| How ubiquitination and autophagy participate in the regulation of the cell response to bacterial infection. | |
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MedLine Citation:
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PMID: 21077843 Owner: NLM Status: In-Process |
Abstract/OtherAbstract:
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Bacterial infection relies on the micro-organism's ability to orchestrate the host's cell signalling such that the immune response is not activated. Conversely, the host cell has dedicated signalling pathways for coping with intrusions by pathogens. The autophagy of foreign micro-organisms (known as xenophagy) has emerged as one of the most powerful of these pathways, although the triggering mode remains largely unknown. In the present paper, we discuss the role that certain post-translational modifications (primarily ubiquitination) may play in the activation of xenophagy and how some bacteria have evolved mechanisms to subvert or hijack this process. In particular, we address the role played by P62/SQSTM1 (sequestosome 1). Finally, we discuss how autophagy can be subverted to eliminate bacteria-induced danger signals. |
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Authors:
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Nicolas Dupont; Nassima Temime-Smaali; Frank Lafont |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Biology of the cell / under the auspices of the European Cell Biology Organization Volume: 102 ISSN: 1768-322X ISO Abbreviation: Biol. Cell Publication Date: 2010 Dec |
Date Detail:
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Created Date: 2010-11-16 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 8108529 Medline TA: Biol Cell Country: England |
Other Details:
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Languages: eng Pagination: 621-34 Citation Subset: IM |
Affiliation:
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Cellular Microbiology of Infectious Pathogens, Center for Infection and Immunity of Lille, Institut Pasteur de Lille, Lille, F-59019, France. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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