ArticleNature communications2020
Aberrant interaction of FUS with the U1 snRNA provides a molecular mechanism of FUS induced amyotrophic lateral sclerosis.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 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.
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Who cites it
48 citing papers in PubMed, 79 citations in OpenAlex.
- Programmable DNA protonuclei reveal environmental context on protein phase separation.Nature communications · 2026Article
- U1 Small Nuclear Ribonucleoprotein Autoantibodies Reflect the Disruption of the Blood-Nerve Barrier in Guillain-Barré Syndrome.International journal of molecular sciences · 2026Article
- RNA G-quadruplexes function as a tunable switch of FUS phase separation.Nucleic acids research · 2026Article
- Systemic Inflammation Triggers Motor Axon Degeneration Via Macrophage IL-1β-Mediated P53/SIRT1/Autophagy Pathway.Inflammation · 2026Article
- Structuring Disorder via Supervised Molecular Dynamics: Uncovering Arginine-Glycine-Glycine-Mediated Ribonucleic Acid-Intrinsically Disordered Region Recognition Mechanisms.Journal of chemical information and modeling · 2026Article
- Gene expression signatures from whole blood predict amyotrophic lateral sclerosis case status and survival.Nature communications · 2025Article
- Splicing factor Sf3b1 facilitates maintenance of neuronal dendrites by modulating mitochondrial health.Cellular and molecular life sciences : CMLS · 2025Article
- G-quadruplex structural motifs modulate protein-RNA interactions within the transcriptome.Genome biology · 2025Article
- QKI ensures splicing fidelity during cardiogenesis by engaging the U6 tri-snRNP to activate splicing at weak 5' splice sites.bioRxiv : the preprint server for biology · 2025Article
- RNA Binding Mechanism of the FUS Zinc Finger in Concert with Its Flanking Intrinsically Disordered Region.Journal of chemical information and modeling · 2025Article
- RNA-binding proteins in ALS and FTD: from pathogenic mechanisms to therapeutic insights.Molecular neurodegeneration · 2025Review
- Single-cell RNA-sequencing reveals early mitochondrial dysfunction unique to motor neurons shared across FUS- and TARDBP-ALS.Nature communications · 2025Article
- LLPS REDIFINE allows the biophysical characterization of multicomponent condensates without tags or labels.Nature communications · 2025Article
- Gene therapy breakthroughs in ALS: a beacon of hope for 20% of ALS patients.Translational neurodegeneration · 2025Review
- RNA dysregulation in neurodegenerative diseases.The EMBO journal · 2025Review
- Molecular Mechanisms of Phase Separation and Amyloidosis of ALS/FTD-linked FUS and TDP-43.Aging and disease · 2024Review
- Understanding Amyotrophic Lateral Sclerosis: Pathophysiology, Diagnosis, and Therapeutic Advances.International journal of molecular sciences · 2024Review
- Adenosine Triphosphate: The Primordial Molecule That Controls Protein Homeostasis and Shapes the Genome-Proteome Interface.Biomolecules · 2024Review
- Specific protein-RNA interactions are mostly preserved in biomolecular condensates.Science advances · 2024Article
- RNAelem: an algorithm for discovering sequence-structure motifs in RNA bound by RNA-binding proteins.Bioinformatics advances · 2024Article
Corrections and comments
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Authors and funding
15 authors at 4 institutions in 5 countries.
Funding
Abstract
Mutations in the RNA-binding protein Fused in Sarcoma (FUS) cause early-onset amyotrophic lateral sclerosis (ALS). However, a detailed understanding of central RNA targets of FUS and their implications for disease remain elusive. Here, we use a unique blend of crosslinking and immunoprecipitation (CLIP) and NMR spectroscopy to identify and characterise physiological and pathological RNA targets of FUS. We find that U1 snRNA is the primary RNA target of FUS via its interaction with stem-loop 3 and provide atomic details of this RNA-mediated mode of interaction with the U1 snRNP. Furthermore, we show that ALS-associated FUS aberrantly contacts U1 snRNA at the Sm site with its zinc finger and traps snRNP biogenesis intermediates in human and murine motor neurons. Altogether, we present molecular insights into a FUS toxic gain-of-function involving direct and aberrant RNA-binding and strengthen the link between two motor neuron diseases, ALS and spinal muscular atrophy (SMA).
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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.