ArticleProceedings of the National Academy of Sciences of the United States of America2018
ALS mutations of FUS suppress protein translation and disrupt the regulation of nonsense-mediated decay.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 112 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
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.
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Who cites it
112 citing papers in PubMed, 187 citations in OpenAlex.
- Contrasting clinical trajectories in two ALS patients with rare FUS variants: implications for variant interpretation, penetrance, and trial readiness.Neurogenetics · 2026Article
- Programmable DNA protonuclei reveal environmental context on protein phase separation.Nature communications · 2026Article
- Human iPSC-Derived Spinal Neurons Carrying the ALS FUS (P525L) Mutation Exhibit Lower Response to Inhibitory Neurotransmitters.Cellular and molecular neurobiology · 2026Article
- Proteasomal-dependent CHK1 degradation leads to DNA damage accumulation in ALS cellular model systems.Cell death & disease · 2026Article
- Targeting RNA binding proteins with small-molecule inhibitors: Advances, challenges, and therapeutic opportunities.Acta pharmaceutica Sinica. B · 2026Review
- Article
- Traditional Chinese botanical medicines and plant-derived bioactive compounds in amyotrophic lateral sclerosis: mechanistic evidence, translational challenges, and therapeutic opportunities.Frontiers in pharmacology · 2026Review
- TARDBP (TDP-43) Knock-in Zebrafish Display a Late-Onset Motor Phenotype and Loss of Large Spinal Cord Motor Neurons.Annals of neurology · 2026Article
- LINE-1 retrotransposition in a mouse TDP-43 model of neurodegeneration marks motor cortex neurons for cell-intrinsic and cell non-autonomous programmed cell death.PLoS genetics · 2025Article
- G-quadruplex structural motifs modulate protein-RNA interactions within the transcriptome.Genome biology · 2025Article
- Nonsense-Mediated mRNA Decay: Mechanisms and Recent Implications in Cardiovascular Diseases.Cells · 2025Review
- ESC models of autism with copy-number variations reveal cell-type-specific translational vulnerability.Cell genomics · 2025Article
- Exploring Protein Misfolding in Amyotrophic Lateral Sclerosis: Structural and Functional Insights.Biomedicines · 2025Review
- Reducing Granules Without Splicing Restoration Alleviates RBM20 Cardiomyopathy.Circulation research · 2025Article
- Rare Diseases, Spotlighting Amyotrophic Lateral Sclerosis, Huntington's Disease, and Myasthenia Gravis: Insights from Landscape Analysis of Current Research.Biochemistry · 2025Review
- Neuromuscular dysfunction in patient-derived FUSNAR molecular medicine · 2025Article
- RNA dysregulation in neurodegenerative diseases.The EMBO journal · 2025Review
- ALS-associated FUS mutation reshapes the RNA and protein composition of stress granules.Nucleic acids research · 2024Article
- Heterogeneous Slowdown of Dynamics in the Condensate of an Intrinsically Disordered Protein.The journal of physical chemistry letters · 2024Article
- Pathogenic tau induces an adaptive elevation in mRNA translation rate at early stages of disease.Aging cell · 2024Article
52 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Amyotrophic lateral sclerosis (ALS) is an incurable neurodegenerative disease characterized by preferential motor neuron death. Approximately 15% of ALS cases are familial, and mutations in the
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.