Rat Prostaglandin E Synthase, Microsomal (PTGES) Protein

Background

Prostaglandin E synthase (PTGES) is an inducible enzyme that catalyzes the conversion of prostaglandin H2 (PGH2) to prostaglandin E2 (PGE2), a bioactive lipid mediator involved in a wide range of physiological and pathological processes, including inflammation, fever, pain perception, and tissue homeostasis. PTGES is typically upregulated in response to pro-inflammatory stimuli such as cytokines (e.g., TNF-α and IL-1β) and oxidative stress, making it a key component of the inflammatory response. It is closely associated with cyclooxygenase-2 (COX-2), as both enzymes are induced during inflammation, and they work in tandem to elevate PGE2 levels. Overexpression of PTGES has been implicated in various diseases, including cancer, rheumatoid arthritis, and cardiovascular disorders, where increased PGE2 production contributes to tumor growth, immune evasion, chronic inflammation, and vascular dysfunction. PTGES is predominantly expressed in the cytoplasm and is regulated by transcriptional and post-translational mechanisms, including phosphorylation. Targeting PTGES has emerged as a potential therapeutic strategy to modulate PGE2 levels while avoiding the side effects associated with COX inhibitors, making it an area of active pharmacological research.