期刊
JOURNAL OF MOLECULAR BIOLOGY
卷 428, 期 9, 页码 1725-1741出版社
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.jmb.2016.03.030
关键词
Autophagy; Autophagy signaling; Atg1/ULK1 regulation; Atg1/ULK1 phosphorylation sites
资金
- Vienna Research Groups for Young Investigators grant from the Vienna Science and Technology Fund [WWTF VRG10-001]
- Austrian Science Fund [FWF P 25522-B20, P 28113-628]
- Austrian Science Fund (FWF) [P 25522, P 28113] Funding Source: researchfish
- Austrian Science Fund (FWF) [P25522, P28113] Funding Source: Austrian Science Fund (FWF)
Autophagy is an intracellular degradation pathway highly conserved in eukaryotic species. It is characterized by selective or bulk trafficking of cytosolic structures ranging from single proteins to cell organelles to the vacuole or a lysosome, in which the autophagic cargo is degraded. Autophagy fulfils a large set of roles, including nutrient mobilization in starvation conditions, clearance of protein aggregates and host defence against intracellular pathogens. Not surprisingly, autophagy has been linked to several human diseases, among them neurodegenerative disorders and cancer. Autophagy is coordinated by the action of the Atg1/ULK1 kinase, which is the target of several important stress signaling cascades. In this review, we will discuss the available information on both upstream regulation and downstream effectors of Atg1/ULK1, with special focus on reported and proposed kinase substrates. (C) 2016 The Authors. Published by Elsevier Ltd.
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