P23 CRISPR Activation Plasmid (h): sc-402670-ACT

Human PTGES3 encodes p23, a conserved HSP90 co-chaperone that stabilizes client protein complexes and modulates ATPase cycling to support protein maturation and signal transduction. p23 is best known for regulating steroid hormone receptor assembly and nuclear signaling, and it also participates in broader proteostasis networks that influence cell stress responses and transcriptional control. Through its integration with chaperone-dependent pathways, PTGES3 can affect cellular proliferation, differentiation, and adaptive responses to proteotoxic stress. Altered chaperone/co-chaperone balance and dysregulated receptor signaling have been associated with disease-relevant phenotypes, including cancer biology and inflammatory signaling contexts, making PTGES3 a useful node for mechanistic studies.

P23 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous PTGES3 expression without altering the underlying DNA sequence.

P23 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the PTGES3 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 PTGES3 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous P23 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native PTGES3 locus and enabling the study of P23-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of P23 pathway restoration in tumor cells with silenced or reduced PTGES3 expression.

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