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Although\n FAIM<\/jats:styled-content>\n 1,\n FAIM<\/jats:styled-content>\n 2, and\n FAIM<\/jats:styled-content>\n 3 inhibit Fas\u2010induced cell death, they are not structurally related, nor do they share expression patterns. Moreover, they inhibit apoptosis through completely different mechanisms.\n FAIM<\/jats:styled-content>\n 1 and\n FAIM<\/jats:styled-content>\n 2 protect neurons from\n DR<\/jats:styled-content>\n \u2010induced apoptosis and are involved in neurite outgrowth and neuronal plasticity.\n FAIM<\/jats:styled-content>\n 1 inhibits Fas ligand\u2010 and tumor necrosis factor alpha\u2010induced apoptosis by direct interaction with Fas receptor and through the stabilization of levels of X\u2010linked inhibitor of apoptosis protein, a potent anti\u2010apoptotic protein that inhibits caspases. Low\n FAIM<\/jats:styled-content>\n 1 levels are found in Alzheimer's disease, thus sensitizing neurons to tumor necrosis factor alpha and prompting neuronal loss.\n FAIM<\/jats:styled-content>\n 2 protects from Fas by direct interaction with Fas receptor, as well as by modulating calcium release at the endoplasmic reticulum through interaction with Bcl\u2010\n xL<\/jats:styled-content>\n . Several studies prove the role of\n FAIM<\/jats:styled-content>\n 2 in diseases of the nervous system, such as ischemia, bacterial meningitis, and neuroblastoma. The less characterized member of the\n FAIM<\/jats:styled-content>\n family is\n FAIM<\/jats:styled-content>\n 3, which is expressed in tissues of the digestive and urinary tracts, bone marrow and testes, and restricted to the cerebellum in the nervous system.\n FAIM<\/jats:styled-content>\n 3 protects against\n DR<\/jats:styled-content>\n \u2010induced apoptosis by inducing the expression of other\n DR<\/jats:styled-content>\n \u2010antagonists such as\n CFLAR<\/jats:styled-content>\n or through the interaction with the\n DR<\/jats:styled-content>\n \u2010adaptor protein Fas\u2010associated via death domain.\n FAIM<\/jats:styled-content>\n 3 null mouse models reveal this protein as an important mediator of inflammatory autoimmune responses such as those triggered in autoimmune encephalomyelitis. Given the differences between\n FAIM<\/jats:styled-content>\n s and the variety of processes in which they are involved, here we sought to provide a concise review about these molecules and their roles in the physiology and pathology of the nervous system.\n <\/jats:p>\n <\/jats:sec>\n \n \n \n \n \n image<\/jats:alt-text>\n <\/jats:graphic>\n <\/jats:boxed-text>\n Even though they share name and inhibit Fas\u2010induced cell death, Fas apoptotic inhibitory molecules (FAIMs) are not structurally related and inhibit apoptosis through completely different mechanisms. In this review, we describe FAIM1, FAIM2, and FAIM3 functions in the nervous system, and their implication in diverse pathologies such as neurodegenerative disease, cancer, or autoimmune diseases.\n <\/jats:p>\n <\/jats:sec>","DOI":"10.1111\/jnc.13729","type":"journal-article","created":{"date-parts":[[2016,7,6]],"date-time":"2016-07-06T09:46:40Z","timestamp":1467798400000},"page":"11-21","source":"Crossref","is-referenced-by-count":37,"title":["Fas apoptosis inhibitory molecules: more than death\u2010receptor antagonists in the nervous system"],"prefix":"10.1111","volume":"139","author":[{"given":"Laura","family":"Planells\u2010Ferrer","sequence":"first","affiliation":[{"name":"Cell Signaling and Apoptosis Group Institut de Recerca de l'Hospital Universitari de la Vall d'Hebron (VHIR) Barcelona Spain"},{"name":"Institut de Neuroci\u00e8ncies Departament de Bioqu\u00edmica i Biologia Molecular Facultat de Medicina Universitat Aut\u00f2noma de Barcelona Bellaterra Spain"},{"name":"Centro de Investigaci\u00f3n Biom\u00e9dica en Red sobre Enfermedades Neurodegenerativas (CIBERNED) Madrid Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jorge","family":"Urresti","sequence":"additional","affiliation":[{"name":"Cell Signaling and Apoptosis Group Institut de Recerca de l'Hospital Universitari de la Vall d'Hebron (VHIR) Barcelona Spain"},{"name":"Institut de Neuroci\u00e8ncies Departament de Bioqu\u00edmica i Biologia Molecular Facultat de Medicina Universitat Aut\u00f2noma de Barcelona Bellaterra Spain"},{"name":"Centro de Investigaci\u00f3n Biom\u00e9dica en Red sobre Enfermedades Neurodegenerativas (CIBERNED) Madrid Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elena","family":"Coccia","sequence":"additional","affiliation":[{"name":"Cell Signaling and Apoptosis Group Institut de Recerca de l'Hospital Universitari de la Vall d'Hebron (VHIR) Barcelona Spain"},{"name":"Institut de Neuroci\u00e8ncies Departament de Bioqu\u00edmica i Biologia Molecular Facultat de Medicina Universitat Aut\u00f2noma de Barcelona Bellaterra Spain"},{"name":"Centro de Investigaci\u00f3n Biom\u00e9dica en Red sobre Enfermedades Neurodegenerativas (CIBERNED) Madrid Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Koen M. 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