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Open AccessJournal ArticleDOI

Beclin 1, an Essential Component and Master Regulator of PI3K-III in Health and Disease.

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TLDR
Beclin 1 seems to function as an adaptor for recruiting multiple proteins that modulate VPS34, enabling the recruitment of a number of autophagy proteins involved in the nucleation of the autophagosome.
Abstract
Autophagy is a cell 'self-digestion' pathway involving the synthesis, trafficking and delivery of autophagosomes to lysosomes for degradation. Beclin 1 is a core component of the class III phosphatidylinositol 3-kinase (PI3K-III) complex, which plays an important role in membrane trafficking and restructuring involved in autophagy, endocytosis, cytokinesis and phagocytosis. To date Beclin 1 has largely been characterized in the context of autophagy; it modulates the lipid kinase activity of PI3K-III catalytic unit VPS34, which generates phosphatidylinositol 3-phosphate (PI(3)P), enabling the recruitment of a number of autophagy proteins involved in the nucleation of the autophagosome. Beclin 1 seems to function as an adaptor for recruiting multiple proteins that modulate VPS34. The recent identification of Beclin 1 protein modifications has shed light on its regulation in autophagy, and the discovery of non-autophagy functions of Beclin 1 has expanded our view of Beclin 1's involvement in tissue homeostasis and human diseases.

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Journal ArticleDOI

Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)

Daniel J. Klionsky, +2983 more
- 08 Feb 2021 - 
TL;DR: In this article, the authors present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes.
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mTOR and Beclin1: Two key autophagy-related molecules and their roles in myocardial ischemia/reperfusion injury.

TL;DR: Mammalian target of rapamycin (mTOR) and Beclin1 are two vital autophagy‐related molecules in myocardial I/R injury playing significant roles in different stages.
Journal ArticleDOI

New frontiers in the treatment of colorectal cancer: Autophagy and the unfolded protein response as promising targets

TL;DR: This review addresses the epidemiology and risk factors of CRC, including genetic mutations leading to the occurrence of the disease and how autophagy and the UPR are involved in the regulation of CRC and how they associate with obesity and inflammatory responses in CRC.
Journal ArticleDOI

Beclin 1 Is Required for Neuron Viability and Regulates Endosome Pathways via the UVRAG-VPS34 Complex

TL;DR: This study reveals the essential role for beclin 1 in neuron survival involving multiple membrane trafficking pathways including endocytosis and autophagy, and suggests that the UVRAG-beclin 2 interaction underlies becl in 1's function in endocyTosis.
Journal ArticleDOI

Interplay Between Lipid Metabolism and Autophagy.

TL;DR: A better understanding of the mechanisms of autophagy and possible links to lipid metabolism will undoubtedly promote potential treatments for a variety of diseases.
References
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Journal ArticleDOI

Autophagy in the Pathogenesis of Disease

TL;DR: This Review summarizes recent advances in understanding the physiological functions of autophagy and its possible roles in the causation and prevention of human diseases.
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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Autophagy: Renovation of Cells and Tissues

TL;DR: It is explored how recent mouse models in combination with advances in human genetics are providing key insights into how the impairment or activation of autophagy contributes to pathogenesis of diverse diseases, from neurodegenerative diseases such as Parkinson disease to inflammatory disorders such as Crohn disease.
Journal ArticleDOI

Bcl-2 antiapoptotic proteins inhibit Beclin 1-dependent autophagy.

TL;DR: Bcl-2 not only functions as an antiapoptotic protein, but also as an antiautophagy protein via its inhibitory interaction with Beclin 1, which may help maintain autophagy at levels that are compatible with cell survival, rather than cell death.
Journal ArticleDOI

Induction of autophagy and inhibition of tumorigenesis by beclin 1.

TL;DR: It is shown that beclin 1 is a mammalian autophagy gene that can inhibit tumorigenesis and is expressed at decreased levels in human breast carcinoma, suggesting that decreased expression of Autophagy proteins may contribute to the development or progression of breast and other human malignancies.
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Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

Daniel J. Klionsky, +2522 more
- 21 Jan 2016 -