Autophagy

Mortimore, Glenn E.; Miotto, Giovanni; Venerando, Rina; Kadowaki, Motoni

doi:10.1007/978-1-4615-5833-0_4

Cited by 82 publications

(59 citation statements)

References 113 publications

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“…It is interesting to note that in the liver these hormones only affected autophagy at intermediate concentrations of amino acids, and not at either very low or very high concentrations of amino acids, when autophagic flux was maximal or minimal, respectively. 24 As we will discuss later, this closely parallels the effect of insulin and glucagon and of amino acids on signal transduction.…”

Section: Inhibition Of Autophagy By Amino Acidsmentioning

confidence: 72%

“…Soon after the discovery of autophagy in the 1960s, 23 it became clear that amino acids, which are produced by autophagic protein breakdown, produce powerful feedback inhibition of autophagic sequestration, and that the process is also inhibited by insulin (in the liver) and activated by glucagon (for a review, see Mortimore et al 24 ). It is interesting to note that in the liver these hormones only affected autophagy at intermediate concentrations of amino acids, and not at either very low or very high concentrations of amino acids, when autophagic flux was maximal or minimal, respectively.…”

Section: Inhibition Of Autophagy By Amino Acidsmentioning

confidence: 99%

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Autophagy and signaling: their role in cell survival and cell death

2005

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Macroautophagy is a vacuolar, self-digesting mechanism responsible for the removal of long-lived proteins and damaged organelles by the lysosome. The discovery of the ATG genes has provided key information about the formation of the autophagosome, and about the role of macroautophagy in allowing cells to survive during nutrient depletion and/or in the absence of growth factors. Two connected signaling pathways encompassing class-I phosphatidylinositol 3-kinase and (mammalian) target of rapamycin play a central role in controlling macroautophagy in response to starvation. However, a considerable body of literature reports that macroautophagy is also a cell death mechanism that can occur either in the absence of detectable signs of apoptosis (via autophagic cell death) or concomitantly with apoptosis. Macroautophagy is activated by signaling pathways that also control apoptosis. The aim of this review is to discuss the signaling pathways that control macroautophagy during cell survival and cell death.

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Section: Inhibition Of Autophagy By Amino Acidsmentioning

confidence: 72%

Section: Inhibition Of Autophagy By Amino Acidsmentioning

confidence: 99%

Autophagy and signaling: their role in cell survival and cell death

2005

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“…The process of macroautophagy (henceforth, referred to as autophagy) was first described in mammals in rat hepatocytes (24,25). Autophagy in mammals is mechanistically identical to the process that occurs in yeast.…”

Section: The Molecular Machinery Of Autophagymentioning

confidence: 99%

Autophagy-Is it a preferred route for lifespan extension?

Dwivedi

Ahnn

2009

BMB Reports

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Autophagy, which is a process of self eating, has gained interest in the past decade due to its both beneficial and controversial roles in various biological phenomena. The discovery of autophagy genes (ATG) in yeast has led to focused research designed to elucidate the mechanism and regulation of this process. The role of autophagy in a variety of biological phenomena, including human disease, is still the subject of debate. However, recent findings suggest that autophagy is a highly regulated process with both beneficial and negative effects. Indeed, studies conducted using various model organisms have demonstrated that increased autophagy leads to an extended lifespan. Despite these findings, it is still unknown if all pathways leading to extended lifespan converge at the process of autophagy or not. Here, an overview of modern developments related to the process of autophagy, its regulation and the molecular machinery involved is presented. In addition, this review focuses on one of the beneficial aspects of autophagy, its role in lifespan regulation. [BMB reports 2009; 42(2): 65-71]

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“…The removal of protein aggregates, as well as misfolded and damaged proteins, occurs via two main degradation pathways, the ubiquitin-proteasome system (UPS) and the autophagy-lysosomal pathway (ALP) (10). Macroautophagy, a prominent constituent of the ALP, is responsible for removal of both soluble and aggregated proteins, as well as damaged organelles, via their sequestration into double-membrane vesicles called autophagosomes, followed by their degradation by catalytic enzymes after autophagosome/lysosome fusion (11,12). Macroautophagy (hereafter, autophagy) has been implicated in bulk degradation of pathologic aggregates, such as the polyglutamine-expanded huntingtin inclusions observed in Huntington disease (13).…”

mentioning

confidence: 99%

Lewy Body-like α-Synuclein Aggregates Resist Degradation and Impair Macroautophagy

Tanik

Schultheiss²,

Volpicelli‐Daley³

et al. 2013

Journal of Biological Chemistry

272

250

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Background: ␣-Synuclein aggregates and macroautophagy are associated with neurodegeneration. Results: Modulation of macroautophagic activity does not affect ␣-synuclein aggregate levels, although these aggregates cause accumulation of immature autophagosomes. Conclusion: ␣-Synuclein aggregates are resistant to degradation and impair autophagy by delaying autophagosome maturation. Significance: Understanding the impact of ␣-synuclein aggregates on autophagy may help elucidate therapies for ␣-synucleinmediated neurodegeneration.

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Autophagy

Cited by 82 publications

References 113 publications

Autophagy and signaling: their role in cell survival and cell death

Autophagy and signaling: their role in cell survival and cell death

Autophagy-Is it a preferred route for lifespan extension?

Lewy Body-like α-Synuclein Aggregates Resist Degradation and Impair Macroautophagy

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