing SUMO-dependent control of cell cycle progression, genome maintenance, and inflammatory signaling, SENP3 is studied in contexts where proteostasis and nuclear organization are perturbed. Dysregulated SENP3 expression or activity has been associated with cancer biology, neurodegenerative processes, and cardiometabolic and inflammatory phenotypes, supporting its use as a mechanistic node in pathway-focused research.
SENP3 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous SENP3 expression without altering the underlying DNA sequence.
SENP3 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the SENP3 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 SENP3 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous SENP3 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native SENP3 locus and enabling the study of SENP3-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of SENP3 pathway restoration in tumor cells with silenced or reduced SENP3 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.