We previously reported that the prostaglandin E-2 (PGE(2)) receptor subtype EP1 is coupled to intracellular Ca2+ mobilization in CHO cells, which is dependent on extracellular Ca2+ 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 Ca2+ mobilization mediated by EP1 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(11) is involved in the Ca2+ mobilization induced by PGE(2). We further investigated the receptor-activated Ca2+ 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 EP1 receptors induce Ca2+ mobilization via G(q) and/or G(11) and Ca2+ influx via TRP. (C) 2002 Elsevier Science (USA). All rights reserved.