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VPS34 complexes from a structural perspective
VPS34 phosphorylates phosphatidylinositol to produce PtdIns3P and is the progenitor of the phosphoinositide 3-kinase (PI3K) family. VPS34 has a simpler domain organization than class I PI3Ks, which belies the complexity of its quaternary organization, with the enzyme always functioning within larger...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
The American Society for Biochemistry and Molecular Biology
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6358306/ https://www.ncbi.nlm.nih.gov/pubmed/30397185 http://dx.doi.org/10.1194/jlr.R089490 |
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author | Ohashi, Yohei Tremel, Shirley Williams, Roger L. |
author_facet | Ohashi, Yohei Tremel, Shirley Williams, Roger L. |
author_sort | Ohashi, Yohei |
collection | PubMed |
description | VPS34 phosphorylates phosphatidylinositol to produce PtdIns3P and is the progenitor of the phosphoinositide 3-kinase (PI3K) family. VPS34 has a simpler domain organization than class I PI3Ks, which belies the complexity of its quaternary organization, with the enzyme always functioning within larger assemblies. PtdIns3P recruits specific recognition modules that are common in protein-sorting pathways, such as autophagy and endocytic sorting. It is best characterized in two heterotetramers, complexes I and II. Complex I is composed of VPS34, VPS15, Beclin 1, and autophagy-related gene (ATG)14L, whereas complex II replaces ATG14L with UVRAG. Because VPS34 can form a component of several distinct complexes, it enables independent regulation of various pathways that are controlled by PtdIns3P. Complexes I and II are critical for early events in autophagy and endocytic sorting, respectively. Autophagy has a complex association with cancer. In early stages, it inhibits tumorigenesis, but in later stages, it acts as a survival factor for tumors. Recently, various disease-associated somatic mutations were found in genes encoding complex I and II subunits. Lipid kinase activities of the complexes are also influenced by posttranslational modifications (PTMs). Mapping PTMs and somatic mutations on three-dimensional models of the complexes suggests mechanisms for how these affect VPS34 activity. |
format | Online Article Text |
id | pubmed-6358306 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | The American Society for Biochemistry and Molecular Biology |
record_format | MEDLINE/PubMed |
spelling | pubmed-63583062019-02-04 VPS34 complexes from a structural perspective Ohashi, Yohei Tremel, Shirley Williams, Roger L. J Lipid Res Thematic Review Series: The Role of Phosphoinositides in Signaling and Disease VPS34 phosphorylates phosphatidylinositol to produce PtdIns3P and is the progenitor of the phosphoinositide 3-kinase (PI3K) family. VPS34 has a simpler domain organization than class I PI3Ks, which belies the complexity of its quaternary organization, with the enzyme always functioning within larger assemblies. PtdIns3P recruits specific recognition modules that are common in protein-sorting pathways, such as autophagy and endocytic sorting. It is best characterized in two heterotetramers, complexes I and II. Complex I is composed of VPS34, VPS15, Beclin 1, and autophagy-related gene (ATG)14L, whereas complex II replaces ATG14L with UVRAG. Because VPS34 can form a component of several distinct complexes, it enables independent regulation of various pathways that are controlled by PtdIns3P. Complexes I and II are critical for early events in autophagy and endocytic sorting, respectively. Autophagy has a complex association with cancer. In early stages, it inhibits tumorigenesis, but in later stages, it acts as a survival factor for tumors. Recently, various disease-associated somatic mutations were found in genes encoding complex I and II subunits. Lipid kinase activities of the complexes are also influenced by posttranslational modifications (PTMs). Mapping PTMs and somatic mutations on three-dimensional models of the complexes suggests mechanisms for how these affect VPS34 activity. The American Society for Biochemistry and Molecular Biology 2019-02 2018-11-05 /pmc/articles/PMC6358306/ /pubmed/30397185 http://dx.doi.org/10.1194/jlr.R089490 Text en Copyright © 2019 Ohashi et al. Published by The American Society for Biochemistry and Molecular Biology, Inc. http://creativecommons.org/licenses/by/4.0/ Author’s Choice—Final version open access under the terms of the Creative Commons CC-BY license. |
spellingShingle | Thematic Review Series: The Role of Phosphoinositides in Signaling and Disease Ohashi, Yohei Tremel, Shirley Williams, Roger L. VPS34 complexes from a structural perspective |
title | VPS34 complexes from a structural perspective |
title_full | VPS34 complexes from a structural perspective |
title_fullStr | VPS34 complexes from a structural perspective |
title_full_unstemmed | VPS34 complexes from a structural perspective |
title_short | VPS34 complexes from a structural perspective |
title_sort | vps34 complexes from a structural perspective |
topic | Thematic Review Series: The Role of Phosphoinositides in Signaling and Disease |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6358306/ https://www.ncbi.nlm.nih.gov/pubmed/30397185 http://dx.doi.org/10.1194/jlr.R089490 |
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