ArticleScientific reports2016
FUS/TLS acts as an aggregation-dependent modifier of polyglutamine disease model mice.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 21 citations in OpenAlex.
- Amyotrophic Lateral Sclerosis: Focus on Cytoplasmic Trafficking and Proteostasis.Molecular neurobiology · 2025Review
- Inhibition of class IIa HDACs reduces mutant HTT aggregation by affecting RNA stability.Frontiers in molecular neuroscience · 2025Article
- Implications of Tau Dysregulation in Huntington's Disease and Potential for New Therapeutics.Journal of Huntington's disease · 2023Review
- Proteomic analysis of heat-stable proteins revealed an increased proportion of proteins with compositionally biased regions.Scientific reports · 2022Article
- Hornerin deposits in neuronal intranuclear inclusion disease: direct identification of proteins with compositionally biased regions in inclusions.Acta neuropathologica communications · 2022Article
- Inactivation of Hippo and cJun-N-terminal Kinase (JNK) signaling mitigate FUS mediated neurodegeneration in vivo.Neurobiology of disease · 2020Article
- FUS P525L mutation causing amyotrophic lateral sclerosis and movement disorders.Brain and behavior · 2020Article
- Role of RNA Binding Proteins with prion-like domains in muscle and neuromuscular diseases.Cell stress · 2020Review
- Widespread remodeling of proteome solubility in response to different protein homeostasis stresses.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Spectrum of tau pathologies in Huntington's disease.Laboratory investigation; a journal of technical methods and pathology · 2019Article
- Tracking Effects of SIL1 Increase: Taking a Closer Look Beyond the Consequences of Elevated Expression Level.Molecular neurobiology · 2018Article
- Sequestration of PRMT1 and Nd1-L mRNA into ALS-linked FUS mutant R521C-positive aggregates contributes to neurite degeneration upon oxidative stress.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
13 authors at 7 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
FUS/TLS is an RNA/DNA-binding protein associated with neurodegenerative diseases including amyotrophic lateral sclerosis and frontotemporal lobar degeneration. Previously, we found that a prion-like domain in the N-terminus of FUS/TLS mediates co-aggregation between FUS/TLS and mutant huntingtin, the gene product of Huntington's disease (HD). Here, we show that heterozygous knockout of FUS/TLS worsened the phenotypes of model mice of (HD, but not spinal and bulbar muscular atrophy (SBMA). This difference was correlated with the degree of pathological association between disease proteins and FUS/TLS. Co-aggregation between FUS/TLS and mutant huntingtin resulted in the depletion of free FUS/TLS protein in HD mice that was detected as a monomer in SDS-PAGE analysis. Recently, we found that FUS/TLS paralogs, TAF15 and EWS, were up-regulated in homozygous FUS/TLS knockout mice. These two proteins were up-regulated in both HD and FUS/TLS heterozygote mice, and were further elevated in HD-TLS
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