PGD2 synthase CRISPR Activation Plasmid (h): sc-402272-ACT

PTGDS encodes prostaglandin D2 synthase (PGD2 synthase), an enzyme that catalyzes conversion of PGH2 to prostaglandin D2, a bioactive lipid mediator in the arachidonic acid/eicosanoid pathway. PGD2 signaling influences inflammatory tone, vascular and smooth muscle responses, sleep–wake regulation, and immune cell chemotaxis through downstream prostanoid receptors and related lipid networks. PTGDS expression is prominent in tissues such as brain and meninges and can modulate local prostaglandin balance that shapes neuroinflammatory and barrier-associated processes. Dysregulated prostaglandin production and PTGDS-associated pathways are studied in contexts including allergic inflammation, neuroinflammation, and tumor microenvironment biology where lipid mediators affect cell state and intercellular signaling.

PGD2 synthase CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous PTGDS expression without altering the underlying DNA sequence.

PGD2 synthase CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the PTGDS 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 PTGDS transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous PGD2 synthase expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native PTGDS locus and enabling the study of PGD2 synthase-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of PGD2 synthase pathway restoration in tumor cells with silenced or reduced PTGDS expression.

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