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Redox Biol. 2016 Apr;7:68-77. doi: 10.1016/j.redox.2015.11.013. Epub 2015 Nov 27.
2
Increased hepatocellular protein carbonylation in human end-stage alcoholic cirrhosis.人类终末期酒精性肝硬化中肝细胞蛋白羰基化增加。
Free Radic Biol Med. 2015 Dec;89:1144-53. doi: 10.1016/j.freeradbiomed.2015.10.420. Epub 2015 Oct 27.
3
Methionine adenosyltransferase α2 sumoylation positively regulate Bcl-2 expression in human colon and liver cancer cells.甲硫氨酸腺苷转移酶α2的类泛素化修饰正向调控人结肠癌细胞和肝癌细胞中Bcl-2的表达。
Oncotarget. 2015 Nov 10;6(35):37706-23. doi: 10.18632/oncotarget.5342.
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Am J Physiol Gastrointest Liver Physiol. 2015 Oct 1;309(7):G566-77. doi: 10.1152/ajpgi.00183.2015. Epub 2015 Aug 6.
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Redox Biol. 2015 Dec;6:33-40. doi: 10.1016/j.redox.2015.06.021. Epub 2015 Jul 6.
6
Advances and New Concepts in Alcohol-Induced Organelle Stress, Unfolded Protein Responses and Organ Damage.酒精诱导的细胞器应激、未折叠蛋白反应及器官损伤的进展与新概念
Biomolecules. 2015 Jun 3;5(2):1099-121. doi: 10.3390/biom5021099.
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8
Increased 4-hydroxynonenal protein adducts in male GSTA4-4/PPAR-α double knockout mice enhance injury during early stages of alcoholic liver disease.在酒精性肝病早期阶段,雄性 GSTA4-4/PPAR-α 双重基因敲除小鼠中增加的 4-羟基壬烯醛蛋白加合物增强了损伤。
Am J Physiol Gastrointest Liver Physiol. 2015 Mar 1;308(5):G403-15. doi: 10.1152/ajpgi.00154.2014. Epub 2014 Dec 11.
9
Transient receptor potential vanilloid 1 gene deficiency ameliorates hepatic injury in a mouse model of chronic binge alcohol-induced alcoholic liver disease.瞬时受体电位香草酸亚型1基因缺陷改善慢性暴饮酒精诱导的酒精性肝病小鼠模型中的肝损伤。
Am J Pathol. 2015 Jan;185(1):43-54. doi: 10.1016/j.ajpath.2014.09.007. Epub 2014 Oct 31.
10
Supplementation of saturated long-chain fatty acids maintains intestinal eubiosis and reduces ethanol-induced liver injury in mice.补充饱和长链脂肪酸可维持小鼠肠道微生态平衡并减轻乙醇诱导的肝损伤。
Gastroenterology. 2015 Jan;148(1):203-214.e16. doi: 10.1053/j.gastro.2014.09.014. Epub 2014 Sep 16.

异常的蛋白质翻译后修饰在酒精性肝损伤发病机制中的作用

Aberrant post-translational protein modifications in the pathogenesis of alcohol-induced liver injury.

作者信息

Osna Natalia A, Carter Wayne G, Ganesan Murali, Kirpich Irina A, McClain Craig J, Petersen Dennis R, Shearn Colin T, Tomasi Maria L, Kharbanda Kusum K

机构信息

Natalia A Osna, Murali Ganesan, Kusum K Kharbanda, Research Service, Veterans Affairs Nebraska-Western Iowa Health Care System, Omaha, NE 68105, United States.

出版信息

World J Gastroenterol. 2016 Jul 21;22(27):6192-200. doi: 10.3748/wjg.v22.i27.6192.

DOI:10.3748/wjg.v22.i27.6192
PMID:27468209
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4945978/
Abstract

It is likely that the majority of proteins will undergo post-translational modification, be it enzymatic or non-enzymatic. These modified protein(s) regulate activity, localization and interaction with other cellular molecules thereby maintaining cellular hemostasis. Alcohol exposure significantly alters several of these post-translational modifications leading to impairments of many essential physiological processes. Here, we present new insights into novel modifications following ethanol exposure and their role in the initiation and progression of liver injury. This critical review condenses the proceedings of a symposium at the European Society for the Biomedical Research on Alcoholism Meeting held September 12-15, 2015, in Valencia, Spain.

摘要

大多数蛋白质可能会经历翻译后修饰,无论是酶促修饰还是非酶促修饰。这些修饰后的蛋白质调节活性、定位以及与其他细胞分子的相互作用,从而维持细胞内稳态。酒精暴露会显著改变其中一些翻译后修饰,导致许多重要生理过程受损。在此,我们阐述了乙醇暴露后新的修饰及其在肝损伤起始和进展中的作用的新见解。这篇重要综述总结了2015年9月12日至15日在西班牙巴伦西亚举行的欧洲酒精中毒生物医学研究学会会议上一个研讨会的会议记录。