AMP-Activated protein kinase and autophagy

被引:137
作者
Meijer, Alfred J.
Codogno, Patrice
机构
[1] Univ Amsterdam, Acad Med Ctr, Dept Med Biochem, NL-1105 AZ Amsterdam, Netherlands
[2] Univ Paris 11, Fac Pharm, INSERM U756, F-92290 Chatenay Malabry, France
关键词
mTOR; rapamycin; energy; amino acids; AICAR; metformin; hepatocytes; HeLa cells; HT-29; cells; LKB1;
D O I
10.4161/auto.3710
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Autophagy is inhibited by TOR-dependent signaling. Interruption of signalling by rapamycin is known to stimulate autophagy, both in mammalian cells and in yeast. However, inactivation of TOR by AMPK has yielded controversial results in the literature with regard to its effect on autophagy: activation of autophogy in yeast but inhibition in hepatocytes. In a recent study, carried out with hepatocytes, HT-29 cells, and HeLa cells, the possible role of AMPK in the control of mammalian autophagy was reexamined. The data suggest that in mammalian cells, as in yeast, AMPK is required for autophagy.
引用
收藏
页码:238 / 240
页数:3
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