ArticleCell reports2019
Mutant FUS and ELAVL4 (HuD) Aberrant Crosstalk 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 42 papers.
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Who cites it
42 citing papers in PubMed, 74 citations in OpenAlex.
- Distinct proteomic CSF profiles in genetic frontotemporal lobar degeneration.Brain : a journal of neurology · 2026Article
- 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
- Stabilized real-time Brillouin microscopy reveals fractal organization of protein condensates in living cells.Nature communications · 2026Article
- Self-driving microscopy detects the onset of protein aggregation and enables intelligent Brillouin imaging.Nature communications · 2025Article
- Highly dynamic mechanical transitions in embryonic cell populations during Drosophila gastrulation.Nature communications · 2025Article
- YAP1 promoter-associated noncoding RNA affects Ewing sarcoma cell tumorigenicity by regulating YAP1 expression.Cellular & molecular biology letters · 2025Article
- Review
- ALS-associated FUS mutation reshapes the RNA and protein composition of stress granules.Nucleic acids research · 2024Article
- HuD impairs neuromuscular junctions and induces apoptosis in human iPSC and Drosophila ALS models.Nature communications · 2024Article
- ePRINT: exonuclease assisted mapping of protein-RNA interactions.Genome biology · 2024Article
- Nicotinamide Mononucleotide (NMN) Works in Type 2 Diabetes through Unexpected Effects in Adipose Tissue, Not by Mitochondrial Biogenesis.International journal of molecular sciences · 2024Article
- Overlapping Neuroimmune Mechanisms and Therapeutic Targets in Neurodegenerative Disorders.Biomedicines · 2023Review
- Cytoplasmic aggregation of mutant FUS causes multistep RNA splicing perturbations in the course of motor neuron pathology.Nucleic acids research · 2023Article
- Emerging Trends in the Field of Inflammation and Proteinopathy in ALS/FTD Spectrum Disorder.Biomedicines · 2023Review
- FUS Alters circRNA Metabolism in Human Motor Neurons Carrying the ALS-Linked P525L Mutation.International journal of molecular sciences · 2023Article
- Digital color-coded molecular barcoding reveals dysregulation of common FUS and FMRP targets in soma and neurites of ALS mutant motoneurons.Cell death discovery · 2023Article
- Phase separation and pathologic transitions of RNP condensates in neurons: implications for amyotrophic lateral sclerosis, frontotemporal dementia and other neurodegenerative disorders.Frontiers in molecular neuroscience · 2023Review
- Emerging Roles for the RNA-Binding Protein HuD (ELAVL4) in Nervous System Diseases.International journal of molecular sciences · 2022Review
- Aberrant NOVA1 function disrupts alternative splicing in early stages of amyotrophic lateral sclerosis.Acta neuropathologica · 2022Article
- SARS-CoV-2 impairs the disassembly of stress granules and promotes ALS-associated amyloid aggregation.Protein & cell · 2022Article
Corrections and comments
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Authors and funding
16 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Amyotrophic lateral sclerosis (ALS) has been genetically linked to mutations in RNA-binding proteins (RBPs), including FUS. Here, we report the RNA interactome of wild-type and mutant FUS in human motor neurons (MNs). This analysis identified a number of RNA targets. Whereas the wild-type protein preferentially binds introns, the ALS mutation causes a shift toward 3' UTRs. Neural ELAV-like RBPs are among mutant FUS targets. As a result, ELAVL4 protein levels are increased in mutant MNs. ELAVL4 and mutant FUS interact and co-localize in cytoplasmic speckles with altered biomechanical properties. Upon oxidative stress, ELAVL4 and mutant FUS are engaged in stress granules. In the spinal cord of FUS ALS patients, ELAVL4 represents a neural-specific component of FUS-positive cytoplasmic aggregates, whereas in sporadic patients it co-localizes with phosphorylated TDP-43-positive inclusions. We propose that pathological mutations in FUS trigger an aberrant crosstalk with ELAVL4 with implications for ALS.
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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.