| Modulation of the CD95-Induced Apoptosis: The Role of CD95 N-Glycosylation. | |
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MedLine Citation:
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PMID: 21625644 Owner: NLM Status: In-Data-Review |
Abstract/OtherAbstract:
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Protein modifications of death receptor pathways play a central role in the regulation of apoptosis. It has been demonstrated that O-glycosylation of TRAIL-receptor (R) is essential for sensitivity and resistance towards TRAIL-mediated apoptosis. In this study we ask whether and how glycosylation of CD95 (Fas/APO-1), another death receptor, influences DISC formation and procaspase-8 activation at the CD95 DISC and thereby the onset of apoptosis. We concentrated on N-glycostructure since O-glycosylation of CD95 was not found. We applied different approaches to analyze the role of CD95 N-glycosylation on the signal transduction: in silico modeling of CD95 DISC, generation of CD95 glycosylation mutants (at N136 and N118), modulation of N-glycosylation by deoxymannojirimycin (DMM) and sialidase from Vibrio cholerae (VCN). We demonstrate that N-deglycosylation of CD95 does not block DISC formation and results only in the reduction of the procaspase-8 activation at the DISC. These findings are important for the better understanding of CD95 apoptosis regulation and reveal differences between apoptotic signaling pathways of the TRAIL and CD95 systems. |
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Authors:
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Olga M Shatnyeva; Andriy V Kubarenko; Claudia E M Weber; Alexander Pappa; Reinhard Schwartz-Albiez; Alexander N R Weber; Peter H Krammer; Inna N Lavrik |
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Publication Detail:
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Type: Journal Article Date: 2011-05-18 |
Journal Detail:
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Title: PloS one Volume: 6 ISSN: 1932-6203 ISO Abbreviation: PLoS ONE Publication Date: 2011 |
Date Detail:
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Created Date: 2011-05-31 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 101285081 Medline TA: PLoS One Country: United States |
Other Details:
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Languages: eng Pagination: e19927 Citation Subset: IM |
Affiliation:
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Division of Immunogenetics, German Cancer Research Center, Heidelberg, Germany. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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