COX2
| Cyclooxygenase-2 | |||||||||
|---|---|---|---|---|---|---|---|---|---|
| Script error: No such module "InfoboxImage". Structure of COX-2 enzyme | |||||||||
| Identifiers | |||||||||
| EC number | 1.14.99.1 | ||||||||
| CAS number | 9077-99-8 | ||||||||
| Databases | |||||||||
| IntEnz | IntEnz view | ||||||||
| BRENDA | BRENDA entry | ||||||||
| ExPASy | NiceZyme view | ||||||||
| KEGG | KEGG entry | ||||||||
| MetaCyc | metabolic pathway | ||||||||
| PRIAM | profile | ||||||||
| PDB structures | RCSB PDB PDBe PDBsum | ||||||||
| Gene Ontology | AmiGO / QuickGO | ||||||||
| |||||||||
Cyclooxygenase-2 (COX-2) is an enzyme that plays a significant role in the inflammatory response and is a target for nonsteroidal anti-inflammatory drugs (NSAIDs). It is one of the two main isoforms of cyclooxygenase, the other being COX-1.
Function[edit | edit source]
COX-2 is an inducible enzyme, meaning its expression is increased in response to inflammatory stimuli. It catalyzes the conversion of arachidonic acid to prostaglandins, which are lipid compounds that have diverse effects, including promoting inflammation, pain, and fever. Unlike COX-1, which is constitutively expressed in most tissues and involved in maintaining normal physiological functions, COX-2 is primarily expressed at sites of inflammation.
Structure[edit | edit source]
COX-2 is a homodimeric enzyme, meaning it consists of two identical subunits. Each subunit has a heme group that is essential for its enzymatic activity. The enzyme is located in the endoplasmic reticulum and the nuclear envelope of cells.
Clinical Significance[edit | edit source]
COX-2 is a major target for NSAIDs, which are commonly used to treat pain and inflammation. Traditional NSAIDs, such as ibuprofen and aspirin, inhibit both COX-1 and COX-2, which can lead to side effects like gastrointestinal bleeding due to COX-1 inhibition. Selective COX-2 inhibitors, such as celecoxib, were developed to reduce these side effects by specifically targeting COX-2.
Regulation[edit | edit source]
The expression of COX-2 is regulated by various cytokines, growth factors, and tumor promoters. It is upregulated in response to pro-inflammatory cytokines such as interleukin-1 (IL-1) and tumor necrosis factor-alpha (TNF-α).
Role in Disease[edit | edit source]
Overexpression of COX-2 has been implicated in various diseases, including cancer, rheumatoid arthritis, and Alzheimer's disease. In cancer, COX-2 may promote tumor growth and metastasis by stimulating angiogenesis and inhibiting apoptosis.
Also see[edit | edit source]
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Contributors: Prab R. Tumpati, MD
