What is the substrate of the enzyme PGH2 synthase?

PGH2 serves as a substrate for cell- and tissue-selective prostanoid synthases and isomerases that produce numerous bioactive prostanoids: prostaglandins D2, E2, F2α, I2, and thromboxane A2.

Which of the following two cyclooxygenase isoenzyme is constitutively expressed?

Two isoforms of COX, COX-1 and COX-2, have been identified by molecular biological methods. The amino acid sequence homology between COX-1 and COX-2 is about 60% for the human enzymes. COX-1 is constitutively expressed in most tissues and cells in animal species.

What does prostaglandin synthase do?

Prostaglandin H synthase (PGHS) is a rate-limiting enzyme in the production of prostaglandins and thromboxane, which are important regulators of vascular function. Under normal physiological conditions, PGHS-dependent vasodilators (such as prostacyclin) modulate vascular tone.

What kind of enzyme is prostaglandin endoperoxide synthase 2?

Prostaglandin-endoperoxide synthase 2. Prostaglandin-endoperoxide synthase 2 (prostaglandin G/H synthase and cyclooxygenase) (The HUGO official symbol is PTGS2; HGNC ID, HGNC:9605 ), also known as cyclooxygenase-2 or COX-2, is an enzyme that in humans is encoded by the PTGS2 gene. In humans it is one of two cyclooxygenases.

Which is cyclooxygenase converts arachidonic acid to prostacyclin?

In humans it is one of two cyclooxygenases. It is involved in the conversion of arachidonic acid to prostaglandin H2, an important precursor of prostacyclin, which is expressed in inflammation . PTGS2 (COX-2), converts arachidonic acid (AA) to prostaglandin endoperoxide H2.

How does PTGS2 affect the development of prostaglandin?

Increased expression of the PTGS2 gene in the fetal membranes is connected to the presence of inflammation, causing uterine prostaglandin gene expression and immunolocalization of prostaglandin pathway proteins in chorionic trophoblast cells and adjacent decidua, or choriodecidua.

Which is COX-2 inhibitor inhibits prostaglandin production?

Prostacyclin relaxes or unsticks platelets, so selective COX-2 inhibitors (coxibs) increase risk of cardiovascular events due to clotting. Non-steroidal anti-inflammatory drugs (NSAIDs) inhibit prostaglandin production by PTGS1 (COX-1) and PTGS2 (COX-2).