ArticleCell reports2019
Antiviral Immune Response as a Trigger of FUS Proteinopathy in Amyotrophic Lateral Sclerosis.
Article in Cell reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
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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
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Who cites it
27 citing papers in PubMed, 46 citations in OpenAlex.
- Breaking β-sheets in FUS prion-like domain preserves phase separation and function but prevents aggregation and toxicity.bioRxiv : the preprint server for biology · 2026Article
- M6A-dependent RNA condensation underlies FUS autoregulation and can be harnessed for ALS therapy development.Science advances · 2025Article
- FUS Mislocalization Rewires a Cortical Gene Network to Drive Cognitive and Behavioral Impairment in ALS.medRxiv : the preprint server for health sciences · 2025Article
- Underestimated virus impaired cognition-more evidence and more work to do.Frontiers in immunology · 2025Review
- The Scientific and Therapeutic Rationale for Off-Label Treatments in Amyotrophic Lateral Sclerosis.Annals of neurology · 2024Review
- Contribution of CNS and extra-CNS infections to neurodegeneration: a narrative review.Journal of neuroinflammation · 2024Review
- Neurotropic virus infection and neurodegenerative diseases: Potential roles of autophagy pathway.CNS neuroscience & therapeutics · 2024Review
- Increased expression of human antiviral protein MxA in FUS proteinopathy in amyotrophic lateral sclerosis.Brain pathology (Zurich, Switzerland) · 2024Article
- Neuronal dysfunction caused by FUSR521G promotes ALS-associated phenotypes that are attenuated by NF-κB inhibition.Acta neuropathologica communications · 2023Article
- Sensing nucleotide composition in virus RNA.Bioscience reports · 2023Review
- Early activation of cellular stress and death pathways caused by cytoplasmic TDP-43 in the rNLS8 mouse model of ALS and FTD.Molecular psychiatry · 2023Article
- Enterovirus infection and its relationship with neurodegenerative diseases.Memorias do Instituto Oswaldo Cruz · 2023Article
- Viruses in neurodegenerative diseases: More than just suspects in crimes.PLoS pathogens · 2022Review
- The Role and Therapeutic Potential of the Integrated Stress Response in Amyotrophic Lateral Sclerosis.International journal of molecular sciences · 2022Review
- ALS-linked cytoplasmic FUS assemblies are compositionally different from physiological stress granules and sequester hnRNPA3, a novel modifier of FUS toxicity.Neurobiology of disease · 2022Article
- Chlorovirus ATCV-1 Accelerates Motor Deterioration in SOD1-G93A Transgenic Mice and Its SOD1 Augments Induction of Inflammatory Factors From Murine Macrophages.Frontiers in neurology · 2022Article
- FUS/TLS Suppresses Enterovirus Replication and Promotes Antiviral Innate Immune Responses.Journal of virology · 2021Article
- The Links between ALS and NF-κB.International journal of molecular sciences · 2021Review
- The Complexity of the cGAS-STING Pathway in CNS Pathologies.Frontiers in neuroscience · 2021Review
- SCASP: A Simple and Robust SDS-Aided Sample Preparation Method for Proteomic Research.Molecular & cellular proteomics : MCP · 2021Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Mutations in the FUS gene cause familial amyotrophic lateral sclerosis (ALS-FUS). In ALS-FUS, FUS-positive inclusions are detected in the cytoplasm of neurons and glia, a condition known as FUS proteinopathy. Mutant FUS incorporates into stress granules (SGs) and can spontaneously form cytoplasmic RNA granules in cultured cells. However, it is unclear what can trigger the persistence of mutant FUS assemblies and lead to inclusion formation. Using CRISPR/Cas9 cell lines and patient fibroblasts, we find that the viral mimic dsRNA poly(I:C) or a SG-inducing virus causes the sustained presence of mutant FUS assemblies. These assemblies sequester the autophagy receptor optineurin and nucleocytoplasmic transport factors. Furthermore, an integral component of the antiviral immune response, type I interferon, promotes FUS protein accumulation by increasing FUS mRNA stability. Finally, mutant FUS-expressing cells are hypersensitive to dsRNA toxicity. Our data suggest that the antiviral immune response is a plausible second hit for FUS proteinopathy.
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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.