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10.1089/ars.2013.5604 http://scihub22266oqcxt.onion/10.1089/ars.2013.5604 C4245843!4245843!24766279     free     free     free Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Antioxid+Redox+Signal 2014 ; 21 (18): 2531-42 Nephropedia Template TP {{tp|p=24766279|t=2014. Sulfhydration of p66Shc at Cysteine59 Mediates the Antioxidant Effect of Hydrogen Sulfide |pdf=|usr=}}{{24766279}} gab.com Text Sulfhydration of p66Shc at Cysteine59 Mediates the Antioxidant Effect of Hydrogen Sulfide JO: Antioxid Redox Signal http://www.kidney.de/pget.php?&tw=1&pmid=24766279 #FOAvip Aims: Mitochondrion is considered as the major source of intracellular reactive oxygen species (ROS). H2S has been reported to be an antioxidant, but its mechanism remains largely elusive. P66Shc is an upstream activator of mitochondrial redox signaling. The aim of this study was to explore whether the antioxidant effect of H2S is mediated by p66Shc. Results: Application of exogenous H2S with its donor, NaHS, or overexpression of its generating enzyme, cystathionine ?-synthase, induced sulfhydration of p66Shc, but inhibited its phosphorylation caused by H2O2/D-galactose in SH-SY5Y cells or in the mice cortex. H2S also decreased mitochondrial ROS production and protected neuronal cells against stress-induced senescence. PKC?II and PP2A are the two key proteins to regulate p66Shc phosphorylation. Although H2S failed to affect the activities of these two proteins, it disrupted their association. Cysteine-59 resides in proximity to serine-36, the phosphorylation site of p66Shc. The C59S mutant attenuated the above-described biological function of H2S. Innovation: We revealed a novel mechanism for the antioxidant effect of H2S and its role in oxidative stress-related diseases. Conclusion: H2S inhibits mitochondrial ROS production via the sulfhydration of Cys-59 residue, which in turn, prevents the phosphorylation of p66Shc. Antioxid. Redox Signal. 21, 2531?2542. Twit Text FOAVip Sulfhydration of p66Shc at Cysteine59 Mediates the Antioxidant Effect of Hydrogen Sulfide ????Antioxid Redox Signal http://www.kidney.de/pget.php?&tw=1&pmid=24766279 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24766279 #FOAvip English Wikipedia <ref>{{Cite pmid|24766279}}</ref> Sulfhydration of p66Shc at Cysteine59 Mediates the Antioxidant Effect of Hydrogen Sulfide #MMPMID24766279 Xie ZZ; Shi MM; Xie L; Wu ZY; Li G; Hua F; Bian JS Antioxid Redox Signal 2014[Dec]; 21 (18): 2531-42 PMID24766279show ga Aims: Mitochondrion is considered as the major source of intracellular reactive oxygen species (ROS). H2S has been reported to be an antioxidant, but its mechanism remains largely elusive. P66Shc is an upstream activator of mitochondrial redox signaling. The aim of this study was to explore whether the antioxidant effect of H2S is mediated by p66Shc. Results: Application of exogenous H2S with its donor, NaHS, or overexpression of its generating enzyme, cystathionine ?-synthase, induced sulfhydration of p66Shc, but inhibited its phosphorylation caused by H2O2/D-galactose in SH-SY5Y cells or in the mice cortex. H2S also decreased mitochondrial ROS production and protected neuronal cells against stress-induced senescence. PKC?II and PP2A are the two key proteins to regulate p66Shc phosphorylation. Although H2S failed to affect the activities of these two proteins, it disrupted their association. Cysteine-59 resides in proximity to serine-36, the phosphorylation site of p66Shc. The C59S mutant attenuated the above-described biological function of H2S. Innovation: We revealed a novel mechanism for the antioxidant effect of H2S and its role in oxidative stress-related diseases. Conclusion: H2S inhibits mitochondrial ROS production via the sulfhydration of Cys-59 residue, which in turn, prevents the phosphorylation of p66Shc. Antioxid. Redox Signal. 21, 2531?2542. äSulfhydration of p66Shc at Cysteine59 Mediates the Antioxidant Effect (epmc).pdf DeepDyve Pubget Overpricing