Format

Send to

Choose Destination
J Mol Biol. 2016 May 8;428(9 Pt A):1725-41. doi: 10.1016/j.jmb.2016.03.030. Epub 2016 Apr 6.

Regulation of Autophagy By Signaling Through the Atg1/ULK1 Complex.

Author information

1
Max F. Perutz Laboratories, Vienna Biocenter, University of Vienna, A-1030 Vienna, Austria.
2
Max F. Perutz Laboratories, Vienna Biocenter, University of Vienna, A-1030 Vienna, Austria. Electronic address: claudine.kraft@univie.ac.at.

Abstract

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.

KEYWORDS:

Atg1/ULK1 phosphorylation sites; Atg1/ULK1 regulation; Atg1/ULK1 substrates; Autophagy; Autophagy signaling

PMID:
27059781
DOI:
10.1016/j.jmb.2016.03.030
[Indexed for MEDLINE]
Free full text

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center