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10.1016/j.molcel.2017.01.032 http://scihub22266oqcxt.onion/10.1016/j.molcel.2017.01.032 C5357178!5357178 !28262504     free     free     free       Mol+Cell 2017 ; 65 (6 ): 1014-1028.e7 Nephropedia Template TP {{tp|p=28262504 |t=2017. Mitochondrial Ca(2+) Uniporter Is a Mitochondrial Luminal Redox Sensor that Augments MCU Channel Activity |pdf=|usr=}}{{28262504 }} gab.com Text Mitochondrial Ca(2+) Uniporter Is a Mitochondrial Luminal Redox Sensor that Augments MCU Channel Activity JO: Mol Cell http://www.kidney.de/pget.php?&tw=1&pmid=28262504 #FOAvip Ca(2+) dynamics and oxidative signaling are fundamental mechanisms for mitochondrial bioenergetics and cell function. The MCU complex is the major pathway by which these signals are integrated in mitochondria. Whether and how these coactive elements interact with MCU have not been established. As an approach toward understanding the regulation of MCU channel by oxidative milieu, we adapted inflammatory and hypoxia models. We identified the conserved cysteine 97 (Cys-97) to be the only reactive thiol in human MCU that undergoes S-glutathionylation. Furthermore, biochemical, structural, and superresolution imaging analysis revealed that MCU oxidation promotes MCU higher order oligomer formation. Both oxidation and mutation of MCU Cys-97 exhibited persistent MCU channel activity with higher [Ca(2+)](m) uptake rate, elevated mROS, and enhanced [Ca(2+)](m) overload-induced cell death. In contrast, these effects were largely independent of MCU interaction with its regulators. These findings reveal a distinct functional role for Cys-97 in ROS sensing and regulation of MCU activity. Twit Text FOAVip Mitochondrial Ca(2+) Uniporter Is a Mitochondrial Luminal Redox Sensor that Augments MCU Channel Activity ????Mol Cell http://www.kidney.de/pget.php?&tw=1&pmid=28262504 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28262504 #FOAvip English Wikipedia <ref>{{Cite pmid|28262504 }}</ref> Mitochondrial Ca(2+) Uniporter Is a Mitochondrial Luminal Redox Sensor that Augments MCU Channel Activity #MMPMID28262504 Dong Z ; Shanmughapriya S ; Tomar D ; Siddiqui N ; Lynch S ; Nemani N ; Breves SL ; Zhang X ; Tripathi A ; Palaniappan P ; Riitano MF ; Worth AM ; Seelam A ; Carvalho E ; Subbiah R ; Jaña F ; Soboloff J ; Peng Y ; Cheung JY ; Joseph SK ; Caplan J ; Rajan S ; Stathopulos PB ; Madesh M Mol Cell 2017[Mar]; 65 (6 ): 1014-1028.e7 PMID28262504 show ga Ca(2+) dynamics and oxidative signaling are fundamental mechanisms for mitochondrial bioenergetics and cell function. The MCU complex is the major pathway by which these signals are integrated in mitochondria. Whether and how these coactive elements interact with MCU have not been established. As an approach toward understanding the regulation of MCU channel by oxidative milieu, we adapted inflammatory and hypoxia models. We identified the conserved cysteine 97 (Cys-97) to be the only reactive thiol in human MCU that undergoes S-glutathionylation. Furthermore, biochemical, structural, and superresolution imaging analysis revealed that MCU oxidation promotes MCU higher order oligomer formation. Both oxidation and mutation of MCU Cys-97 exhibited persistent MCU channel activity with higher [Ca(2+)](m) uptake rate, elevated mROS, and enhanced [Ca(2+)](m) overload-induced cell death. In contrast, these effects were largely independent of MCU interaction with its regulators. These findings reveal a distinct functional role for Cys-97 in ROS sensing and regulation of MCU activity. |*Calcium Signaling/drug effects [MESH] |*Ion Channel Gating/drug effects [MESH] |Animals [MESH] |COS Cells [MESH] |Calcium Channels/chemistry/genetics/*metabolism [MESH] |Calcium/*metabolism [MESH] |Cell Death [MESH] |Cell Hypoxia [MESH] |Chlorocebus aethiops [MESH] |Cysteine [MESH] |Endothelial Cells/drug effects/*metabolism/pathology [MESH] |Energy Metabolism [MESH] |Glutathione/metabolism [MESH] |HEK293 Cells [MESH] |HeLa Cells [MESH] |Humans [MESH] |Lipopolysaccharides/pharmacology [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Mice, Knockout [MESH] |Mitochondria/drug effects/*metabolism/pathology [MESH] |Mitochondrial Membranes/drug effects/*metabolism/pathology [MESH] |Mutation [MESH] |Oxidation-Reduction [MESH] |Protein Multimerization [MESH] |Protein Processing, Post-Translational [MESH] |Protein Structure, Quaternary [MESH] |Reactive Oxygen Species/*metabolism [MESH] |Structure-Activity Relationship [MESH] |Thrombin/pharmacology [MESH] |Time Factors [MESH]Mitochondrial Ca(2+) Uniporter Is a Mitochondrial Luminal Redox Sensor(epmc).pdf DeepDyve Pubget Overpricing