ArticleScientific reports2016
FAIM-L regulation of XIAP degradation modulates Synaptic Long-Term Depression and Axon Degeneration.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 16 citations in OpenAlex.
- Cell death in glioblastoma and the central nervous system.Cellular oncology (Dordrecht, Netherlands) · 2025Review
- Phosphoprofile reorganization of the actin binding protein Drebrin during long term depression.Frontiers in molecular neuroscience · 2025Article
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- Article
- Non-Canonical Roles of Apoptotic Caspases in the Nervous System.Frontiers in cell and developmental biology · 2022Review
- Mutagenic Consequences of Sublethal Cell Death Signaling.International journal of molecular sciences · 2021Review
- FAIM-L - SIVA-1: Two Modulators of XIAP in Non-Apoptotic Caspase Function.Frontiers in cell and developmental biology · 2021Review
- FAIM-S functions as a negative regulator of NF-κB pathway and blocks cell cycle progression in NSCLC cells.Cell cycle (Georgetown, Tex.) · 2020Article
- SIVA-1 regulates apoptosis and synaptic function by modulating XIAP interaction with the death receptor antagonist FAIM-L.Cell death & disease · 2020Article
- Article
- Effect of Enterococcus faecalis 2001 on colitis and depressive-like behavior in dextran sulfate sodium-treated mice: involvement of the brain-gut axis.Journal of neuroinflammation · 2019Article
- FAIM: An Antagonist of Fas-Killing and Beyond.Cells · 2019Review
- Apoptosis versus axon pruning: Molecular intersection of two distinct pathways for axon degeneration.Neuroscience research · 2019Review
- Physiological functions of non-apoptotic caspase activity in the nervous system.Seminars in cell & developmental biology · 2018Review
- More alive than dead: non-apoptotic roles for caspases in neuronal development, plasticity and disease.Cell death and differentiation · 2017Review
- Identification and characterization of new isoforms of human fas apoptotic inhibitory molecule (FAIM).PloS one · 2017Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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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