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GAPDH inhibits intracellular pathways during starvation for cellular energy homeostasis
Nature ( IF 64.8 ) Pub Date : 2018-09-01 , DOI: 10.1038/s41586-018-0475-6
Jia-Shu Yang 1 , Jia-Wei Hsu 1 , Seung-Yeol Park 1 , Jian Li 1 , William M Oldham 2 , Galina V Beznoussenko 3 , Alexander A Mironov 3 , Joseph Loscalzo 4 , Victor W Hsu 1
Affiliation  

Starvation poses a fundamental challenge to cell survival. Whereas the role of autophagy in promoting energy homeostasis in this setting has been extensively characterized1, other mechanisms are less well understood. Here we reveal that glyceraldehyde 3-phosphate dehydrogenase (GAPDH) inhibits coat protein I (COPI) transport by targeting a GTPase-activating protein (GAP) towards ADP-ribosylation factor 1 (ARF1) to suppress COPI vesicle fission. GAPDH inhibits multiple other transport pathways, also by targeting ARF GAPs. Further characterization suggests that this broad inhibition is activated by the cell during starvation to reduce energy consumption. These findings reveal a remarkable level of coordination among the intracellular transport pathways that underlies a critical mechanism of cellular energy homeostasis.During starvation, glyceraldehyde 3-phosphate dehydrogenase (GAPDH) targets GTPase-activating proteins to inhibit multiple intracellular transport pathways, thereby promoting energy homeostasis.

中文翻译:

GAPDH在细胞能量稳态饥饿期间抑制细胞内途径

饥饿对细胞生存构成了根本性挑战。尽管自噬在这种环境中促进能量稳态的作用已得到广泛表征,但其他机制尚不清楚。在这里,我们揭示了甘油醛 3-磷酸脱氢酶 (GAPDH) 通过将 GTP 酶激活蛋白 (GAP) 靶向 ADP-核糖基化因子 1 (ARF1) 来抑制外壳蛋白 I (COPI) 的转运,从而抑制 COPI 囊泡分裂。GAPDH 还通过靶向 ARF GAP 抑制多种其他运输途径。进一步的表征表明,这种广泛的抑制作用在饥饿期间被细胞激活以减少能量消耗。这些发现揭示了细胞内运输途径之间的显着协调水平,这是细胞能量稳态的关键机制的基础。在饥饿期间,
更新日期:2018-09-01
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