TY - JOUR
T1 - FAIM-L regulation of XIAP degradation modulates Synaptic Long-Term Depression and Axon Degeneration
AU - Martínez-Mármol, Ramón
AU - Barneda-Zahonero, Bruna
AU - Soto, David
AU - Andrés, Rosa Maria
AU - Coccia, Elena
AU - Gasull, Xavier
AU - Planells-Ferrer, Laura
AU - Moubarak, Rana S.
AU - Soriano, Eduardo
AU - Comella, Joan X.
PY - 2016/10/21
Y1 - 2016/10/21
N2 - © 2016 The Author(s). 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.
AB - © 2016 The Author(s). 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.
U2 - https://doi.org/10.1038/srep35775
DO - https://doi.org/10.1038/srep35775
M3 - Article
VL - 6
M1 - 35775
ER -