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10.1038/srep24919 http://scihub22266oqcxt.onion/10.1038/srep24919 C4847119!4847119!27118599     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Sci+Rep 2016 ; 6 (ä): ä Nephropedia Template TP {{tp|p=27118599|t=2016. Accumulation of isolevuglandin-modified protein in normal and fibrotic lung |pdf=|usr=}}{{27118599}} gab.com Text Accumulation of isolevuglandin-modified protein in normal and fibrotic lung JO: Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=27118599 #FOAvip Protein lysine modification by ?-ketoaldehyde isomers derived from arachidonic acid, termed isolevuglandins (IsoLGs), is emerging as a mechanistic link between pathogenic reactive oxygen species and disease progression. However, the questions of whether covalent modification of proteins by IsoLGs are subject to genetic regulation and the identity of IsoLG-modified proteins remain unclear. Herein we show that Nrf2 and Nox2 are key regulators of IsoLG modification in pulmonary tissue and report on the identity of proteins analyzed by LC-MS following immunoaffinity purification of IsoLG-modified proteins. Gene ontology analysis revealed that proteins in numerous cellular pathways are susceptible to IsoLG modification. Although cells tolerate basal levels of modification, exceeding them induces apoptosis. We found prominent modification in a murine model of radiation-induced pulmonary fibrosis and in idiopathic pulmonary fibrosis, two diseases considered to be promoted by gene-regulated oxidant stress. Based on these results we hypothesize that IsoLG modification is a hitherto unrecognized sequelae that contributes to radiation-induced pulmonary injury and IPF. Twit Text FOAVip Accumulation of isolevuglandin-modified protein in normal and fibrotic lung ????Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=27118599 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27118599 #FOAvip English Wikipedia <ref>{{Cite pmid|27118599}}</ref> Accumulation of isolevuglandin-modified protein in normal and fibrotic lung #MMPMID27118599 Mont S; Davies SS; Roberts second LJ; Mernaugh RL; McDonald WH; Segal BH; Zackert W; Kropski JA; Blackwell TS; Sekhar KR; Galligan JJ; Massion PP; Marnett LJ; Travis EL; Freeman ML Sci Rep 2016[]; 6 (ä): ä PMID27118599show ga Protein lysine modification by ?-ketoaldehyde isomers derived from arachidonic acid, termed isolevuglandins (IsoLGs), is emerging as a mechanistic link between pathogenic reactive oxygen species and disease progression. However, the questions of whether covalent modification of proteins by IsoLGs are subject to genetic regulation and the identity of IsoLG-modified proteins remain unclear. Herein we show that Nrf2 and Nox2 are key regulators of IsoLG modification in pulmonary tissue and report on the identity of proteins analyzed by LC-MS following immunoaffinity purification of IsoLG-modified proteins. Gene ontology analysis revealed that proteins in numerous cellular pathways are susceptible to IsoLG modification. Although cells tolerate basal levels of modification, exceeding them induces apoptosis. We found prominent modification in a murine model of radiation-induced pulmonary fibrosis and in idiopathic pulmonary fibrosis, two diseases considered to be promoted by gene-regulated oxidant stress. Based on these results we hypothesize that IsoLG modification is a hitherto unrecognized sequelae that contributes to radiation-induced pulmonary injury and IPF. äAccumulation of isolevuglandin-modified protein in normal and fibrotic(epmc).pdf DeepDyve Pubget Overpricing