Abstract
Biosynthesis of prostacyclin (PGI2) is catalyzed serially by phospholipase A2 which liberates arachidonic acid from the prostaglandin H2 synthase, a bifunctional enzyme which catalyzes the conversion of arachidonic acid to prostaglandin G2 and subsequently to prostaglandin H2, and PGI2 synthase (PGIS, EC 5.3.99.4) which catalyzes the formation of PGI2 from prostaglandin H2. PGIS has been shown to be widely distributed, predominantly in vascular endothelial and smooth muscle cells [1,2]. An impaired synthesis of PGI2 has been implicated in the development of essential hypertension (EH), or cerebral infarction (CI). We already determined the organization of this gene [3]. The purpose of this study was to search for possible point mutations in all 10 exons and 5′-flanking region of the PGIS gene in patients with EH or CI.
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Nakayama, T., Soma, M., Rehemudula, D., Kanmatsuse, K. (2001). Mutation of the Human Prostacyclin Synthase Gene. In: Samuelsson, B., Paoletti, R., Folco, G.C., Granström, E., Nicosia, S. (eds) Advances in Prostaglandin and Leukotriene Research. Medical Science Symposia Series, vol 16. Springer, Dordrecht. https://doi.org/10.1007/978-94-015-9721-0_11
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DOI: https://doi.org/10.1007/978-94-015-9721-0_11
Publisher Name: Springer, Dordrecht
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