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Article

Wild-type FUS corrects ALS-like disease induced by cytoplasmic mutant FUS through autoregulation.

Molecular neurodegeneration - 6 Sept 2021

Sanjuan-Ruiz Inmaculada, Govea-Perez Noé, McAlonis-Downes Melissa, Dieterle Stéphane, Megat Salim, Dirrig-Grosch Sylvie, Picchiarelli Gina, Piol Diana, Zhu Qiang, Myers Brian, Lee Chao-Zong, Cleveland Don W, Lagier-Tourenne Clotilde, Da Cruz Sandrine, Dupuis Luc

Abstract excerpt

Mutations in FUS, an RNA-binding protein involved in multiple steps of RNA metabolism, are associated with the most severe forms of amyotrophic lateral sclerosis (ALS). Accumulation of cytoplasmic FUS is likely to be a major culprit in the toxicity of FUS mutations. Thus, preventing cytoplasmic mislocalization of the FUS protein may represent a valuable therapeutic strategy. FUS binds to its own pre-mRNA creating...

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Identifiers

PMID: 34488813
DOI: 10.1186/s13024-021-00477-w
PMCID: PMC8419956

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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Wild-type FUS corrects ALS-like disease induced by cytoplasmic mutant FUS through autoregulation.PMID 34488813Read ↗

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