期刊
AUTOPHAGY
卷 3, 期 4, 页码 381-383出版社
TAYLOR & FRANCIS INC
DOI: 10.4161/auto.4240
关键词
AMP-activated protein kinase; autophagy; calcium; CaMKK-beta; mTORC1; signaling
类别
Autophagy is a lysosomal pathway involved in the turnover of cellular macromolecules and organelles. Starvation and various other stresses increase autophagic activity above the low basal levels observed in unstressed cells, where it is kept down by mammalian target of rapamycin complex 1 (mTORC1). In starved cells, LKB1 activates AMP-activated protein kinase (AMPK) that inhibits mTORC1 activity via a pathway involving tuberous sclerosis complex 1 and 2 (TSC1/2) and its substrate Rheb. The present study suggests that AMPK inhibits mTORC1 and autophagy also in nonstarved cells. Various Ca2+ mobilizing agents (vitamin D compounds, thapsigargin, ATP and ionomycin) activate AMPK via activation of Ca2+/calmodulin-dependent kinase kinase-beta (CaMKK-(3), and this pathway is required for Ca2+-induced autophagy. Thus, we propose that an increase in free cytosolic Ca2+ ([Ca2+](c)) induces autophagy via the CaMKK/beta-AMPK-TSC1/ 2-Rheb-mTORC1 signaling pathway and that AMPK is a more general regulator of autophagy than previously expected.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据