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COX-1

PTGS1
Pghs1.png
Identifiers
Aliases PTGS1, COX1, COX3, PCOX1, PES-1, PGG/HS, PGHS-1, PGHS1, PHS1, PTGHS, prostaglandin-endoperoxide synthase 1
External IDs MGI: 97797 HomoloGene: 743 GeneCards: PTGS1
Targeted by Drug
aspirin, bromfenac, diclofenac, fenoprofen, flurbiprofen, ibuprofen, ketoprofen, ketorolac, meclofenamic acid, mefenamic acid, meloxicam, naproxen, nimesulide, oxaprozin, acetaminophen, phenylbutazone, piroxicam, suprofen
RNA expression pattern
PBB GE PTGS1 205127 at tn.png

PBB GE PTGS1 205128 x at tn.png

PBB GE PTGS1 215813 s at tn.png
More reference expression data
Orthologs
Species Human Mouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)

NM_008969

RefSeq (protein)

NP_032995.1
NP_032995

Location (UCSC) Chr 9: 122.37 – 122.4 Mb Chr 2: 36.23 – 36.25 Mb
PubMed search

NM_001271368
NM_080591

NM_008969

NP_001258297
NP_542158

NP_032995.1
NP_032995

Cyclooxygenase 1 (COX-1), also known as prostaglandin G/H synthase 1, prostaglandin-endoperoxide synthase 1 or prostaglandin H2 synthase 1, is an enzyme that in humans is encoded by the PTGS1 gene. In humans it is one of two cyclooxygenases.

Cyclooxygenase (COX) is the central enzyme in the biosynthetic pathway to prostaglandins from arachidonic acid. This protein was purified more than 20 years ago and cloned in 1988.

There are two isozymes of COX encoded by distinct gene products: a constitutive COX-1 (this enzyme) and an inducible COX-2, which differ in their regulation of expression and tissue distribution. The expression of these two transcripts is differentially regulated by relevant cytokines and growth factors. This gene encodes COX-1, which regulates angiogenesis in endothelial cells. COX-1 is also involved in cell signaling and maintaining tissue homeostasis. A splice variant of COX-1 termed COX-3 was identified in the CNS of dogs, but does not result in a functional protein in humans. Two smaller COX-1-derived proteins (the partial COX-1 proteins PCOX-1A and PCOX-1B) have also been discovered, but their precise roles are yet to be described.


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Wikipedia

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