COX1 / Cyclooxygenase 1 overexpression 293T lysate (whole cell)

Supplementary information

This supplementary information is collated from multiple sources and compiled automatically.

Cyclooxygenase 1 (COX-1) also known as COX1 cyclooxygenase-1 COX one and the COX1 protein is an important enzyme in the conversion of arachidonic acid to prostaglandins. It is a heme-containing dimer enzyme with a molecular weight of approximately 70 kDa. COX-1 is widely expressed in most tissues and cell types where it plays a significant role in maintaining homeostatic functions. This protein is constitutively active meaning it is often active under normal physiological conditions.

Biological function summary

COX-1 is involved in producing prostaglandins that regulate a variety of normal physiological processes including gastric mucosal protection renal blood flow and platelet aggregation. Unlike COX-2 COX-1 is not induced by inflammatory stimuli and is not part of an inducible complex. It serves to maintain essential physiological functions in various organs and systems making its activity critical for cellular maintenance.

Pathways

COX-1 is primarily involved in the prostaglandin biosynthesis pathway. It converts arachidonic acid into prostaglandin H2 a precursor for other prostaglandins and thromboxanes. Thromboxane A2 produced from this pathway plays an important role in platelet aggregation and vasoconstriction linking COX-1's functions with hemostatic processes. Another protein involved in this pathway is thromboxane synthase which further processes the products of COX-1 activity.

COX-1’s role connects it closely to conditions like peptic ulcers and cardiovascular diseases. Inhibition of COX-1 by nonsteroidal anti-inflammatory drugs (NSAIDs) can lead to gastric mucosal damage contributing to the development of peptic ulcers. Additionally due to its involvement in platelet aggregation COX-1 affects thrombotic diseases. COX-1's interactions with proteins such as COX-2 become relevant in inflammation and pain management where selective inhibition of COX-2 is sought to reduce adverse effects related to COX-1.