ArticleMolecular and cellular biology2020
Cdc48/VCP and Endocytosis Regulate TDP-43 and FUS Toxicity and Turnover.
Article in Molecular and cellular biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
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Who cites it
15 citing papers in PubMed, 32 citations in OpenAlex.
- The p97 adaptor p47/NSFL1C is necessary for stress granule dissolution after heat stress.bioRxiv : the preprint server for biology · 2026Article
- Rsp5/NEDD4 and ESCRT regulate TDP-43 toxicity and turnover via an endolysosomal clearance mechanism.The Journal of cell biology · 2026Article
- Decoding TDP-43: the molecular chameleon of neurodegenerative diseases.Acta neuropathologica communications · 2024Review
- Saccharomyces cerevisiae as a research tool for RNA-mediated human disease.Wiley interdisciplinary reviews. RNA · 2023Review
- Transcriptomic Profiling Reveals Discrete Poststroke Dementia Neuronal and Gliovascular Signatures.Translational stroke research · 2023Article
- The Role of TDP-43 in Neurodegenerative Disease.Molecular neurobiology · 2022Review
- Nuclear RNA transcript levels modulate nucleocytoplasmic distribution of ALS/FTD-associated protein FUS.Scientific reports · 2022Article
- Review
- Mechanisms of TDP-43 Proteinopathy Onset and Propagation.International journal of molecular sciences · 2021Review
- TDP-43 and FUS mislocalization in VCP mutant motor neurons is reversed by pharmacological inhibition of the VCP D2 ATPase domain.Brain communications · 2021Article
- Stress Granule Assembly Can Facilitate but Is Not Required for TDP-43 Cytoplasmic Aggregation.Biomolecules · 2020Article
- The role of TDP-43 mislocalization in amyotrophic lateral sclerosis.Molecular neurodegeneration · 2020Review
- Cell-Clearing Systems Bridging Repeat Expansion Proteotoxicity and Neuromuscular Junction Alterations in ALS and SBMA.International journal of molecular sciences · 2020Review
- Mice Carrying ALS Mutant TDP-43, but Not Mutant FUS, Display In Vivo Defects in Axonal Transport of Signaling Endosomes.Cell reports · 2020Article
- Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Amyotrophic lateral sclerosis (ALS) is a fatal motor neuron degenerative disease. TDP-43 (TAR DNA-binding protein 43) and FUS (fused in sarcoma) are aggregation-prone RNA-binding proteins that in ALS can mislocalize to the cytoplasm of affected motor neuron cells, often forming cytoplasmic aggregates in the process. Such mislocalization and aggregation are implicated in ALS pathology, though the mechanism(s) of TDP-43 and FUS cytoplasmic toxicity remains unclear. Recently, we determined that the endocytic function aids the turnover (i.e., protein degradation) of TDP-43 and reduces TDP-43 toxicity. Here, we identified that Cdc48 and Ubx3, a Cdc48 cofactor implicated in endocytic function, regulates the turnover and toxicity of TDP-43 and FUS expressed in
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Registered trials
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