dc.contributor.author |
Martínez-Mármol, Ramón |
dc.contributor.author |
Barneda Zahonero, Bruna |
dc.contributor.author |
Soto, David |
dc.contributor.author |
Andrés, Rosa María |
dc.contributor.author |
Coccia, Elena |
dc.contributor.author |
Gasull, Xavier |
dc.contributor.author |
Planells Ferrer, Laura |
dc.contributor.author |
Moubarak, Rana S. |
dc.contributor.author |
Soriano García, Eduardo |
dc.contributor.author |
Comella i Carnicé, Joan Xavier, |
dc.date |
2016 |
dc.identifier |
https://ddd.uab.cat/record/206003 |
dc.identifier |
urn:10.1038/srep35775 |
dc.identifier |
urn:oai:ddd.uab.cat:206003 |
dc.identifier |
urn:pmid:27767058 |
dc.identifier |
urn:recercauab:ARE-83902 |
dc.identifier |
urn:articleid:20452322v6p35775 |
dc.identifier |
urn:scopus_id:84992425328 |
dc.identifier |
urn:wos_id:000385822500001 |
dc.identifier |
urn:oai:egreta.uab.cat:publications/59f6c93a-a974-440d-9e6d-22eed85d47d9 |
dc.identifier |
urn:pmc-uid:5073314 |
dc.identifier |
urn:pmcid:PMC5073314 |
dc.identifier |
urn:oai:pubmedcentral.nih.gov:5073314 |
dc.format |
application/pdf |
dc.language |
eng |
dc.publisher |
|
dc.relation |
Scientific reports ; Vol. 6 (2016), art. 35775 |
dc.rights |
open access |
dc.rights |
Aquest document està subjecte a una llicència d'ús Creative Commons. Es permet la reproducció total o parcial, la distribució, la comunicació pública de l'obra i la creació d'obres derivades, fins i tot amb finalitats comercials, sempre i quan es reconegui l'autoria de l'obra original. |
dc.rights |
https://creativecommons.org/licenses/by/4.0/ |
dc.title |
FAIM-L regulation of XIAP degradation modulates synaptic long-term depression and axon degeneration |
dc.type |
Article |
dc.description.abstract |
Caspases have recently emerged as key regulators of axonal pruning and degeneration and of longterm 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.. |