PTGES
PTGES (prostaglandin E synthase, also known as mPGES-1, MGST-IV and PIG12) is a glutathione-dependent membrane enzyme of the MAPEG family. It is the terminal enzyme of the COX-2-mediated prostaglandin E2 biosynthetic pathway and acts in inflammation, fever and pain. Browse Assay Genie's current range of PTGES research reagents below, or read on for the biology behind the target.
PTGES catalyses the glutathione-dependent oxidoreduction of prostaglandin endoperoxide H2 (PGH2) to prostaglandin E2 (PGE2) in response to inflammatory stimuli. It is the terminal enzyme of the cyclooxygenase (COX)-2-mediated PGE2 pathway. The enzyme also converts PGH3, derived from eicosapentaenoate, to PGE3, although PGH2 remains the preferred substrate. Beyond this, it catalyses the oxidoreduction of endocannabinoids into prostaglandin glycerol esters and of PGG2 into 15-hydroperoxy-PGE2, and shows low glutathione transferase and glutathione-dependent peroxidase activities towards 1-chloro-2,4-dinitrobenzene and 5-hydroperoxyicosatetraenoic acid (5-HPETE). UniProt records a key role for the enzyme in the inflammatory response, fever and pain.
The PTGES gene encodes a protein of the MAPEG superfamily, and HGNC places it in the prostaglandin E synthase gene group. UniProt lists the protein in the membrane and in the perinuclear region of the cytoplasm. Researchers working with the PTGES protein will also meet it under the names mPGES-1, MGST-IV, PIG12, MGST1-L1, TP53I12 and MGST1L1. Mouse and rat both carry a Ptges ortholog.
NCBI Gene reports that PTGES expression is induced by the proinflammatory cytokine interleukin 1 beta (IL1B). It can also be induced by the tumour suppressor TP53, and the enzyme may be involved in TP53-induced apoptosis. Knockout studies in mice suggest that the gene may contribute to the pathogenesis of collagen-induced arthritis and mediate acute pain during inflammatory responses. These links make it a frequent subject in studies of inflammatory signalling and lipid mediators.
PTGES acts as the terminal enzyme of COX-2-mediated PGE2 synthesis and responds to inflammatory stimuli, including induction by IL-1 beta.
UniProt assigns PTGES a key role in fever and pain, and mouse knockout data suggest it mediates acute pain during inflammation.
Knockout studies in mice suggest PTGES contributes to the pathogenesis of collagen-induced arthritis.
PTGES converts PGH2 to PGE2 and PGH3 to PGE3, and also acts on endocannabinoids and PGG2.
PTGES is the terminal enzyme of the COX-2-mediated prostaglandin E2 pathway. It catalyses the glutathione-dependent conversion of PGH2 to PGE2 in response to inflammatory stimuli. UniProt assigns it a key role in inflammation, fever and pain.
Aliases include mPGES-1, MGST-IV, PIG12, MGST1-L1, TP53I12 and MGST1L1. The HGNC name is prostaglandin E synthase. The enzyme belongs to the MAPEG family and carries EC number 5.3.99.3. Gene and protein searches may use any of these names.
Mouse and rat both have a Ptges ortholog. NCBI Gene notes that mouse knockout studies suggest a contribution to collagen-induced arthritis and to acute pain during inflammatory responses. Check the datasheet of any product for its validated reactivity.
Other prostaglandin E synthases, upstream COX-2 pathway members and regulators of PTGES expression with products at Assay Genie.
Gene and protein annotations from HGNC, NCBI Gene and UniProt O14684; product specifications from Assay Genie datasheets.