PSA/KLK3/Kallikrein 3/Prostate Specific Antigen CRISPR Activation Plasmid (h): sc-400448-ACT

KLK3 encodes prostate-specific antigen (PSA), a secreted kallikrein-related serine protease that participates in proteolytic processing of seminal plasma proteins and regulation of extracellular protease cascades. PSA/KLK3 expression is strongly regulated by androgen receptor signaling and is tightly linked to prostate epithelial differentiation and luminal cell identity. As a component of tissue remodeling and extracellular matrix–adjacent proteolysis, KLK3 activity intersects with pathways governing secretion, protease activation/inhibition balance, and microenvironmental dynamics. Dysregulated KLK3 transcription is widely used as a molecular readout of androgen-responsive programs and prostate pathophysiology in experimental models.

PSA/KLK3/Kallikrein 3/Prostate Specific Antigen CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous KLK3 expression without altering the underlying DNA sequence.

PSA/KLK3/Kallikrein 3/Prostate Specific Antigen CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the KLK3 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 KLK3 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous PSA/KLK3/Kallikrein 3/Prostate Specific Antigen expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native KLK3 locus and enabling the study of PSA/KLK3/Kallikrein 3/Prostate Specific Antigen-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of PSA/KLK3/Kallikrein 3/Prostate Specific Antigen pathway restoration in tumor cells with silenced or reduced KLK3 expression.

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