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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 Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28486130 &cmd=llinks): Failed to open stream: HTTP request failed! 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Gastric Acid Secretion from Parietal Cells Is Mediated by a Ca(2+) Efflux Channel in the Tubulovesicle |pdf=|usr=}}{{28486130 }} gab.com Text Gastric Acid Secretion from Parietal Cells Is Mediated by a Ca(2+) 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-ATPase-rich tubulovesicles (TVs) toward apical membranes in response to histamine stimulation via cyclic AMP 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 Ca(2+) 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 Ca(2+) release from TV stores. Hence, we demonstrated that ML1, acting as a Ca(2+) channel in TVs, links transmitter-initiated cyclic nucleotide signaling with Ca(2+)-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 Ca(2+) 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 Ca(2+) 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 PMID28486130 show ga Gastric acid secretion by parietal cells requires trafficking and exocytosis of H/K-ATPase-rich tubulovesicles (TVs) toward apical membranes in response to histamine stimulation via cyclic AMP 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 Ca(2+) 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 Ca(2+) release from TV stores. Hence, we demonstrated that ML1, acting as a Ca(2+) channel in TVs, links transmitter-initiated cyclic nucleotide signaling with Ca(2+)-dependent TV exocytosis in parietal cells, providing a regulatory mechanism that could be targeted to manage acid-related gastric diseases. |Animals [MESH] |Biological Transport/physiology [MESH] |Calcium/*metabolism [MESH] |Cell Membrane/*metabolism [MESH] |Exocytosis/*physiology [MESH] |Gastric Acid/*metabolism [MESH] |H(+)-K(+)-Exchanging ATPase/metabolism [MESH] |Histamine/metabolism [MESH] |Mice [MESH] |Parietal Cells, Gastric/*metabolism [MESH]Gastric Acid Secretion from Parietal Cells Is Mediated by a Ca(2+) Eff(epmc).pdf DeepDyve Pubget Overpricing