ArticleRare diseases (Austin, Tex.)2014
FUS-regulated RNA metabolism and DNA damage repair: Implications for amyotrophic lateral sclerosis and frontotemporal dementia pathogenesis.
Article in Rare diseases (Austin, Tex.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed, 37 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
- From Yeast to Therapeutics: Modeling Neurodegenerative Diseases in Saccharomyces cerevisiae.Yeast (Chichester, England) · 2025Review
- Review
- Disease-disease interactions: molecular links of neurodegenerative diseases with cancer, viral infections, and type 2 diabetes.Translational neurodegeneration · 2025Review
- Integrative Transcriptomic and Network-Based Analysis of Neuromuscular Diseases.International journal of molecular sciences · 2025Article
- Molecular hallmarks of ageing in amyotrophic lateral sclerosis.Cellular and molecular life sciences : CMLS · 2024Review
- "Boundary residues" between the folded RNA recognition motif and disordered RGG domains are critical for FUS-RNA binding.The Journal of biological chemistry · 2023Article
- Genetic Interaction of tRNA-Dependent Mistranslation with Fused in Sarcoma Protein Aggregates.Genes · 2023Article
- FUS Microphase Separation: Regulation by Nucleic Acid Polymers and DNA Repair Proteins.International journal of molecular sciences · 2022Article
- The Complex Mechanisms by Which Neurons Die Following DNA Damage in Neurodegenerative Diseases.International journal of molecular sciences · 2022Review
- Wild-Type and Mutant FUS Expression Reduce Proliferation and Neuronal Differentiation Properties of Neural Stem Progenitor Cells.International journal of molecular sciences · 2021Article
- Aberrant Phase Separation of FUS Leads to Lysosome Sequestering and Acidification.Frontiers in cell and developmental biology · 2021Article
- Nucleolin Rescues TDP-43 Toxicity in Yeast and Human Cell Models.Frontiers in cellular neuroscience · 2021Article
- Fused in Sarcoma (FUS) in DNA Repair: Tango with Poly(ADP-ribose) Polymerase 1 and Compartmentalisation of Damaged DNA.International journal of molecular sciences · 2020Review
- Complex karyotype with crypticOncology letters · 2020Article
- Risk Factors and Emerging Therapies in Amyotrophic Lateral Sclerosis.International journal of molecular sciences · 2019Review
- A context-based ABC model for literature-based discovery.PloS one · 2019Article
- Disease-modifying effects of metabolic perturbations in ALS/FTLD.Molecular neurodegeneration · 2018Review
- FUS interacts with ATP synthase beta subunit and induces mitochondrial unfolded protein response in cellular and animal models.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Arginine methylation of translocated in liposarcoma (TLS) inhibits its binding to long noncoding RNA, abrogating TLS-mediated repression of CBP/p300 activity.The Journal of biological chemistry · 2018Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cytoplasmic inclusion of RNA binding protein FUS/TLS in neurons and glial cells is a characteristic pathology of a subgroup of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). Dysregulation of RNA metabolism caused by FUS cytoplasmic inclusion emerges to be a key event in FUS-associated ALS/FTD pathogenesis. Our recent discovery of a FUS autoregulatory mechanism and its dysregulation in ALS-FUS mutants demonstrated that dysregulated alternative splicing can directly exacerbate the pathological FUS accumulation. We show here that FUS targets RNA for pre-mRNA alternative splicing and for the processing of long intron-containing transcripts, and that these targets are enriched for genes in neurogenesis and gene expression regulation. We also identify that FUS RNA targets are enriched for genes in the DNA damage response pathway. Together, the data support a model in which dysregulated RNA metabolism and DNA damage repair together may render neurons more vulnerable and accelerate neurodegeneration in ALS and FTD.
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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.