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10.1016/j.devcel.2017.04.003 http://scihub22266oqcxt.onion/10.1016/j.devcel.2017.04.003 C5497767!5497767!28486130     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Dev+Cell 2017 ; 41 (3): 262-273.e6 Nephropedia Template TP {{tp|p=28486130|t=2017. Gastric acid secretion from parietal cells is mediated by a Ca2+ efflux channel in the tubulovesicle |pdf=|usr=}}{{28486130}} gab.com Text Gastric acid secretion from parietal cells is mediated by a Ca2+ efflux channel in the tubulovesicle JO: Dev Cell http://www.kidney.de/pget.php?&tw=1&pmid=28486130 #FOAvip Gastric acid secretion by parietal cells requires trafficking and exocytosis of H-K-ATPaserich tubulovesicles (TVs) toward apical membranes in response to histamine stimulation via cAMP elevation. Here, we found that TRPML1 (ML1), a protein that is mutated in type IV Mucolipidosis (ML-IV), is a tubulovesicular channel essential for TV exocytosis and acid secretion. Whereas ML-IV patients are reportedly achlorhydric, transgenic overexpression of ML1 in mouse parietal cells induced constitutive acid secretion. Gastric acid secretion was blocked and stimulated by ML1 inhibitors and agonists, respectively. Organelle-targeted Ca2+ imaging and direct patch-clamping of apical vacuolar membranes revealed that ML1 mediates a PKA-activated conductance on TV membranes that is required for histamine-induced Ca2+ release from TV stores. Hence, we demonstrated that ML1, acting as a Ca2+ channel in TVs, links transmitter-initiated cyclic nucleotide signaling with Ca2+-dependent TV exocytosis in parietal cells, providing a regulatory mechanism that could be targeted to manage acid-related gastric diseases. Twit Text FOAVip Gastric acid secretion from parietal cells is mediated by a Ca2+ efflux channel in the tubulovesicle ????Dev Cell http://www.kidney.de/pget.php?&tw=1&pmid=28486130 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28486130 #FOAvip English Wikipedia <ref>{{Cite pmid|28486130}}</ref> Gastric acid secretion from parietal cells is mediated by a Ca2+ efflux channel in the tubulovesicle #MMPMID28486130 Sahoo N; Gu M; Zhang X; Raval N; Yang J; Bekier M; Calvo R; Patnaik S; Wang W; King G; Samie M; Gao Q; Sahoo S; Sundaresan S; Keeley TM; Wang Y; Marugan J; Ferrer M; Samuelson LC; Merchant JL; Xu H Dev Cell 2017[May]; 41 (3): 262-273.e6 PMID28486130show ga Gastric acid secretion by parietal cells requires trafficking and exocytosis of H-K-ATPaserich tubulovesicles (TVs) toward apical membranes in response to histamine stimulation via cAMP elevation. Here, we found that TRPML1 (ML1), a protein that is mutated in type IV Mucolipidosis (ML-IV), is a tubulovesicular channel essential for TV exocytosis and acid secretion. Whereas ML-IV patients are reportedly achlorhydric, transgenic overexpression of ML1 in mouse parietal cells induced constitutive acid secretion. Gastric acid secretion was blocked and stimulated by ML1 inhibitors and agonists, respectively. Organelle-targeted Ca2+ imaging and direct patch-clamping of apical vacuolar membranes revealed that ML1 mediates a PKA-activated conductance on TV membranes that is required for histamine-induced Ca2+ release from TV stores. Hence, we demonstrated that ML1, acting as a Ca2+ channel in TVs, links transmitter-initiated cyclic nucleotide signaling with Ca2+-dependent TV exocytosis in parietal cells, providing a regulatory mechanism that could be targeted to manage acid-related gastric diseases. äGastric acid secretion from parietal cells is mediated by a Ca2+ efflu(epmc).pdf DeepDyve Pubget Overpricing