Rapamycin requires AMPK activity and p27 expression for promoting autophagy-dependent Tsc2-null cell survival
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- 作者：Tania Camposa ; Javiera Ziehea ; 1 ; Francisco Fuentes-Villalobosa ; Orlando Riquelmea ; Daniela Peñ ; aa ; Rodrigo Troncosob ; c ; Sergio Lavanderob ; d ; Violeta Morina ; Roxana Pincheiraa ; Ariel F. Castroa ; arcastro@udec.cl" class="auth_mail" title="E-mail the corresponding author
- 关键词：AMPK ; 5&prime ; AMP-activated protein kinase ; Atg13 ; autophagy-related protein 13 ; CDK ; cyclin-dependent kinase ; DAPI ; 4&prime ; 6-diamidino-2-phenylindole ; DMEM ; Dulbecco's modified eagle's medium ; DMSO ; dimethyl sulfoxide ; FDA ; US Food and Drug Administration ; GFP ; green fluorescent protein ; LAM ; lymphangioleiomyomatosis ; LC3 ; microtubule-associated protein light Chain 3 ; LKB1 ; liver kinase B1 ; MEK1/2 ; mitogen-activated protein kinase kinase 1/2 ; mTORC1 ; mammalian/mechanistic target of rapamycin
- 刊名：Biochimica et Biophysica Acta (BBA)-Molecular Cell Research
- 出版年：2016
- 出版时间：June 2016
- 年：2016
- 卷：1863
- 期：6
- 页码：1200-1207
- 全文大小：2025 K
文摘
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An AMPK/p27 axis drives activation of autophagy in rapamycin-treated Tsc2-null cells.
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p27 can induce rapamycin-dependent autophagy in the absence of AMPK activity.
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N-terminal domain of p27 is sufficient for rapamycin-dependent autophagy.
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Rapamycin requires p27 to induce autophagy-dependent Tsc2-null cell survival.