| Cell cycle-dependent induction of autophagy, mitophagy and reticulophagy. | |
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MedLine Citation:
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PMID: 17890908 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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When added to cells, a variety of autophagy inducers that operate through distinct mechanisms and target different organelles for autophagic destruction (mitochondria in mitophagy, endoplasmic reticulum in reticulophagy) rarely induce autophagic vacuolization in more than 50% or the cells. Here we show that this heterogeneity may be explained by cell cycle-specific effects. The BH3 mimetic ABT737, lithium, rapamycin, tunicamycin or nutrient depletion stereotypically induce autophagy preferentially in the G(1) and S phases of the cell cycle, as determined by simultaneous monitoring of cell cycle markers and the cytoplasmic aggregation of GFP-LC3 in autophagic vacuoles. These results point to a hitherto neglected crosstalk between autophagic vacuolization and cell cycle regulation. |
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Authors:
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Ezgi Tasdemir; M Chiara Maiuri; Nicolas Tajeddine; Ilio Vitale; Alfredo Criollo; José Miguel Vicencio; John A Hickman; Olivier Geneste; Guido Kroemer |
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Publication Detail:
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Type: Comparative Study; Journal Article; Research Support, Non-U.S. Gov't Date: 2007-07-02 |
Journal Detail:
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Title: Cell cycle (Georgetown, Tex.) Volume: 6 ISSN: 1551-4005 ISO Abbreviation: Cell Cycle Publication Date: 2007 Sep |
Date Detail:
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Created Date: 2007-10-01 Completed Date: 2007-11-12 Revised Date: 2008-09-23 |
Medline Journal Info:
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Nlm Unique ID: 101137841 Medline TA: Cell Cycle Country: United States |
Other Details:
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Languages: eng Pagination: 2263-7 Citation Subset: IM |
Affiliation:
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INSERM, Villejuif, France. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Apoptosis / physiology Autophagy / physiology* Cell Cycle / physiology* Cell Differentiation / physiology Endoplasmic Reticulum / pathology, physiology* HCT116 Cells Humans Mitochondria / pathology, physiology* Rats |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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