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Dynamics and diversity in autophagy mechanisms: lessons from yeast

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TLDR
The discovery of autophagy in yeast and the genetic tractability of this organism have allowed us to identify genes that are responsible for this process, which has led to the explosive growth of this research field seen today.
Abstract
Autophagy is a fundamental function of eukaryotic cells and is well conserved from yeast to humans. The most remarkable feature of autophagy is the synthesis of double membrane-bound compartments that sequester materials to be degraded in lytic compartments, a process that seems to be mechanistically distinct from conventional membrane traffic. The discovery of autophagy in yeast and the genetic tractability of this organism have allowed us to identify genes that are responsible for this process, which has led to the explosive growth of this research field seen today. Analyses of autophagy-related (Atg) proteins have unveiled dynamic and diverse aspects of mechanisms that underlie membrane formation during autophagy.

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GSK3-TIP60-ULK1 signaling pathway links growth factor deprivation to autophagy.

TL;DR: These findings uncover an activating pathway that integrates protein phosphorylation and acetylation to connect growth factor deprivation to autophagy when deprived of serum but not glucose.
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Free Radicals in Cross Talk Between Autophagy and Apoptosis

TL;DR: Understanding of mechanisms that regulate the cross talk between cell fates is essential for discovery of therapeutic tools in the strenuous fight against various disorders, including neurodegeneration and cancer.
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The ESCRT Complexes

TL;DR: This review will describe the structure and function of the six complexes noted above and summarize current knowledge of their mechanistic roles in cellular pathways and in disease.
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MAPK/JNK signalling: a potential autophagy regulation pathway.

TL;DR: Herein, MAPK/JNK signalling is proposed as a potential autophagy regulation pathway for the transcription-dependent or independent role.
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Plant NBR1 is a selective autophagy substrate and a functional hybrid of the mammalian autophagic adapters NBR1 and p62/SQSTM1

TL;DR: It is shown that AtNBR1 is an autophagy substrate degraded in the vacuole dependent on the polymerization property of the PB1 domain and of expression of AtATG7, which is similar to mammalian NBR1 and p62.
References
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Journal ArticleDOI

Autophagy fights disease through cellular self-digestion

TL;DR: Understanding autophagy may ultimately allow scientists and clinicians to harness this process for the purpose of improving human health, and to play a role in cell death.
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TOR signaling in growth and metabolism.

TL;DR: The physiological consequences of mammalianTORC1 dysregulation suggest that inhibitors of mammalian TOR may be useful in the treatment of cancer, cardiovascular disease, autoimmunity, and metabolic disorders.
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p62/SQSTM1 Binds Directly to Atg8/LC3 to Facilitate Degradation of Ubiquitinated Protein Aggregates by Autophagy

TL;DR: It is demonstrated that the previously reported aggresome-like induced structures containing ubiquitinated proteins in cytosolic bodies are dependent on p62 for their formation and p62 is required both for the formation and the degradation of polyubiquitin-containing bodies by autophagy.
Journal ArticleDOI

Autophagy: process and function

TL;DR: In this review, the process of autophagy is summarized, and the role of autophileagy is discussed in a process-based manner.
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