| Reovirus infection or ectopic expression of outer capsid protein micro1 induces apoptosis independently of the cellular proapoptotic proteins Bax and Bak. | |
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MedLine Citation:
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PMID: 20980509 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Mammalian orthoreoviruses induce apoptosis in vivo and in vitro; however, the specific mechanism by which apoptosis is induced is not fully understood. Recent studies have indicated that the reovirus outer capsid protein μ1 is the primary determinant of reovirus-induced apoptosis. Ectopically expressed μ1 induces apoptosis and localizes to intracellular membranes. Here we report that ectopic expression of μ1 activated both the extrinsic and intrinsic apoptotic pathways with activation of initiator caspases-8 and -9 and downstream effector caspase-3. Activation of both pathways was required for μ1-induced apoptosis, as specific inhibition of either caspase-8 or caspase-9 abolished downstream effector caspase-3 activation. Similar to reovirus infection, ectopic expression of μ1 caused release into the cytosol of cytochrome c and smac/DIABLO from the mitochondrial intermembrane space. Pancaspase inhibitors did not prevent cytochrome c release from cells expressing μ1, indicating that caspases were not required. Additionally, μ1- or reovirus-induced release of cytochrome c occurred efficiently in Bax(-/-)Bak(-/-) mouse embryonic fibroblasts (MEFs). Finally, we found that reovirus-induced apoptosis occurred in Bax(-/-)Bak(-/-) MEFs, indicating that reovirus-induced apoptosis occurs independently of the proapoptotic Bcl-2 family members Bax and Bak. |
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Authors:
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Meagan L Wisniewski; Brenda G Werner; Louis G Hom; Lynne J Anguish; Caroline M Coffey; John S L Parker |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't Date: 2010-10-27 |
Journal Detail:
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Title: Journal of virology Volume: 85 ISSN: 1098-5514 ISO Abbreviation: J. Virol. Publication Date: 2011 Jan |
Date Detail:
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Created Date: 2010-12-14 Completed Date: 2011-01-20 Revised Date: 2011-08-01 |
Medline Journal Info:
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Nlm Unique ID: 0113724 Medline TA: J Virol Country: United States |
Other Details:
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Languages: eng Pagination: 296-304 Citation Subset: IM |
Affiliation:
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Baker Institute for Animal Health, College of Veterinary Medicine, Cornell University, Hungerford Hill Road, Ithaca, NY 14853, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Apoptosis / physiology* CHO Cells Capsid Proteins / genetics, metabolism*, pharmacology Carrier Proteins / genetics, metabolism Caspases / genetics, metabolism Cell Line Cricetinae Cricetulus Cytochromes c / genetics, metabolism Cytosol / metabolism Fibroblasts / virology Hela Cells Humans Intracellular Membranes / metabolism Mammalian orthoreovirus 3 / pathogenicity* Mice Mitochondria / metabolism Mitochondrial Proteins / genetics, metabolism Orthoreovirus, Mammalian / pathogenicity* bcl-2 Homologous Antagonist-Killer Protein / genetics, metabolism* bcl-2-Associated X Protein / genetics, metabolism* |
| Grant Support | |
ID/Acronym/Agency:
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R01 AI063036/AI/NIAID NIH HHS; T32 AI07618/AI/NIAID NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Capsid Proteins; 0/Carrier Proteins; 0/Mitochondrial Proteins; 0/bcl-2 Homologous Antagonist-Killer Protein; 0/bcl-2-Associated X Protein; 9007-43-6/Cytochromes c; EC 3.4.22.-/Caspases |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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