| Literature DB >> 12413954 |
Hiroyuki Tabata1, Satoshi Tanaka, Yukihiko Sugimoto, Hideaki Kanki, Shuji Kaneko, Atsushi Ichikawa.
Abstract
We previously reported that the prostaglandin E(2) (PGE(2)) receptor subtype EP(1) is coupled to intracellular Ca(2+) mobilization in CHO cells, which is dependent on extracellular Ca(2+) in a pertussis toxin-insensitive manner [H. Katoh, et al., Biochim. Biophys. Acta 1244 (1995) 41-48]. However, it remains unknown about the signal transduction involved in this response. To investigate the mechanism regulating Ca(2+) mobilization mediated by EP(1) receptors in detail, we performed a series of experiments using the Xenopus laevis oocyte expression system and found that endogenous G(q) and/or G(11), and not G(i1) is involved in the Ca(2+) mobilization induced by PGE(2). We further investigated the receptor-activated Ca(2+) channel (RACC)-related response by introducing mRNA for mouse transient receptor potential 5 (TRP5), a possible candidate for the RACC, and found effective coupling between them. These results suggest that the EP(1) receptors induce Ca(2+) mobilization via G(q) and/or G(11) and Ca(2+) influx via TRP.Entities:
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Year: 2002 PMID: 12413954 DOI: 10.1016/s0006-291x(02)02455-5
Source DB: PubMed Journal: Biochem Biophys Res Commun ISSN: 0006-291X Impact factor: 3.575