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lüll TRPV5 is internalized via clathrin-dependent endocytosis to enter a Ca2+-controlled recycling pathway van de Graaf SF; Rescher U; Hoenderop JG; Verkaart S; Bindels RJ; Gerke VJ Biol Chem 2008[Feb]; 283 (7): 4077-86The epithelial Ca(2+) channel TRPV5 plays an essential role in transcellular Ca(2+) transport and is one of the most Ca(2+)-selective members of the transient receptor potential superfamily. Regulation of the abundance of TRPV5 at the cell surface is critical in body Ca(2+) homeostasis. However, little is known about the mechanisms underlying TRPV5 endo- and exocytosis. Here, we show that TRPV5 is constitutively internalized in a dynamin- and clathrin-dependent manner. Internalized TRPV5 first appears in small vesicular structures and then localizes to perinuclear structures positive for Rab11a. TRPV5 has a half-life of more than 8 h and is stable even after internalization from the cell surface for more than 3 h. Disruption of cell surface delivery of newly synthesized TRPV5 by brefeldin A does not reduce TRPV5-mediated Ca(2+) influx in cells, suggesting the presence of a stable intracellular pool of the channel capable of recycling back to the surface. Furthermore, the endocytic recycling kinetics is decreased upon treatment with Ca(2+) chelator BAPTA-AM, indicating that the channel's trafficking pathways are dynamically controlled by Ca(2+).|*Endocytosis[MESH]|Base Sequence[MESH]|Calcium/*metabolism[MESH]|Cell Line[MESH]|Clathrin/*metabolism[MESH]|DNA Primers[MESH]|Humans[MESH]|Mutagenesis, Site-Directed[MESH]|TRPV Cation Channels/genetics/*metabolism[MESH] |