| Redox regulation of the intrinsic pathway in neuronal apoptosis. | |
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MedLine Citation:
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PMID: 20812874 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Two principal pathways exist by which cells can undergo apoptotic death, known as the extrinsic and the intrinsic pathways. Binding of a ligand to a death receptor activates the extrinsic pathway. In the intrinsic pathway, an apoptotic stimulus, such as neurotrophin withdrawal or exposure to a toxin, causes a proapoptotic member of the Bcl-2 family of proteins, such as Bax, to permeabilize the outer mitochondrial membrane. This allows redistribution of cytochrome c from the mitochondrial intermembrane space into the cytoplasm, where it causes activation of caspase proteases and, subsequently, cell death. A dramatic increase occurs in mitochondria-derived reactive oxygen species (ROS) during the apoptotic death of sympathetic, cerebellar granule, and cortical neurons. These ROS lie downstream of Bax in each cell type. Here I review possible mechanisms by which Bax causes increased ROS during neuronal apoptosis. I also discuss evidence that these ROS are an important part of the apoptotic cascade in these cells. Finally, I discuss evidence that suggests that neurotrophins prevent release of cytochrome c in neurons through activation of an antioxidant pathway. |
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Authors:
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James L Franklin |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Review Date: 2011-01-08 |
Journal Detail:
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Title: Antioxidants & redox signaling Volume: 14 ISSN: 1557-7716 ISO Abbreviation: Antioxid. Redox Signal. Publication Date: 2011 Apr |
Date Detail:
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Created Date: 2011-03-22 Completed Date: 2012-02-08 Revised Date: 2012-04-16 |
Medline Journal Info:
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Nlm Unique ID: 100888899 Medline TA: Antioxid Redox Signal Country: United States |
Other Details:
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Languages: eng Pagination: 1437-48 Citation Subset: IM |
Affiliation:
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Department of Pharmaceutical and Biomedical Sciences, University of Georgia, 250 Green St., Athens, GA 30602, USA. jlfrankl@rx.uga.edu |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Apoptosis* Cytochromes c / metabolism Humans Nerve Growth Factors / metabolism Neurons / metabolism*, pathology* Oxidation-Reduction Reactive Oxygen Species / metabolism bcl-2-Associated X Protein / metabolism |
| Grant Support | |
ID/Acronym/Agency:
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R01NS37110/NS/NINDS NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Nerve Growth Factors; 0/Reactive Oxygen Species; 0/bcl-2-Associated X Protein; 9007-43-6/Cytochromes c |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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