| How phosphoinositide 3-phosphate controls growth downstream of amino acids and autophagy downstream of amino acid withdrawal. | |
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MedLine Citation:
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PMID: 22260663 Owner: NLM Status: In-Data-Review |
Abstract/OtherAbstract:
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The simple phosphoinositide PtdIns3P has been shown to control cell growth downstream of amino acid signalling and autophagy downstream of amino acid withdrawal. These opposing effects depend in part on the existence of distinct complexes of Vps34 (vacuolar protein sorting 34), the kinase responsible for the majority of PtdIns3P synthesis in cells: one complex is activated after amino acid withdrawal to induce autophagy and another regulates mTORC1 (mammalian target of rapamycin complex 1) activation when amino acids are present. However, lipid-dependent signalling almost always exhibits a spatial dimension, related to the site of formation of the lipid signal. In the case of PtdIns3P-regulated autophagy induction, recent data suggest that PtdIns3P accumulates in a membrane compartment dynamically connected to the endoplasmic reticulum that constitutes a platform for the formation of some autophagosomes. For PtdIns3P-regulated mTORC1 activity, a spatial context is not yet known: several possibilities can be envisaged based on the known effects of PtdIns3P on the endocytic system and on recent data suggesting that activation of mTORC1 depends on its localization on lysosomes. |
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Authors:
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Nicholas T Ktistakis; Maria Manifava; Priya Schoenfelder; Sergio Rotondo |
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Publication Detail:
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Type: Journal Article |
Journal Detail:
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Title: Biochemical Society transactions Volume: 40 ISSN: 1470-8752 ISO Abbreviation: Biochem. Soc. Trans. Publication Date: 2012 Feb |
Date Detail:
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Created Date: 2012-01-20 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 7506897 Medline TA: Biochem Soc Trans Country: England |
Other Details:
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Languages: eng Pagination: 37-43 Citation Subset: IM |
Affiliation:
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Signalling Programme, Babraham Institute, Cambridge CB22 3AT, U.K. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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