|Expression of a dominant negative form of Daxx in vivo rescues motoneurons from Fas (CD95)-induced cell death.|
|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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|Type: Comparative Study; Journal Article; Research Support, Non-U.S. Gov't|
|Title: Journal of neurobiology Volume: 62 ISSN: 0022-3034 ISO Abbreviation: J. Neurobiol. Publication Date: 2005 Feb|
|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|
|Languages: eng Pagination: 178-88 Citation Subset: IM|
|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.|
|APA/MLA Format Download EndNote Download BibTex|
Adaptor Proteins, Signal Transducing
Antigens, CD95 / physiology*
Apoptosis* / radiation effects
Carrier Proteins / genetics, metabolism*
Cell Count / methods
Fas Ligand Protein
Fluorescent Antibody Technique / methods
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
Mice, Inbred C57BL
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*
|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 18.104.22.168/Nitric Oxide Synthase; EC 22.214.171.124/Nitric Oxide Synthase Type I; EC 126.96.36.199/Nos1 protein, mouse; EC 188.8.131.52/JNK Mitogen-Activated Protein Kinases|
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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