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10.1681/ASN.2008080873 http://scihub22266oqcxt.onion/10.1681/ASN.2008080873 19423690!2723979!19423690     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=19423690&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Am+Soc+Nephrol 2009 ; 20 (8): 1693-704 Nephropedia Template TP {{tp|p=19423690|t=2009. Parathyroid hormone activates TRPV5 via PKA-dependent phosphorylation |pdf=|usr=}}{{19423690}} gab.com Text Parathyroid hormone activates TRPV5 via PKA-dependent phosphorylation JO: J Am Soc Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=19423690 #FOAvip Low extracellular calcium (Ca(2+)) promotes release of parathyroid hormone (PTH), which acts on multiple organs to maintain overall Ca(2+) balance. In the distal part of the nephron, PTH stimulates active Ca(2+) reabsorption via the adenylyl cyclase-cAMP-protein kinase A (PKA) pathway, but the molecular target of this pathway is unknown. The transient receptor potential vanilloid 5 (TRPV5) channel constitutes the luminal gate for Ca(2+) entry in the distal convoluted tubule and has several putative PKA phosphorylation sites. Here, we investigated the effect of PTH-induced cAMP signaling on TRPV5 activity. Using fluorescence resonance energy transfer, we studied cAMP and Ca(2+) dynamics during PTH stimulation of HEK293 cells that coexpressed the PTH receptor and TRPV5. PTH increased cAMP levels, followed by a rise in TRPV5-mediated Ca(2+) influx. PTH (1 to 31) and forskolin, which activate the cAMP pathway, mimicked the stimulation of TRPV5 activity. Remarkably, TRPV5 activation was limited to conditions of strong intracellular Ca(2+) buffering. Cell surface biotinylation studies demonstrated that forskolin did not affect TRPV5 expression on the cell surface, suggesting that it alters the single-channel activity of a fixed number of TRPV5 channels. Application of the PKA catalytic subunit, which phosphorylated TRPV5, directly increased TRPV5 channel open probability. Alanine substitution of threonine-709 abolished both in vitro phosphorylation and PTH-mediated stimulation of TRPV5. In summary, PTH activates the cAMP-PKA signaling cascade, which rapidly phosphorylates threonine-709 of TRPV5, increasing the channel's open probability and promoting Ca(2+) reabsorption in the distal nephron. Twit Text FOAVip Parathyroid hormone activates TRPV5 via PKA-dependent phosphorylation ????J Am Soc Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=19423690 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=19423690 #FOAvip English Wikipedia <ref>{{Cite pmid|19423690}}</ref> Parathyroid hormone activates TRPV5 via PKA-dependent phosphorylation #MMPMID19423690 de Groot T; Lee K; Langeslag M; Xi Q; Jalink K; Bindels RJ; Hoenderop JG J Am Soc Nephrol 2009[Aug]; 20 (8): 1693-704 PMID19423690show ga Low extracellular calcium (Ca(2+)) promotes release of parathyroid hormone (PTH), which acts on multiple organs to maintain overall Ca(2+) balance. In the distal part of the nephron, PTH stimulates active Ca(2+) reabsorption via the adenylyl cyclase-cAMP-protein kinase A (PKA) pathway, but the molecular target of this pathway is unknown. The transient receptor potential vanilloid 5 (TRPV5) channel constitutes the luminal gate for Ca(2+) entry in the distal convoluted tubule and has several putative PKA phosphorylation sites. Here, we investigated the effect of PTH-induced cAMP signaling on TRPV5 activity. Using fluorescence resonance energy transfer, we studied cAMP and Ca(2+) dynamics during PTH stimulation of HEK293 cells that coexpressed the PTH receptor and TRPV5. PTH increased cAMP levels, followed by a rise in TRPV5-mediated Ca(2+) influx. PTH (1 to 31) and forskolin, which activate the cAMP pathway, mimicked the stimulation of TRPV5 activity. Remarkably, TRPV5 activation was limited to conditions of strong intracellular Ca(2+) buffering. Cell surface biotinylation studies demonstrated that forskolin did not affect TRPV5 expression on the cell surface, suggesting that it alters the single-channel activity of a fixed number of TRPV5 channels. Application of the PKA catalytic subunit, which phosphorylated TRPV5, directly increased TRPV5 channel open probability. Alanine substitution of threonine-709 abolished both in vitro phosphorylation and PTH-mediated stimulation of TRPV5. In summary, PTH activates the cAMP-PKA signaling cascade, which rapidly phosphorylates threonine-709 of TRPV5, increasing the channel's open probability and promoting Ca(2+) reabsorption in the distal nephron. |*Calcium Signaling[MESH] |Calcium/*metabolism[MESH] |Cell Line[MESH] |Colforsin[MESH] |Cyclic AMP-Dependent Protein Kinases/*metabolism[MESH] |Cyclic AMP/metabolism[MESH] |Fluorescence Resonance Energy Transfer[MESH] |Humans[MESH] |Parathyroid Hormone/*metabolism[MESH] |Phosphatidylinositol 4,5-Diphosphate/metabolism[MESH] |Phosphorylation[MESH] |Receptor, Parathyroid Hormone, Type 1/metabolism[MESH] |TRPV Cation Channels/*metabolism[MESH]Parathyroid hormone activates TRPV5 via PKA-dependent phosphorylation (epmc).pdf DeepDyve Pubget Overpricing