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10.1038/srep32257

http://scihub22266oqcxt.onion/10.1038/srep32257
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C5006047!5006047!27577858
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suck abstract from ncbi


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pmid27577858      Sci+Rep 2016 ; 6 (ä): ä
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  • Acetylated ?-Tubulin Regulated by N-Acetyl-Seryl-Aspartyl-Lysyl-Proline(Ac-SDKP) Exerts the Anti-fibrotic Effect in Rat Lung Fibrosis Induced by Silica #MMPMID27577858
  • Xiaojun W; Yan L; Hong X; Xianghong Z; Shifeng L; Dingjie X; Xuemin G; Lijuan Z; Bonan Z; Zhongqiu W; Ruimin W; Brann D; Fang Y
  • Sci Rep 2016[]; 6 (ä): ä PMID27577858show ga
  • Silicosis is the most serious occupational disease in China. The objective of this study was to screen various proteins related to mechanisms of the pathogenesis of silicosis underlying the anti-fibrotic effect of N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) using proteomic profile analysis. We also aimed to explore a potential mechanism of acetylated ?-tubulin (?-Ac-Tub) regulation by Ac-SDKP. Two-dimensional electrophoresis (2-DE) and matrix-assisted laser desorption ionization time-of-flight mass spectrometry (MALDI-TOF/TOF MS) were used to assess the different protein expression profiles between control and silicosis rats treated with or without Ac-SDKP. Twenty-nine proteins were identified to be potentially involved in the progression of silicosis and the anti-fibrotic effect of Ac-SDKP. Our current study finds that 1) the lost expression of Ac-Tub-? may be a new mechanism in rat silicosis; 2) treatment of silicotic rats with N-acetyl-Seryl-Aspartyl-Lysyl-Proline (Ac-SDKP) inhibits myofibroblast differentiation and collagen deposition accompanied by stabilizing the expression of ?-Ac-Tub in vivo and in vitro, which is related with deacetylase family member 6 (HDAC6) and ?-tubulin acetyl transferase (?-TAT1). Our data suggest that ?-Ac-Tub regulation by Ac-SDKP may potentially be a new anti-fibrosis mechanism.
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