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NOK 介导糖酵解和与核 PDC 相关的组蛋白乙酰化。

NOK mediates glycolysis and nuclear PDC associated histone acetylation.

机构信息

Department of Microbiology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences and School of Basic Medicine, Peking Union Medical College, Beijing 100005, China.

State Key Laboratory of Proteomics, Genetic Laboratory of Development and Diseases, Institute of Biotechnology, Beijing 100071, China.

出版信息

Front Biosci (Landmark Ed). 2017 Jun 1;22(10):1792-1804. doi: 10.2741/4572.

Abstract

NOK is a potent oncogene that can transform normal cells to cancer cells. We hypothesized that NOK might impact cancer cell metabolism and histone acetylation. We show that NOK localizes in the mitochondria, and while it minimally impacts tricarboxylic acid (TCA) cycle, it markedly inhibits the process of electron transport and oxidative phosphorylation processes and dramatically enhances aerobic glycolysis in cancer cells. NOK promotes the mitochondrial-nuclear translocation of pyruvate dehydrogenase complex (PDC), and enhances histone acetylation in the nucleus. Together, these findings show that NOK mediates glycolysis and nuclear PDC associated histone acetylation.

摘要

NOK 是一种有效的癌基因,能够将正常细胞转化为癌细胞。我们假设 NOK 可能会影响癌细胞的代谢和组蛋白乙酰化。我们发现 NOK 定位于线粒体中,虽然它对三羧酸 (TCA) 循环的影响很小,但它明显抑制电子传递和氧化磷酸化过程,并显著增强癌细胞中的有氧糖酵解。NOK 促进丙酮酸脱氢酶复合物 (PDC) 的线粒体-核易位,并增强核内组蛋白乙酰化。这些发现表明,NOK 介导糖酵解和与核 PDC 相关的组蛋白乙酰化。

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