| Calpains and delayed calcium deregulation in excitotoxicity. | |
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MedLine Citation:
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PMID: 21110090 Owner: NLM Status: In-Process |
Abstract/OtherAbstract:
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Overactivation of glutamate receptors results in neurodegeneration in a variety of brain pathologies, including ischemia, epilepsy, traumatic brain injury and slow-progressing neurodegenerative disorders. In all these pathologies, it is well accepted that the calcium-dependent cysteine proteases calpains are key players in the mechanisms of neuronal cell death. Many research groups have been actively pursuing to establish a link between the deregulation of intracellular Ca(2+) homeostasis associated with excitotoxicity and calpain activity. It is well established that these two events are connected and interact synergistically to promote neurodegeneration, but whether calpain activity depends on or contributes to Ca(2+) deregulation is still under debate. |
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Authors:
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Inês M Araújo; Bruno P Carreira; Caetana M Carvalho; Arsélio P Carvalho |
Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2010-11-26 |
Journal Detail:
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Title: Neurochemical research Volume: 35 ISSN: 1573-6903 ISO Abbreviation: Neurochem. Res. Publication Date: 2010 Dec |
Date Detail:
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Created Date: 2010-12-16 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 7613461 Medline TA: Neurochem Res Country: United States |
Other Details:
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Languages: eng Pagination: 1966-9 Citation Subset: IM |
Affiliation:
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Center for Neuroscience and Cell Biology, University of Coimbra, Largo Marquês de Pombal, 3004-517 Coimbra, Portugal. inaraujo@cnc.cj.uc.pt |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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