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lüll G protein-coupled receptor signaling via Src kinase induces endogenous human transient receptor potential vanilloid type 6 (TRPV6) channel activation Spehr J; Gelis L; Osterloh M; Oberland S; Hatt H; Spehr M; Neuhaus EMJ Biol Chem 2011[Apr]; 286 (15): 13184-92Ca(2+) homeostasis plays a critical role in a variety of cellular processes. We showed previously that stimulation of the prostate-specific G protein-coupled receptor (PSGR) enhances cytosolic Ca(2+) and inhibits proliferation of prostate cells. Here, we analyzed the signaling mechanisms underlying the PSGR-mediated Ca(2+) increase. Using complementary molecular, biochemical, electrophysiological, and live-cell imaging techniques, we found that endogenous Ca(2+)-selective transient receptor potential vanilloid type 6 (TRPV6) channels are critically involved in the PSGR-induced Ca(2+) signal. Biophysical characterization of the current activated by PSGR stimulation revealed characteristic properties of TRPV6. The molecular identity of the involved channel was confirmed using RNA interference targeting TrpV6. TRPV6-mediated Ca(2+) influx depended on Src kinase activity. Src kinase activation occurred independently of G protein activation, presumably by direct interaction with PSGR. Taken together, we report that endogenous TRPV6 channels are activated downstream of a G protein-coupled receptor and present the first physiological characterization of these channels in situ.|Calcium Channels/genetics/*metabolism[MESH]|Calcium Signaling/*physiology[MESH]|Calcium/*metabolism[MESH]|Cell Line[MESH]|Enzyme Activation/physiology[MESH]|Humans[MESH]|Male[MESH]|Prostate/cytology/metabolism[MESH]|RNA Interference[MESH]|Receptors, G-Protein-Coupled/genetics/*metabolism[MESH]|TRPV Cation Channels/genetics/*metabolism[MESH]|src-Family Kinases/genetics/*metabolism[MESH] |