Document Detail

Expression of a dominant negative form of Daxx in vivo rescues motoneurons from Fas (CD95)-induced cell death.
MedLine Citation:
PMID:  15459896     Owner:  NLM     Status:  MEDLINE    
Fas-induced death of motoneurons in vitro has been shown to involve two signaling cascades that act together to execute the death program: a Fas-Daxx-ASK-1-p38 kinase-nNOS branch, which controls transcriptional and post-translational events, and the second classical Fas-FADD-caspase-8 branch. To analyze the role of Daxx in the developmental motoneuron cell death, we studied Fas-dependent cell death in motoneurons from transgenic mice that overexpress a dominant-negative form of Daxx. Motoneurons purified from these transgenic mice are resistant to Fas-induced death. This protective effect is specific to Fas because ultraviolet irradiation-triggered death is not affected by the transgene. The Daxx and the FADD pathways work in parallel because only Daxx, but not FADD, is involved in the transcriptional control of neuronal nitric oxide synthase and nitric oxide production. Nevertheless, we do not observe involvement of Daxx in developmental motoneuronal cell death, as the pattern of naturally occurring programmed cell death in vivo is normal in transgenic mice overexpressing the dominant negative form of Daxx, suggesting that Daxx-independent pathways are used during development.
Cedric Raoul; Catherine Barthelemy; Arnaud Couzinet; David Hancock; Brigitte Pettmann; Anne-Odile Hueber
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of neurobiology     Volume:  62     ISSN:  0022-3034     ISO Abbreviation:  J. Neurobiol.     Publication Date:  2005 Feb 
Date Detail:
Created Date:  2004-12-14     Completed Date:  2005-04-11     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  0213640     Medline TA:  J Neurobiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  178-88     Citation Subset:  IM    
Copyright Information:
2004 Wiley Periodicals, Inc
INSERM U. 382, Developmental Biology Institute of Marseille (CNRS-INSERM-Univ. Méditerranée-AP Marseille), Campus de Luminy-Case 907, 13288 Marseille, France.
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MeSH Terms
Adaptor Proteins, Signal Transducing / metabolism
Antigens, CD95 / physiology*
Apoptosis* / radiation effects
Carrier Proteins / genetics,  metabolism*
Cell Count / methods
Embryo, Mammalian
Fas Ligand Protein
Fluorescent Antibody Technique / methods
Genes, Dominant
Green Fluorescent Proteins / metabolism
In Situ Nick-End Labeling / methods
Indoles / diagnostic use
Intracellular Signaling Peptides and Proteins / genetics,  metabolism*
JNK Mitogen-Activated Protein Kinases / metabolism
Membrane Glycoproteins
Mice, Inbred C57BL
Mice, Transgenic
Motor Neurons / cytology*
Nerve Tissue Proteins / metabolism
Nitric Oxide Synthase / metabolism
Nitric Oxide Synthase Type I
Nuclear Proteins / genetics,  metabolism*
Peptides / metabolism
RNA, Messenger / biosynthesis
Reverse Transcriptase Polymerase Chain Reaction / methods
Spinal Cord / cytology*
Time Factors
Reg. No./Substance:
0/Adaptor Proteins, Signal Transducing; 0/Antigens, CD95; 0/Carrier Proteins; 0/Daxx protein, mouse; 0/Fas Ligand Protein; 0/Fasl protein, mouse; 0/Indoles; 0/Intracellular Signaling Peptides and Proteins; 0/Membrane Glycoproteins; 0/Nerve Tissue Proteins; 0/Nuclear Proteins; 0/Peptides; 0/RNA, Messenger; 147336-22-9/Green Fluorescent Proteins; 47165-04-8/DAPI; 98849-88-8/FLAG peptide; EC Oxide Synthase; EC Oxide Synthase Type I; EC protein, mouse; EC Mitogen-Activated Protein Kinases

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