| Endoplasmic reticulum: ER stress regulates mitochondrial bioenergetics. | |
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MedLine Citation:
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PMID: 22064245 Owner: NLM Status: Publisher |
Abstract/OtherAbstract:
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Endoplasmic reticulum (ER) stress activates an adaptive unfolded protein response (UPR) that facilitates cellular repair, however, under prolonged ER stress, the UPR can ultimately trigger apoptosis thereby terminating damaged cells. The molecular mechanisms responsible for execution of the cell death program are relatively well characterized, but the metabolic events taking place during the adaptive phase of ER stress remain largely undefined. Here we discuss emerging evidence regarding the metabolic changes that occur during the onset of ER stress and how ER influences mitochondrial function through mechanisms involving calcium transfer, thereby facilitating cellular adaptation. Finally, we highlight how dysregulation of ER-mitochondrial calcium homeostasis during prolonged ER stress is emerging as a novel mechanism implicated in the onset of metabolic disorders. |
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Authors:
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Roberto Bravo; Tomás Gutierrez; Felipe Paredes; Damián Gatica; Andrea E Rodriguez; Zully Pedrozo; Mario Chiong; Valentina Parra; Andrew F G Quest; Beverly A Rothermel; Sergio Lavandero |
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Publication Detail:
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Type: JOURNAL ARTICLE Date: 2011-11-2 |
Journal Detail:
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Title: The international journal of biochemistry & cell biology Volume: - ISSN: 1878-5875 ISO Abbreviation: - Publication Date: 2011 Nov |
Date Detail:
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Created Date: 2011-11-8 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 9508482 Medline TA: Int J Biochem Cell Biol Country: - |
Other Details:
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Languages: ENG Pagination: - Citation Subset: - |
Copyright Information:
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Copyright © 2011. Published by Elsevier Ltd. |
Affiliation:
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Centro Estudios Moleculares de la Celula, Facultad Ciencias Quimicas y Farmaceuticas, Chile. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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