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Post-translational modifications of Beclin 1 provide multiple strategies for autophagy regulation

Hill, Sandra M ; Wrobel, Lidia ; Rubinsztein, David C

Cell death and differentiation, 2019-03, Vol.26 (4), p.617-629 [Periódico revisado por pares]

England: Nature Publishing Group

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Título:
Post-translational modifications of Beclin 1 provide multiple strategies for autophagy regulation
Autor: Hill, Sandra M ; Wrobel, Lidia ; Rubinsztein, David C
Assuntos: 1-Phosphatidylinositol 3-kinase ; aging ; Animals ; Autophagy ; Autophagy - genetics ; Autophagy-Related Proteins - metabolism ; Basic Medicine ; Beclin 1 ; Beclin-1 - genetics ; Beclin-1 - metabolism ; Biological Sciences ; Biologiska vetenskaper ; Cancer ; Class III Phosphatidylinositol 3-Kinases - genetics ; Class III Phosphatidylinositol 3-Kinases - metabolism ; Homeostasis ; Humans ; Medicinska grundvetenskaper ; Membrane structure ; Neurodegeneration ; Phagocytosis ; Phagosomes - enzymology ; Phagosomes - genetics ; Phagosomes - metabolism ; Phosphatidylinositol 3-Kinases - genetics ; Phosphatidylinositol 3-Kinases - metabolism ; Phosphatidylinositol Phosphates - metabolism ; Phosphorylation ; Post-translation ; post-translational modifications ; Protein Processing, Post-Translational ; Review ; Signal transduction ; Signal Transduction - genetics ; Translation ; Ubiquitination
É parte de: Cell death and differentiation, 2019-03, Vol.26 (4), p.617-629
Notas: ObjectType-Article-2
SourceType-Scholarly Journals-1
ObjectType-Feature-3
ObjectType-Review-1
Descrição: Autophagy is a conserved intracellular degradation pathway essential for protein homeostasis, survival and development. Defects in autophagic pathways have been connected to a variety of human diseases, including cancer and neurodegeneration. In the process of macroautophagy, cytoplasmic cargo is enclosed in a double-membrane structure and fused to the lysosome to allow for digestion and recycling of material. Autophagosome formation is primed by the ULK complex, which enables the downstream production of PI(3)P, a key lipid signalling molecule, on the phagophore membrane. The PI(3)P is generated by the PI3 kinase (PI3K) complex, consisting of the core components VPS34, VPS15 and Beclin 1. Beclin 1 is a central player in autophagy and constitutes a molecular platform for the regulation of autophagosome formation and maturation. Post-translational modifications of Beclin 1 affect its stability, interactions and ability to regulate PI3K activity, providing the cell with a plethora of strategies to fine-tune the levels of autophagy. Being such an important regulator, Beclin 1 is a potential target for therapeutic intervention and interfering with the post-translational regulation of Beclin 1 could be one way of manipulating the levels of autophagy. In this review, we provide an overview of the known post-translational modifications of Beclin 1 that govern its role in autophagy and how these modifications are maintained by input from several upstream signalling pathways. ▓.
Editor: England: Nature Publishing Group
Idioma: Inglês

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Post-translational modifications of Beclin 1 provide multiple strategies for autophagy regulation

Hill, Sandra M ; Wrobel, Lidia ; Rubinsztein, David C

England: Nature Publishing Group

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