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Originally published In Press as doi:10.1074/jbc.R600038200 on February 28, 2007

J. Biol. Chem., Vol. 282, Issue 16, 11613-11617, April 20, 2007
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Prostaglandin E Receptors*

Yukihiko Sugimoto{ddagger} and Shuh Narumiya§1

From the {ddagger}Department of Physiological Chemistry, Graduate School of Pharmaceutical Sciences and the §Department of Pharmacology, Faculty of Medicine, Kyoto University, Kyoto 606-8501, Japan

Prostaglandin (PG) E2 exerts its actions by acting on a group of G-protein-coupled receptors (GPCRs). There are four GPCRs responding to PGE2 designated subtypes EP1, EP2, EP3, and EP4 and multiple splicing isoforms of the subtype EP3. The EP subtypes exhibit differences in signal transduction, tissue localization, and regulation of expression. This molecular and biochemical heterogeneity of PGE receptors leads to PGE2 being the most versatile prostanoid. Studies on knock-out mice deficient in each EP subtype have defined PGE2 actions mediated by each subtype and identified the role each EP subtype plays in various physiological and pathophysiological responses. Here we review recent advances in PGE receptor research.


* This minireview will be reprinted in the 2007 Minireview Compendium, which will be available in January, 2008. Work in our laboratories was supported in part by grants-in-aid for scientific research from the Ministry of Education, Culture, Sports Science and Technology of Japan and from the Ministry of Health and Labor of Japan.

1 To whom correspondence should be addressed. E-mail: snaru{at}mfour.med.kyoto-u.ac.jp.


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