| Autophagy: a target for retinoic acids. | |
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MedLine Citation:
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PMID: 20953149 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Autophagy is an intracellular catabolic process that responds with great sensitivity to nutrient availability, implying that certain macro- or micro-nutrients are involved. We found that retinoic acid promotes autophagosome maturation through a pathway independent from the classic nuclear retinoid receptors. Retinoic acid redistributes the cation-independent mannose-6-phosphate receptor from the trans-Golgi region to maturing autophagosomal structures inducing their acidification. Manipulation of the autophagic activity by retinoids could have enormous health implications, since they are essential dietary components and frequently used pharmaceuticals. |
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Authors:
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Yogendra Rajawat; Zoe Hilioti; Ioannis Bossis |
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Publication Detail:
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Type: Journal Article Date: 2010-11-16 |
Journal Detail:
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Title: Autophagy Volume: 6 ISSN: 1554-8635 ISO Abbreviation: Autophagy Publication Date: 2010 Nov |
Date Detail:
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Created Date: 2010-11-16 Completed Date: 2011-03-02 Revised Date: 2011-06-30 |
Medline Journal Info:
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Nlm Unique ID: 101265188 Medline TA: Autophagy Country: United States |
Other Details:
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Languages: eng Pagination: 1224-6 Citation Subset: IM |
Affiliation:
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Department of Veterinary Medicine, University of Maryland, College Park, MD, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Autophagy
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drug effects* Hela Cells Humans Models, Biological Phagosomes / drug effects, metabolism Receptor, IGF Type 2 / metabolism Receptors, Retinoic Acid / metabolism Recombinant Fusion Proteins / metabolism Sirolimus / pharmacology Tretinoin / pharmacology* trans-Golgi Network / drug effects, metabolism |
| Chemical | |
Reg. No./Substance:
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0/Receptor, IGF Type 2; 0/Receptors, Retinoic Acid; 0/Recombinant Fusion Proteins; 302-79-4/Tretinoin; 53123-88-9/Sirolimus |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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