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作 者:Terytty Yang Li Yu Sun Yu Liang Qing Liu Yuzhe Shi Chen-Song Zhang Cixiong Zhang Lintao Song Pu Zhang Xianzhong Zhang Xiaotong Li Tao Chen Hui-Ying Huang Xiadi He Yi Wang Yu-Qing Wu Shaoxuan Chen Ming Jiang Canhe Chen Changchuan Xie James Y.Yang Yan Lin Shimin Zhao Zhiyun Ye Shu-Yong Lin Daniel Tsun-yee Chiu 林圣彩[2]
机构地区:[1]不详 [2]厦门大学生命科学学院
出 处:《科学新闻》2017年第4期84-84,共1页Science News
基 金:国家自然科学基金重点项目;国家科技部(973课题);国家基础科学人才培养基金等的经费支持
摘 要:在细胞感受到环境中营养物质和生长因子的提供量发生改变后,代谢通路的重编程对于维持此时胞内的稳态是非常重要的过程。ULK1和ULK2是传递外界应激信号至自噬发生的重要整合因子。Metabolic reprogramming is fundamental to biological homeostasis, enabling cells to adjust metabolic routes after sensing altered availability of fuels and growth factors. ULK1 and ULK2 represent key integrators that relay metabolic stress signals to the autophagy machinery. Here, we demonstrate that, during deprivation of amino acid and growth factors, ULK1/2 directly phosphorylate key glycolytic enzymes including hexokinase (HK), phosphofructokinase 1 (PFK1), enolase 1 (ENO1), and the gluconeogenic enzyme fructose-1,6-bisphosphatase (FBP1). Phosphorylation of these enzymes leads to enhanced HK activity to sustain glucose uptake but reduced activity of FBP1 to block the gluconeogenic route and reduced activity of PFK1 and ENO1 to moderate drop of glucose-6-phosphate and to repartition more carbon flux to pentose phosphate pathway (PPP), maintaining cellular energy and redox homeostasis at cellular and organismal levels. These results identify ULK1/ 2 as a bifurcate-signaling node that sustains glucose metabolic fluxes besides initiation of autophagy in response to nutritional deprivation.
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