ArticleCellular and molecular life sciences : CMLS2011
Muscleblind participates in RNA toxicity of expanded CAG and CUG repeats in Caenorhabditis elegans.
Article in Cellular and molecular life sciences : CMLS, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed.
- NMR structures of small molecules bound to a model of a CUG RNA repeat expansion.Bioorganic & medicinal chemistry letters · 2024Review
- NMR structures of small molecules bound to a model of an RNA CUG repeat expansion.bioRxiv : the preprint server for biology · 2024Article
- Review
- Current Status of Gene Therapy Research in Polyglutamine Spinocerebellar Ataxias.International journal of molecular sciences · 2021Review
- Huntington's disease brain-derived small RNAs recapitulate associated neuropathology in mice.Acta neuropathologica · 2021Article
- Huntington disease: new insights into molecular pathogenesis and therapeutic opportunities.Nature reviews. Neurology · 2020Review
- Gene Therapy for Neurodegenerative Diseases: Slowing Down the Ticking Clock.Frontiers in neuroscience · 2020Review
- Development of an AAV-Based MicroRNA Gene Therapy to Treat Machado-Joseph Disease.Molecular therapy. Methods & clinical development · 2019Article
- Models and mechanisms of repeat expansion disorders: a worm's eye view.Journal of genetics · 2018Review
- Role of non-coding RNAs in non-aging-related neurological disorders.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2018Review
- Review
- Protein sequestration as a normal function of long noncoding RNAs and a pathogenic mechanism of RNAs containing nucleotide repeat expansions.Human genetics · 2017Review
- Review
- RNA toxicity induced by expanded CAG repeats in Huntington's disease.Brain pathology (Zurich, Switzerland) · 2016Review
- Nuclear retention of full-length HTT RNA is mediated by splicing factors MBNL1 and U2AF65.Scientific reports · 2015Article
- Non-coding RNA in neural function, disease, and aging.Frontiers in genetics · 2015Review
- The role of the immune system in triplet repeat expansion diseases.Mediators of inflammation · 2015Review
- RAN translation and frameshifting as translational challenges at simple repeats of human neurodegenerative disorders.Nucleic acids research · 2014Review
- Ataxin-3 protein and RNA toxicity in spinocerebellar ataxia type 3: current insights and emerging therapeutic strategies.Molecular neurobiology · 2014Review
- Worming forward: amyotrophic lateral sclerosis toxicity mechanisms and genetic interactions in Caenorhabditis elegans.Frontiers in genetics · 2014Review
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have utilized Caenorhabditis elegans as a model to investigate the toxicity and underlying mechanism of untranslated CAG repeats in comparison to CUG repeats. Our results indicate that CAG repeats can be toxic at the RNA level in a length-dependent manner, similar to that of CUG repeats. Both CAG and CUG repeats of toxic length form nuclear foci and co-localize with C. elegans muscleblind (CeMBL), implying that CeMBL may play a role in repeat RNA toxicity. Consistently, the phenotypes of worms expressing toxic CAG and CUG repeats, including shortened life span and reduced motility rate, were partially reversed by CeMbl over-expression. These results provide the first experimental evidence to show that the RNA toxicity induced by expanded CAG and CUG repeats can be mediated, at least in part, through the functional alteration of muscleblind in worms.
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