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. Author manuscript; available in PMC: 2013 Jun 17.
Published in final edited form as: Compr Physiol. 2012 Oct 1;2(4):2683–2731. doi: 10.1002/cphy.c110033

Figure 15.

Figure 15

GqPCRs regulates not only voltage-dependent cation channels, but also transient receptor potential (TRP) and leak cation channels. GqPCRs-induced depletion of Ca2+-store facilitates activation of Ca2+-store operated NSCCs, such as TRPC (1–6, 7), TRPM (3, 7, 8) and TRPV6. On the other hand, TRPM4/5 may be directly activated by elevation of internal Ca2+ concentration (300, 576). GqPCRs seem to modulate activity of K2P (TASK, TREK, and TRESK) and sodium-leak-channel-nonspecific (NALCN) channels. In particular, GqPCRs act through Src protein controls NALCN channels through both UNC-79 and UNC-80 (316, 317, 491, 540). Abbreviations; P2K (“two-pore” potassium channels, TASK, TREK, and TRESK channels), TRPM (transient receptor potential melastatin), TRPV(transient receptor potential vanilloid), TRPC (transient receptor potential canonical), Ca2+ store operated NSCCs (nonselective cation currents), and Src (sarcoma) is a proto-oncogenic and nonreceptor tyrosine kinase.