ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013
FAIM-L is an IAP-binding protein that inhibits XIAP ubiquitinylation and protects from Fas-induced apoptosis.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.
- Brain multi-omic Mendelian randomisation to identify novel drug targets for gliomagenesis.Human molecular genetics · 2025Pooled it
- FAIM modulates HCC progression via enhancing HMGA1 interaction with CDK7 and promoting its phosphorylation level.Journal of translational medicine · 2025Article
- Cell death in glioblastoma and the central nervous system.Cellular oncology (Dordrecht, Netherlands) · 2025Review
- Gene expression networks regulated by human personality.Molecular psychiatry · 2024Review
- Article
- Article
- Non-Canonical Roles of Apoptotic Caspases in the Nervous System.Frontiers in cell and developmental biology · 2022Review
- 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
- FAIM: An Antagonist of Fas-Killing and Beyond.Cells · 2019Review
- Genome-Wide Bimolecular Fluorescence Complementation-Based Proteomic Analysis ofFrontiers in immunology · 2018Article
- 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
- FAIM-L regulation of XIAP degradation modulates Synaptic Long-Term Depression and Axon Degeneration.Scientific reports · 2016Article
- Loss of Fas apoptosis inhibitory molecule leads to spontaneous obesity and hepatosteatosis.Cell death & disease · 2016Article
- Neurodegeneration and neuroinflammation: two processes, one target.Neural regeneration research · 2015Article
- Amyloid-β reduces the expression of neuronal FAIM-L, thereby shifting the inflammatory response mediated by TNFα from neuronal protection to death.Cell death & disease · 2015Article
- Selective inhibition of esophageal cancer cells by combination of HDAC inhibitors and Azacytidine.Epigenetics · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The neuronal long isoform of Fas Apoptotic Inhibitory Molecule (FAIM-L) protects from death receptor (DR)-induced apoptosis, yet its mechanism of protection remains unknown. Here, we show that FAIM-L protects rat neuronal Type II cells from Fas-induced apoptosis. XIAP has previously emerged as a molecular discriminator that is upregulated in Type II and downregulated in Type I apoptotic signaling. We demonstrate that FAIM-L requires sustained endogenous levels of XIAP to protect Type II cells as well as murine cortical neurons from Fas-induced apoptosis. FAIM-L interacts with the BIR2 domain of XIAP through an IAP-binding motif, the mutation of which impairs the antiapoptotic function of FAIM-L. Finally, we report that FAIM-L inhibits XIAP auto-ubiquitinylation and maintains its stability, thus conferring protection from apoptosis. Our results bring new understanding of the regulation of endogenous XIAP by a DR antagonist, pointing out at FAIM-L as a promising therapeutic tool for protection from apoptosis in pathological situations where XIAP levels are decreased.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.