SENP1 CRISPR Activation Plasmid (h): sc-417768-ACT

Human SENP1 (sentrin-specific protease 1) is a SUMO protease that removes SUMO modifications from target proteins, thereby regulating SUMOylation-dependent control of protein stability, localization, and transcriptional activity. Through dynamic deSUMOylation, SENP1 influences nuclear–cytoplasmic signaling, cell-cycle progression, DNA damage responses, and stress-adaptive transcriptional programs, including pathways linked to hypoxia and metabolic regulation. Altered SENP1 activity has been associated with dysregulated transcription factor signaling, aberrant proliferation, and changes in proteostasis that are frequently explored in cancer biology and other conditions characterized by perturbed SUMO pathway homeostasis.

SENP1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous SENP1 expression without altering the underlying DNA sequence.

SENP1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the SENP1 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 SENP1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous SENP1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native SENP1 locus and enabling the study of SENP1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of SENP1 pathway restoration in tumor cells with silenced or reduced SENP1 expression.

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