ULK1/2 Constitute a Bifurcate Node Controlling Glucose Metabolic Fluxes in Addition to Autophagy
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- 作者：Terytty Yang Li1 ; Yu Sun1 ; Yu Liang1 ; Qing Liu1 ; Yuzhe Shi1 ; Chen-Song Zhang1 ; Cixiong Zhang1 ; Lintao Song1 ; Pu Zhang2 ; Xianzhong Zhang2 ; Xiaotong Li1 ; Tao Chen1 ; Hui-Ying Huang1 ; Xiadi He3 ; Yi Wang4 ; Yu-Qing Wu1 ; Shaoxuan Chen1 ; Ming Jiang1 ; Canhe Chen1 ; Changchuan Xie1 ; James Y. Yang1 ; Yan Lin3 ; Shimin Zhao3 ; Zhiyun Ye1 ; Shu-Yong Lin1 ; Daniel Tsun-yee Chiu5 ; 6 ; Sheng-Cai Lin1 ; linsc@xmu.edu.cn" class="auth_mail" title="E-mail the corresponding author
- 刊名：Molecular Cell
- 出版年：2016
- 出版时间：5 May 2016
- 年：2016
- 卷：62
- 期：3
- 页码：359-370
- 全文大小：2750 K
文摘
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ULK1/2 deficiency leads to reduction of glycolysis during nutritional stresses
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HK1, PFK1, FBP1, and ENO1 are direct substrates of the ULK1 kinase
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ULK1 regulates activities of glycolytic enzymes and sustains glycolysis and PPP flux
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ULK1/2 reprogram glucose metabolic fluxes independently of autophagy