ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2007
The long form of Fas apoptotic inhibitory molecule is expressed specifically in neurons and protects them against death receptor-triggered apoptosis.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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
44 citing papers in PubMed, 77 citations in OpenAlex.
- Cell death in glioblastoma and the central nervous system.Cellular oncology (Dordrecht, Netherlands) · 2025Review
- Mendelian randomization of plasma proteomics identifies novel ALS-associated proteins and their GO enrichment and KEGG pathway analyses.BMC neurology · 2025Article
- Article
- Small Heat Shock Proteins Collaborate with FAIM to Prevent Accumulation of Misfolded Protein Aggregates.International journal of molecular sciences · 2022Article
- The nucleocapsid protein of rice stripe virus in cell nuclei of vector insect regulates viral replication.Protein & cell · 2022Article
- FAIM Enhances the Efficacy of Mesenchymal Stem Cell Transplantation by Inhibiting JNK-Induced c-FLIP Ubiquitination and Degradation.Stem cells international · 2022Article
- FAIM-L - SIVA-1: Two Modulators of XIAP in Non-Apoptotic Caspase Function.Frontiers in cell and developmental biology · 2021Review
- Fas Apoptosis Inhibitory Molecule Blocks and Dissolves Pathological Amyloid-β Species.Frontiers in molecular neuroscience · 2021Article
- 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 Is a Non-redundant Defender of Cellular Viability in the Face of Heat and Oxidative Stress and Interferes With Accumulation of Stress-Induced Protein Aggregates.Frontiers in molecular biosciences · 2020Article
- FAIM Opposes Aggregation of Mutant SOD1 That Typifies Some Forms of Familial Amyotrophic Lateral Sclerosis.Frontiers in neuroscience · 2020Article
- A meta-analysis of genome-wide association studies of epigenetic age acceleration.PLoS genetics · 2019Article
- FAIM: An Antagonist of Fas-Killing and Beyond.Cells · 2019Review
- Surveillance of Tumour Development: The Relationship Between Tumour-Associated RNAs and Ribonucleases.Frontiers in pharmacology · 2019Review
- Genome-Wide Bimolecular Fluorescence Complementation-Based Proteomic Analysis ofFrontiers in immunology · 2018Article
- The systemic tumor response to RNase A treatment affects the expression of genes involved in maintaining cell malignancy.Oncotarget · 2017Article
- 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
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Death receptors (DRs) and their ligands are expressed in developing nervous system. However, neurons are generally resistant to death induction through DRs and rather their activation promotes neuronal outgrowth and branching. These results suppose the existence of DRs antagonists expressed in the nervous system. Fas apoptosis inhibitory molecule (FAIM(S)) was first identified as a Fas antagonist in B-cells. Soon after, a longer alternative spliced isoform with unknown function was identified and named FAIM(L). FAIM(S) is widely expressed, including the nervous system, and we have shown previously that it promotes neuronal differentiation but it is not an anti-apoptotic molecule in this system. Here, we demonstrate that FAIM(L) is expressed specifically in neurons, and its expression is regulated during the development. Expression could be induced by NGF through the extracellular regulated kinase pathway in PC12 (pheochromocytoma cell line) cells. Contrary to FAIM(S), FAIM(L) does not increase the neurite outgrowth induced by neurotrophins and does not interfere with nuclear factor kappaB pathway activation as FAIM(S) does. Cells overexpressing FAIM(L) are resistant to apoptotic cell death induced by DRs such as Fas or tumor necrosis factor R1. Reduction of endogenous expression by small interfering RNA shows that endogenous FAIM(L) protects primary neurons from DR-induced cell death. The detailed analysis of this antagonism shows that FAIM(L) can bind to Fas receptor and prevent the activation of the initiator caspase-8 induced by Fas. In conclusion, our results indicate that FAIM(L) could be responsible for maintaining initiator caspases inactive after receptor engagement protecting neurons from the cytotoxic action of death ligands.
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.