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10.1016/j.jmb.2010.01.014 http://scihub22266oqcxt.onion/10.1016/j.jmb.2010.01.014 C2825087!2825087!20070945     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Mol+Biol 2010 ; 396 (4): 858-69 Nephropedia Template TP {{tp|p=20070945|t=2010. TRPM7 Activates m-Calpain by Stress-Dependent Stimulation of p38 MAPK and c-Jun N-Terminal Kinase |pdf=|usr=}}{{20070945}} gab.com Text TRPM7 Activates m-Calpain by Stress-Dependent Stimulation of p38 MAPK and c-Jun N-Terminal Kinase JO: J Mol Biol http://www.kidney.de/pget.php?&tw=1&pmid=20070945 #FOAvip TRPM7 is a Ca2+ and Mg2+ permeant ion channel in possession of its own kinase domain. In a previous study we showed that overexpression of the channel-kinase in HEK-293 cells produced cell rounding and loss of adhesion which was dependent upon the Ca2+-dependent protease m-calpain. The TRPM7-elicited change in cell morphology was channel-dependent and occurred without any significant increase in cytosolic Ca2+. Here we demonstrate that overexpression of TRPM7 increased levels of cellular reactive oxygen species (ROS) and nitric oxide (NO), causing the activation of p38 MAP kinase (p38 MAPK) and c-Jun N-terminal kinase (JNK). Application of inhibitors of p38 MAPK and JNK blocked TRPM7-induced cell rounding and activation of m-calpain, without affecting the phosphorylation state of the protease. Overexpression of TRPM7 increased intracellular Mg2+; however, when the concentrations of either external Ca2+ or Mg2+ was increased to favor permeation of one divalent cation over the other, a similar increase in cell rounding and calpain activity was detected, indicating that TRPM7-mediated activation of m-calpain is not dependent on the nature of the divalent conducted by the channel. Application of inhibitors of nitric oxide synthase and mitochondrial-derived ROS reduced TRPM7-induced increases in nitric oxide and ROS production, blocked the change in cell morphology, and reduced cellular calpain activity. Collectively, our data reveal that excessive TRPM7 channel activity causes oxidative and nitrosative stress, producing cell rounding mediated by p38 MAPK/JNK dependent activation of m-calpain. Twit Text FOAVip TRPM7 Activates m-Calpain by Stress-Dependent Stimulation of p38 MAPK and c-Jun N-Terminal Kinase ????J Mol Biol http://www.kidney.de/pget.php?&tw=1&pmid=20070945 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=20070945 #FOAvip English Wikipedia <ref>{{Cite pmid|20070945}}</ref> TRPM7 Activates m-Calpain by Stress-Dependent Stimulation of p38 MAPK and c-Jun N-Terminal Kinase #MMPMID20070945 Su LT; Chen HC; González-Pagán O; Overton JD; Xie J; Yue L; Runnels LW J Mol Biol 2010[Mar]; 396 (4): 858-69 PMID20070945show ga TRPM7 is a Ca2+ and Mg2+ permeant ion channel in possession of its own kinase domain. In a previous study we showed that overexpression of the channel-kinase in HEK-293 cells produced cell rounding and loss of adhesion which was dependent upon the Ca2+-dependent protease m-calpain. The TRPM7-elicited change in cell morphology was channel-dependent and occurred without any significant increase in cytosolic Ca2+. Here we demonstrate that overexpression of TRPM7 increased levels of cellular reactive oxygen species (ROS) and nitric oxide (NO), causing the activation of p38 MAP kinase (p38 MAPK) and c-Jun N-terminal kinase (JNK). Application of inhibitors of p38 MAPK and JNK blocked TRPM7-induced cell rounding and activation of m-calpain, without affecting the phosphorylation state of the protease. Overexpression of TRPM7 increased intracellular Mg2+; however, when the concentrations of either external Ca2+ or Mg2+ was increased to favor permeation of one divalent cation over the other, a similar increase in cell rounding and calpain activity was detected, indicating that TRPM7-mediated activation of m-calpain is not dependent on the nature of the divalent conducted by the channel. Application of inhibitors of nitric oxide synthase and mitochondrial-derived ROS reduced TRPM7-induced increases in nitric oxide and ROS production, blocked the change in cell morphology, and reduced cellular calpain activity. Collectively, our data reveal that excessive TRPM7 channel activity causes oxidative and nitrosative stress, producing cell rounding mediated by p38 MAPK/JNK dependent activation of m-calpain. äTRPM7 Activates m-Calpain by Stress-Dependent Stimulation of p38 MAPK (epmc).pdf DeepDyve Pubget Overpricing