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Times Cited: 232
Times Cited
Times Co-cited
Similarity
CAG expansions in a novel gene for Machado-Joseph disease at chromosome 14q32.1.
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Calpastatin-mediated inhibition of calpains in the mouse brain prevents mutant ataxin 3 proteolysis, nuclear localization and aggregation, relieving Machado-Joseph disease.
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Calpain inhibition is sufficient to suppress aggregation of polyglutamine-expanded ataxin-3.
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Overexpression of the autophagic beclin-1 protein clears mutant ataxin-3 and alleviates Machado-Joseph disease.
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An isoform of ataxin-3 accumulates in the nucleus of neuronal cells in affected brain regions of SCA3 patients.
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Deranged calcium signaling and neurodegeneration in spinocerebellar ataxia type 3.
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Calpain inhibition reduces ataxin-3 cleavage alleviating neuropathology and motor impairments in mouse models of Machado-Joseph disease.
Ana Teresa Simões, Nélio Gonçalves, Rui Jorge Nobre, Carlos Bandeira Duarte, Luís Pereira de Almeida. Hum Mol Genet 2014
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Nuclear localization of ataxin-3 is required for the manifestation of symptoms in SCA3: in vivo evidence.
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Calpain-mediated ataxin-3 cleavage in the molecular pathogenesis of spinocerebellar ataxia type 3 (SCA3).
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Polyglutamine tracts regulate beclin 1-dependent autophagy.
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CRISPR/Cas9-Targeted Deletion of Polyglutamine in Spinocerebellar Ataxia Type 3-Derived Induced Pluripotent Stem Cells.
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A mutant ataxin-3 putative-cleavage fragment in brains of Machado-Joseph disease patients and transgenic mice is cytotoxic above a critical concentration.
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The polyglutamine neurodegenerative protein ataxin-3 binds polyubiquitylated proteins and has ubiquitin protease activity.
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Autophagy Promoted the Degradation of Mutant ATXN3 in Neurally Differentiated Spinocerebellar Ataxia-3 Human Induced Pluripotent Stem Cells.
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Ataxin-3 is a histone-binding protein with two independent transcriptional corepressor activities.
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Clinical features, neurogenetics and neuropathology of the polyglutamine spinocerebellar ataxias type 1, 2, 3, 6 and 7.
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Induced pluripotent stem cells from patients with Huntington's disease show CAG-repeat-expansion-associated phenotypes.
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Unravelling Endogenous MicroRNA System Dysfunction as a New Pathophysiological Mechanism in Machado-Joseph Disease.
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Induced pluripotent stem cell - derived neurons for the study of spinocerebellar ataxia type 3.
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Genetic correction of Huntington's disease phenotypes in induced pluripotent stem cells.
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The deubiquitinating enzyme ataxin-3, a polyglutamine disease protein, edits Lys63 linkages in mixed linkage ubiquitin chains.
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Ataxin-3 represses transcription via chromatin binding, interaction with histone deacetylase 3, and histone deacetylation.
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Polyglutamine-expanded ataxin-3 causes cerebellar dysfunction of SCA3 transgenic mice by inducing transcriptional dysregulation.
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Silencing mutant ATXN3 expression resolves molecular phenotypes in SCA3 transgenic mice.
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A combinatorial approach to identify calpain cleavage sites in the Machado-Joseph disease protein ataxin-3.
Jonasz J Weber, Matthias Golla, Giambattista Guaitoli, Pimthanya Wanichawan, Stefanie N Hayer, Stefan Hauser, Ann-Christin Krahl, Maike Nagel, Sebastian Samer, Eleonora Aronica,[...]. Brain 2017
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Toward RNAi therapy for the polyglutamine disease Machado-Joseph disease.
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Calpain Inhibition Is Protective in Machado-Joseph Disease Zebrafish Due to Induction of Autophagy.
Maxinne Watchon, Kristy C Yuan, Nick Mackovski, Adam J Svahn, Nicholas J Cole, Claire Goldsbury, Silke Rinkwitz, Thomas S Becker, Garth A Nicholson, Angela S Laird. J Neurosci 2017
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CK2-dependent phosphorylation determines cellular localization and stability of ataxin-3.
Thorsten Mueller, Peter Breuer, Ina Schmitt, Jochen Walter, Bernd O Evert, Ullrich Wüllner. Hum Mol Genet 2009
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Evaluation of Antisense Oligonucleotides Targeting ATXN3 in SCA3 Mouse Models.
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Induced pluripotent stem cells from a spinal muscular atrophy patient.
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Ataxin-3 suppresses polyglutamine neurodegeneration in Drosophila by a ubiquitin-associated mechanism.
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Identification and functional dissection of localization signals within ataxin-3.
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Proteolytic cleavage of polyglutamine-expanded ataxin-3 is critical for aggregation and sequestration of non-expanded ataxin-3.
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Axonal inclusions in spinocerebellar ataxia type 3.
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Generation of human-induced pluripotent stem cells to model spinocerebellar ataxia type 2 in vitro.
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Vulnerability of Purkinje Cells Generated from Spinocerebellar Ataxia Type 6 Patient-Derived iPSCs.
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Evidence for proteasome involvement in polyglutamine disease: localization to nuclear inclusions in SCA3/MJD and suppression of polyglutamine aggregation in vitro.
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Polyglutamine spinocerebellar ataxias - from genes to potential treatments.
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Serotonergic signalling suppresses ataxin 3 aggregation and neurotoxicity in animal models of Machado-Joseph disease.
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Co-cited is the co-citation frequency, indicating how many articles cite the article together with the query article. Similarity is the co-citation as percentage of the times cited of the query article or the article in the search results, whichever is the lowest. These numbers are calculated for the last 100 citations when articles are cited more than 100 times.