Emerging regulation and functions of autophagy

被引:1019
作者
Boya, Patricia [1 ]
Reggiori, Fulvio [2 ,3 ]
Codogno, Patrice [4 ]
机构
[1] CSIC, Ctr Invest Biol, Dept Cellular & Mol Biol, Madrid 28040, Spain
[2] Univ Med Ctr Utrecht, Dept Cell Biol, NL-3584 CX Utrecht, Netherlands
[3] Univ Med Ctr Utrecht, Inst Biomembranes, NL-3584 CX Utrecht, Netherlands
[4] Univ Paris 05, INSERM U845, Necker Growth & Signaling Res Ctr, F-75014 Paris, France
关键词
SELECTIVE AUTOPHAGY; UNCONVENTIONAL SECRETION; ENDOPLASMIC-RETICULUM; INDEPENDENTLY TARGET; AEROBIC GLYCOLYSIS; MEDIATED CLEAVAGE; ATG PROTEINS; TUMOR-GROWTH; CELL-DEATH; PHOSPHORYLATION;
D O I
10.1038/ncb2788
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Autophagy maintains cell, tissue and organism homeostasis through degradation. Complex post-translational modulation of the Atg (autophagy-related) proteins adds additional entry points for crosstalk with other cellular processes and helps define cell-type-specific regulations of autophagy. Beyond the simplistic view of a process exclusively dedicated to the turnover of cellular components, recent data have uncovered unexpected functions for autophagy and the autophagy-related genes, such as regulation of metabolism, membrane transport and modulation of host defenses - indicating the novel frontiers lying ahead.
引用
收藏
页码:713 / 720
页数:8
相关论文
共 91 条
[11]   Autophagy Proteins Regulate the Secretory Component of Osteoclastic Bone Resorption [J].
DeSelm, Carl J. ;
Miller, Brian C. ;
Zou, Wei ;
Beatty, Wandy L. ;
van Meel, Helena ;
Takahata, Yoshifumi ;
Klumperman, Judith ;
Tooze, Sharon A. ;
Teitelbaum, Steven L. ;
Virgin, Herbert W. .
DEVELOPMENTAL CELL, 2011, 21 (05) :966-974
[12]   Astrocyte dysfunction triggers neurodegeneration in a lysosomal storage disorder [J].
Di Malta, Chiara ;
Fryer, John D. ;
Settembre, Carmine ;
Ballabio, Andrea .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2012, 109 (35) :E2334-E2342
[13]   Autophagy-based unconventional secretory pathway for extracellular delivery of IL-1β [J].
Dupont, Nicolas ;
Jiang, Shanya ;
Pilli, Manohar ;
Ornatowski, Wojciech ;
Bhattacharya, Dhruva ;
Deretic, Vojo .
EMBO JOURNAL, 2011, 30 (23) :4701-4711
[14]   Unconventional secretion of Acb1 is mediated by autophagosomes [J].
Duran, Juan M. ;
Anjard, Christophe ;
Stefan, Chris ;
Loomis, William F. ;
Malhotra, Vivek .
JOURNAL OF CELL BIOLOGY, 2010, 188 (04) :527-536
[15]   Glutaminolysis yields a metabolic by-product that stimulates autophagy [J].
Eng, Christina H. ;
Abraham, Robert T. .
AUTOPHAGY, 2010, 6 (07) :968-970
[16]   Chronic Expression of RCAN1-1L Protein Induces Mitochondrial Autophagy and Metabolic Shift from Oxidative Phosphorylation to Glycolysis in Neuronal Cells [J].
Ermak, Gennady ;
Sojitra, Sonal ;
Yin, Fei ;
Cadenas, Enrique ;
Cuervo, Ana Maria ;
Davies, Kelvin J. A. .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2012, 287 (17) :14088-14098
[17]   Liver autophagy contributes to the maintenance of blood glucose and amino acid levels [J].
Ezaki, Junji ;
Matsumoto, Naomi ;
Takeda-Ezaki, Mitsue ;
Komatsu, Masaaki ;
Takahashi, Katsuyuki ;
Hiraoka, Yuka ;
Taka, Hikari ;
Fujimura, Tsutomu ;
Takehana, Kenji ;
Yoshida, Mitsutaka ;
Iwata, Junichi ;
Tanida, Isei ;
Furuya, Norihiko ;
Zheng, Dong-Mei ;
Tada, Norihiro ;
Tanaka, Keiji ;
Kominami, Eiki ;
Ueno, Takashi .
AUTOPHAGY, 2011, 7 (07) :727-736
[18]   Autophagy machinery mediates macroendocytic processing and entotic cell death by targeting single membranes [J].
Florey, Oliver ;
Kim, Sung Eun ;
Sandoval, Cynthia P. ;
Haynes, Cole M. ;
Overholtzer, Michael .
NATURE CELL BIOLOGY, 2011, 13 (11) :1335-U118
[19]   Metabolic Profiling of Hypoxic Cells Revealed a Catabolic Signature Required for Cell Survival [J].
Frezza, Christian ;
Zheng, Liang ;
Tennant, Daniel A. ;
Papkovsky, Dmitri B. ;
Hedley, Barbara A. ;
Kalna, Gabriela ;
Watson, David G. ;
Gottlieb, Eyal .
PLOS ONE, 2011, 6 (09)
[20]   Non-apoptotic functions of apoptosis-regulatory proteins [J].
Galluzzi, Lorenzo ;
Kepp, Oliver ;
Trojel-Hansen, Christina ;
Kroemer, Guido .
EMBO REPORTS, 2012, 13 (04) :322-330