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Phosphoregulation of the autophagy machinery by kinases and phosphatases.

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TLDR
In this paper, the authors summarize the current knowledge on kinases and phosphatases acting on the core autophagy machinery and discuss the relevance of phosphoregulation for the overall process of autophagocytosis.
Abstract
Eukaryotic cells use post-translational modifications to diversify and dynamically coordinate the function and properties of protein networks within various cellular processes. For example, the process of autophagy strongly depends on the balanced action of kinases and phosphatases. Highly conserved from the budding yeast Saccharomyces cerevisiae to humans, autophagy is a tightly regulated self-degradation process that is crucial for survival, stress adaptation, maintenance of cellular and organismal homeostasis, and cell differentiation and development. Many studies have emphasized the importance of kinases and phosphatases in the regulation of autophagy and identified many of the core autophagy proteins as their direct targets. In this review, we summarize the current knowledge on kinases and phosphatases acting on the core autophagy machinery and discuss the relevance of phosphoregulation for the overall process of autophagy.

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ER-phagy: mechanisms, regulation, and diseases connected to the lysosomal clearance of the endoplasmic reticulum

TL;DR: ER-phagy is dysfunctional in specific human diseases and its regulators are subverted by pathogens, highlighting its crucial role for cell and organism life.
Journal ArticleDOI

Molecular regulation of autophagosome formation

TL;DR: The current knowledge about the molecular regulation of autophagosome formation is described, with a particular focus on budding yeast and mammalian cells.
Journal ArticleDOI

Molecular regulation of autophagosome formation

TL;DR: A review of the current knowledge about the molecular regulation of autophagosome formation, with a particular focus on budding yeast and mammalian cells, can be found in this article , where the authors describe the current state-of-the-art in autophagy.
Journal ArticleDOI

The AMPK pathway in fatty liver disease

TL;DR: A detailed description of each signaling axis of the AMPK pathway, as well as a discussion of its mechanism of action and therapeutic significance, is performed in this review.
Journal ArticleDOI

Post-Translational Modifications of ATG4B in the Regulation of Autophagy

Na Yeon Park, +2 more
- 01 Apr 2022 - 
TL;DR: Recent advances in understanding of the effect of post-translational modification on the regulation, activity, and function of ATG4, the main protease that controls autophagy are reviewed.
References
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Journal ArticleDOI

The split protein phosphatase system.

TL;DR: The set of potentially generalizable principles outlined in this review may facilitate the study of these poorly understood enzymes and the identification of their physiological substrates.
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ULK1-mediated phosphorylation of ATG16L1 promotes xenophagy, but destabilizes the ATG16L1 Crohn's mutant.

TL;DR: The results show that ATG16L1 is a novel target of ULK 1 kinase and that ULK1 signalling to ATG 16L1 has been shown to be a double‐edged sword, enhancing the function of the wild‐type ATG15L1, but promoting degradation of caATG16 L1.
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ULK1-ATG13 and their mitotic phospho-regulation by CDK1 connect autophagy to cell cycle

TL;DR: Combining mass spectrometry and site-directed mutagenesis, it is found that CDK1-induced ULK 1-ATG13 phosphorylation promotes mitotic autophagy and cell cycle progression and double knockout of ULK1 and ATG13 could block cell Cycle progression and significantly decrease cancer cell proliferation in cell line and mouse models.
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Endothelial PKA activity regulates angiogenesis by limiting autophagy through phosphorylation of ATG16L1.

TL;DR: Results indicate that endothelial PKA activity mediates a critical switch from active sprouting to quiescence in part through phosphorylation of ATG16L1, which in turn reduces endothelial autophagy.
Journal ArticleDOI

TOPK inhibits autophagy by phosphorylating ULK1 and promotes glioma resistance to TMZ

TL;DR: It is demonstrated that TOPK could inhibit the initiation and progression of autophagy in glioma cells and provides insight into the problem of TMZ-resistance in GBM treatment.
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