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The long form of fas apoptotic inhibitory molecule is expressed specifically in neurons and protects them against death receptor-triggered apoptosis
Segura, Miguel F. (Universitat de Lleida. Departament de Ciències Mèdiques Bàsiques)
Solé, Carme (Universitat de Lleida. Departament de Ciències Mèdiques Bàsiques)
Pascual, Marta (Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas)
Moubarak, Rana S. (Universitat Autònoma de Barcelona. Institut de Neurociències)
Pérez García, M. José (Universitat de Lleida. Departament de Ciències Mèdiques Bàsiques)
Gozzelino, Raffaella (Universitat de Lleida. Departament de Ciències Mèdiques Bàsiques)
Iglesias Guimarais, Victoria (Universitat Autònoma de Barcelona. Institut de Neurociències)
Badiola Benito, Nahuai (Universitat Autònoma de Barcelona. Institut de Neurociències)
Bayascas Ramírez, José Ramón (Universitat Autònoma de Barcelona. Departament de Bioquímica i de Biologia Molecular)
Llecha, Nuria (Universitat de Lleida. Departament de Ciències Mèdiques Bàsiques)
Rodríguez Álvarez, José (Universitat Autònoma de Barcelona. Departament de Bioquímica i Biologia Molecular)
Soriano García, Eduardo (Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas)
Yuste Mateos, Víctor J. (Víctor José) (Universitat Autònoma de Barcelona. Departament de Bioquímica i Biologia Molecular)
Comella i Carnicé, Joan Xavier, 1963- (Universitat Autònoma de Barcelona. Institut de Neurociències)

Date: 2007
Abstract: Death receptors (DRs) and their ligands are expressed in developing nervous system. However, neurons are generally resistant to death induction through DRs and rather their activation promotes neuronal outgrowth and branching. These results suppose the existence of DRs antagonists expressed in the nervous system. Fas apoptosis inhibitory molecule (FAIMS ) was first identified as a Fas antagonist in B-cells. Soon after, a longer alternative spliced isoform with unknown function was identified and named FAIML. FAIMS is widely expressed, including the nervous system, and we have shown previously that it promotes neuronal differentiation but it is not an anti-apoptotic molecule in this system. Here, we demonstrate that FAIML is expressed specifically in neurons, and its expression is regulated during the development. Expression could be induced by NGF through the extracellular regulated kinase pathway in PC12(pheochromocytoma cell line) cells. Contrary to FAIMS , FAIML does not increase the neurite outgrowth induced by neurotrophins and does not interfere with nuclear factor ĸB pathway activation as FAIMS does. Cells overexpressing FAIML are resistant to apoptotic cell death induced by DRs such as Fas or tumor necrosis factor R1. Reduction of endogenous expression by small interfering RNA shows that endogenousFAIML protects primary neurons from DR-induced cell death. The detailed analysis of this antagonism shows thatFAIML can bind to Fas receptor and prevent the activation of the initiator caspase-8 induced by Fas. In conclusion, our results indicate that FAIML could be responsible for maintaining initiator caspases inactive after receptor engagement protecting neurons from the cytotoxic action of death ligands.
Rights: Aquest document està subjecte a una llicència d'ús Creative Commons. Es permet la reproducció total o parcial, la comunicació pública de l'obra i la creació d'obres derivades, sempre que no sigui amb finalitats comercials i que es distribueixin sota la mateixa llicència que regula l'obra original. Cal que es reconegui l'autoria de l'obra original. Creative Commons
Language: Anglès.
Document: article ; recerca ; publishedVersion
Subject: FAIM ; Apoptosis ; Fas/CD95 ; TNF ; Neurotrophic factor ; Neuron ; Apoptosi ; Factor neurotròfic ; Neurona
Published in: The Journal of neuroscience, Vol. 27 Núm. 42 (October 2007) , p. 11228-11241, ISSN 1529-2401

DOI: 10.1523/JNEUROSCI.3462-07.2007
PMID: 17942717


14 p, 1.2 MB

The record appears in these collections:
Research literature > UAB research groups literature > Research Centres and Groups (scientific output) > Health sciences and biosciences > Institut de Neurociències (INc)
Articles > Research articles
Articles > Published articles

 Record created 2014-10-27, last modified 2019-09-09



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