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Fas/CD95 regulatory protein Faim2 is neuroprotective after transient brain ischemia.
MedLine Citation:
PMID:  21209208     Owner:  NLM     Status:  In-Process    
Abstract/OtherAbstract:
Death receptor (DR) signaling has a major impact on the outcome of numerous neurological diseases, including ischemic stroke. DRs mediate not only cell death signals, but also proinflammatory responses and cell proliferation. Identification of regulatory proteins that control the switch between apoptotic and alternative DR signaling opens new therapeutic opportunities. Fas apoptotic inhibitory molecule 2 (Faim2) is an evolutionary conserved, neuron-specific inhibitor of Fas/CD95-mediated apoptosis. To investigate its role during development and in disease models, we generated Faim2-deficient mice. The ubiquitous null mutation displayed a viable and fertile phenotype without overt deficiencies. However, lack of Faim2 caused an increase in susceptibility to combined oxygen-glucose deprivation in primary neurons in vitro as well as in caspase-associated cell death, stroke volume, and neurological impairment after cerebral ischemia in vivo. These processes were rescued by lentiviral Faim2 gene transfer. In summary, we provide evidence that Faim2 is a novel neuroprotective molecule in the context of cerebral ischemia.
Authors:
Arno Reich; Christopher Spering; Karen Gertz; Christoph Harms; Ellen Gerhardt; Golo Kronenberg; Klaus A Nave; Markus Schwab; Simone C Tauber; Anja Drinkut; Kristian Harms; Chrstioph P Beier; Aaron Voigt; Sandra Göbbels; Matthias Endres; Jörg B Schulz
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  The Journal of neuroscience : the official journal of the Society for Neuroscience     Volume:  31     ISSN:  1529-2401     ISO Abbreviation:  J. Neurosci.     Publication Date:  2011 Jan 
Date Detail:
Created Date:  2011-01-06     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8102140     Medline TA:  J Neurosci     Country:  United States    
Other Details:
Languages:  eng     Pagination:  225-33     Citation Subset:  IM    
Affiliation:
Department of Neurology, University Hospital and Medical School, RWTH Aachen University, D-52074 Aachen, Germany.
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