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Título:	FAIM-L regulation of XIAP degradation modulates Synaptic Long-Term Depression and Axon Degeneration
Autor/a:	Martínez Mármol, Ramón; Barneda Zahonero, Bruna; Soto del Cerro, David; Andrés, Rosa Maria; Coccia, Elena; Gasull Casanova, Xavier; Planells-Ferrer, Laura; Moubarak, Rana S.; Soriano García, Eduardo; Comella i Carnicé, Joan Xavier, 1963-
Notas:	Caspases have recently emerged as key regulators of axonal pruning and degeneration and of long-term depression (LTD), a long-lasting form of synaptic plasticity. However, the mechanism underlying these functions remains unclear. In this context, XIAP has been shown to modulate these processes. The neuron-specific form of FAIM protein (FAIM-L) is a death receptor antagonist that stabilizes XIAP protein levels, thus preventing death receptor-induced neuronal apoptosis. Here we show that FAIM-L modulates synaptic transmission, prevents chemical-LTD induction in hippocampal neurons, and thwarts axon degeneration after nerve growth factor (NGF) withdrawal. Additionally, we demonstrate that the participation of FAIM-L in these two processes is dependent on its capacity to stabilize XIAP protein levels. Our data reveal FAIM-L as a regulator of axonal degeneration and synaptic plasticity.
Materia(s):	-Apoptosi -Malalties del sistema nerviós -Apoptosis -Nervous system diseases
Derechos:	cc-by (c) Martínez-Mármol, Ramón et al., 2016 http://creativecommons.org/licenses/by/3.0/es
Tipo de documento:	Artículo Artículo - Versión publicada
Editor:	Nature Publishing Group
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