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Si us plau utilitzeu sempre aquest identificador per citar o enllaçar aquest document: https://hdl.handle.net/2445/116597
FAIM-L regulation of XIAP degradation modulates Synaptic Long-Term Depression and Axon Degeneration
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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.
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MARTÍNEZ MÁRMOL, Ramón, BARNEDA ZAHONERO, Bruna, SOTO DEL CERRO, David, ANDRÉS, Rosa maría, COCCIA, Elena, GASULL CASANOVA, Xavier, PLANELLS FERRER, Laura, MOUBARAK, Rana s., SORIANO GARCÍA, Eduardo, COMELLA I CARNICÉ, Joan xavier. FAIM-L regulation of XIAP degradation modulates Synaptic Long-Term Depression and Axon Degeneration. _Scientific Reports_. 2016. Vol. 6, núm. 35775. [consulta: 13 de febrer de 2026]. ISSN: 2045-2322. [Disponible a: https://hdl.handle.net/2445/116597]