
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
KLK5 CRISPR Activation Plasmid (h) | sc-404042-ACT | 20 µg | $397.00 |
Kallikrein-related peptidase 5 (KLK5) is a secreted trypsin-like serine protease that participates in extracellular proteolytic cascades controlling epidermal desquamation, barrier homeostasis, and innate defense. KLK5 regulates processing of structural proteins and activates other kallikreins, contributing to pericellular matrix remodeling and signaling through protease-activated receptors (PARs). Dysregulated KLK5 activity has been linked to inflammatory skin phenotypes and altered epithelial differentiation, and KLK5 expression is frequently studied as a marker of epithelial state and microenvironmental remodeling. In cancer biology and dermatology research, KLK5 is used to investigate protease-driven changes in invasion, cytokine signaling, and barrier-associated pathways.
KLK5 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous KLK5 expression without altering the underlying DNA sequence.
KLK5 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the KLK5 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 KLK5 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous KLK5 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native KLK5 locus and enabling the study of KLK5-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of KLK5 pathway restoration in tumor cells with silenced or reduced KLK5 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.