Title : Aspirin acetylates nitric oxide synthase type 3 in platelets thereby increasing its activity.

Pub. Date : 2009 Jul 1

PMID : 19377066






7 Functional Relationships(s)
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1 The aim of the present study was to determine the mechanism by which aspirin acutely increases the activity of NO synthase type 3 (NOS-3), the predominant NOS isoform expressed by platelets, and specifically whether this occurs through an increase in its acetylation. Aspirin nitric oxide synthase 3 Homo sapiens
2 At all concentrations tested, aspirin increased the activity of NOS-3 from platelets. Aspirin nitric oxide synthase 3 Homo sapiens
3 Serine phosphorylation of NOS-3 in platelets was decreased, and this was especially marked for serine-1177 phosphorylation, whereas acetylation of NOS-3 was increased, by aspirin incubation. Aspirin nitric oxide synthase 3 Homo sapiens
4 Serine phosphorylation of NOS-3 in platelets was decreased, and this was especially marked for serine-1177 phosphorylation, whereas acetylation of NOS-3 was increased, by aspirin incubation. Aspirin nitric oxide synthase 3 Homo sapiens
5 HeLa cells transfected with NOS-3 exhibited an increase in NO biosynthesis following aspirin exposure, and this was associated with acetylation of the enzyme on both serine-765 and serine-771. Aspirin nitric oxide synthase 3 Homo sapiens
6 CONCLUSION: Aspirin acetylates NOS-3 acutely in platelets, and this causes an increase in its activity as well as a decrease in its phosphorylation. Aspirin nitric oxide synthase 3 Homo sapiens
7 It is also possible that aspirin indirectly affects NOS-3 activity by acetylating other substrates within the platelet, but this remains to be determined. Aspirin nitric oxide synthase 3 Homo sapiens