| Apoptosis caused by cathepsins does not require Bid signaling in an in vivo model of progressive myoclonus epilepsy (EPM1). | |
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MedLine Citation:
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PMID: 12934064 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Apoptosis can be mediated by mechanisms other than the traditional caspase-mediated cleavage cascade. There is growing recognition that alternative proteolytic enzymes such as the lysosomal cathepsin proteases can initiate or propagate proapoptotic signals, but it is currently unclear how cathepsins achieve these actions. Recent in vitro evidence suggests that cathepsins cleave the proapoptotic Bcl-2 family member Bid, thereby activating it and allowing it to induce the mitochondrial release of cytochrome c and subsequent apoptosis. We have tested this hypothesis in vivo by breeding mice that lack cathepsin inhibition (cystatin B-deficient mice) to Bid-deficient mice, to determine whether the apoptosis caused by cathepsins is dependent on Bid signaling. We found that cathepsins are still able to promote apoptosis even in the absence of Bid, indicating that these proteases mediate apoptosis via a different pathway, or that some other molecule can functionally substitute for Bid in this system. |
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Authors:
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M K Houseweart; A Vilaythong; X-M Yin; B Turk; J L Noebels; R M Myers |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S. |
Journal Detail:
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Title: Cell death and differentiation Volume: 10 ISSN: 1350-9047 ISO Abbreviation: Cell Death Differ. Publication Date: 2003 Dec |
Date Detail:
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Created Date: 2003-11-19 Completed Date: 2004-07-13 Revised Date: 2008-11-21 |
Medline Journal Info:
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Nlm Unique ID: 9437445 Medline TA: Cell Death Differ Country: England |
Other Details:
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Languages: eng Pagination: 1329-35 Citation Subset: IM |
Affiliation:
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Department of Genetics, School of Medicine, Stanford University, 300 Pasteur Drive, Stanford, CA 94305-5120, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Age Factors Animals Apoptosis* Ataxia BH3 Interacting Domain Death Agonist Protein Blotting, Western Carrier Proteins / metabolism* Cathepsins / metabolism* Cell Death Cerebellum / metabolism Cystatin B Cystatins / genetics Cytochromes c / metabolism Disease Models, Animal Electroencephalography Genotype In Situ Nick-End Labeling Lysosomes / metabolism Mice Mice, Knockout Mitochondria / metabolism Myoclonic Epilepsies, Progressive / metabolism, pathology* Phenotype Proto-Oncogene Proteins c-bcl-2 / metabolism Signal Transduction* |
| Grant Support | |
ID/Acronym/Agency:
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CA 83817/CA/NCI NIH HHS; NS29709/NS/NINDS NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/BH3 Interacting Domain Death Agonist Protein; 0/Bid protein, mouse; 0/Carrier Proteins; 0/Cstb protein, mouse; 0/Cystatins; 0/Proto-Oncogene Proteins c-bcl-2; 88844-95-5/Cystatin B; 9007-43-6/Cytochromes c; EC 3.4.-/Cathepsins |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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