Expanded polyglutamine domain possesses nuclear export activity which modulates subcellular localization and toxicity of polyQ disease protein via exportin-1. (Q39596478)

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scientific article published on 7 February 2011

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English	Expanded polyglutamine domain possesses nuclear export activity which modulates subcellular localization and toxicity of polyQ disease protein via exportin-1.	scientific article published on 7 February 2011

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21 January 2020

Expanded polyglutamine domain possesses nuclear export activity which modulates subcellular localization and toxicity of polyQ disease protein via exportin-1 (English)

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21 January 2020

Norbert Perrimon

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21 January 2020

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21 January 2020

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21 January 2020

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Hoi Yeung Li

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Wing Man Chan

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21 January 2020

Ho Tsoi

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21 January 2020

Chi Chung Wu

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21 January 2020

Tat Cheung Cheng

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21 January 2020

Pang Chui Shaw

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21 January 2020

Ho Yin Edwin Chan

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21 January 2020

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7 February 2011

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21 January 2020

Human Molecular Genetics

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21 January 2020

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21 January 2020

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21 January 2020

1738-1750

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21 January 2020

Trinucleotide Repeat Disorders

1 reference

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Nuclear localization of ataxin-3 is required for the manifestation of symptoms in SCA3: in vivo evidence

1 reference

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Ataxin-1 nuclear localization and aggregation: role in polyglutamine-induced disease in SCA1 transgenic mice.

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C-termini of P/Q-type Ca2+ channel alpha1A subunits translocate to nuclei and promote polyglutamine-mediated toxicity

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Nuclear localization of a non-caspase truncation product of atrophin-1, with an expanded polyglutamine repeat, increases cellular toxicity

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Nuclear targeting of mutant Huntingtin increases toxicity

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Huntingtin acts in the nucleus to induce apoptosis but death does not correlate with the formation of intranuclear inclusions.

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Nuclear-targeting of mutant huntingtin fragments produces Huntington's disease-like phenotypes in transgenic mice

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Nuclear accumulation of truncated atrophin-1 fragments in a transgenic mouse model of DRPLA.

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21 January 2018

Contribution of nuclear and extranuclear polyQ to neurological phenotypes in mouse models of Huntington's disease

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Nucleocytoplasmic transport signals affect the age at onset of abnormalities in knock-in mice expressing polyglutamine within an ectopic protein context

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Karyopherins: from nuclear-transport mediators to nuclear-function regulators

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Dynamic nuclear pore complexes: life on the edge.

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Ectopically expressed CAG repeats cause intranuclear inclusions and a progressive late onset neurological phenotype in the mouse.

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Polyglutamine expansion of huntingtin impairs its nuclear export

1 reference

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21 January 2018

Ataxin-7 can export from the nucleus via a conserved exportin-dependent signal.

1 reference

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21 January 2018

CRM1 is an export receptor for leucine-rich nuclear export signals

1 reference

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21 January 2018

Nuclear transport as a target for cell growth

1 reference

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21 January 2018

Leptomycin B is an inhibitor of nuclear export: inhibition of nucleo-cytoplasmic translocation of the human immunodeficiency virus type 1 (HIV-1) Rev protein and Rev-dependent mRNA

1 reference

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21 January 2018

Disruption of the toxic conformation of the expanded polyglutamine stretch leads to suppression of aggregate formation and cytotoxicity

1 reference

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21 January 2018

Ataxin-3 suppresses polyglutamine neurodegeneration in Drosophila by a ubiquitin-associated mechanism.

1 reference

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21 January 2018

Genome-wide screen for modifiers of ataxin-3 neurodegeneration in Drosophila

1 reference

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21 January 2018

Genetic modulation of polyglutamine toxicity by protein conjugation pathways in Drosophila

1 reference

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21 January 2018

Histone deacetylase inhibitors arrest polyglutamine-dependent neurodegeneration in Drosophila

1 reference

https://api.crossref.org/works/10.1093%2FHMG%2FDDR049

21 January 2018

Sodium dodecyl sulfate-insoluble oligomers are involved in polyglutamine degeneration.

1 reference

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21 January 2018

Chaperone suppression of alpha-synuclein toxicity in a Drosophila model for Parkinson's disease

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Modulation of neurodegeneration by molecular chaperones

1 reference

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21 January 2018

Dynamic regulation of molecular chaperone gene expression in polyglutamine disease.

1 reference

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21 January 2018

Polyglutamine-expanded ataxin-3 causes cerebellar dysfunction of SCA3 transgenic mice by inducing transcriptional dysregulation.

1 reference

https://api.crossref.org/works/10.1093%2FHMG%2FDDR049

21 January 2018

Polyglutamine gene function and dysfunction in the ageing brain

1 reference

https://api.crossref.org/works/10.1093%2FHMG%2FDDR049

21 January 2018

Huntingtin modulates transcription, occupies gene promoters in vivo, and binds directly to DNA in a polyglutamine-dependent manner

1 reference

https://api.crossref.org/works/10.1093%2FHMG%2FDDR049

21 January 2018

Suppression of polyglutamine-mediated neurodegeneration in Drosophila by the molecular chaperone HSP70.

1 reference

https://api.crossref.org/works/10.1093%2FHMG%2FDDR049

21 January 2018

Alpha-synuclein acts in the nucleus to inhibit histone acetylation and promote neurotoxicity

1 reference

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21 January 2018

Exon 1 of the HD gene with an expanded CAG repeat is sufficient to cause a progressive neurological phenotype in transgenic mice

1 reference

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21 January 2018

Formation of neuronal intranuclear inclusions underlies the neurological dysfunction in mice transgenic for the HD mutation

1 reference

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Nuclear accumulation of polyglutamine disease proteins and neuropathology

1 reference

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21 January 2018

The identification of a functional nuclear localization signal in the Huntington disease protein

1 reference

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21 January 2018

Interference of Crx-dependent transcription by ataxin-7 involves interaction between the glutamine regions and requires the ataxin-7 carboxy-terminal region for nuclear localization

1 reference

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21 January 2018

Nuclear import of the human androgen receptor

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Nuclear localization of the spinocerebellar ataxia type 7 protein, ataxin-7

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Identification and characterization of a ligand-regulated nuclear export signal in androgen receptor

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Huntingtin contains a highly conserved nuclear export signal

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Identification and functional dissection of localization signals within ataxin-3.

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Nucleocytoplasmic shuttling activity of ataxin-3.

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The roles of proteolysis and nuclear localisation in the toxicity of the polyglutamine diseases. A review

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Leptomycin B inactivates CRM1/exportin 1 by covalent modification at a cysteine residue in the central conserved region

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Ataxin-3 represses transcription via chromatin binding, interaction with histone deacetylase 3, and histone deacetylation

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Disruption of Axonal Transport by Loss of Huntingtin or Expression of Pathogenic PolyQ Proteins in Drosophila

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Suppression of neuropil aggregates and neurological symptoms by an intracellular antibody implicates the cytoplasmic toxicity of mutant huntingtin

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Progressive decrease in chaperone protein levels in a mouse model of Huntington's disease and induction of stress proteins as a therapeutic approach

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Mutant Huntingtin reduces HSP70 expression through the sequestration of NF-Y transcription factor.

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Polyglutamine expansion induces a protein-damaging stress connecting heat shock protein 70 to the JNK pathway

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Expanded polyglutamine protein forms nuclear inclusions and causes neural degeneration in Drosophila

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Use of double-stranded RNA interference in Drosophila cell lines to dissect signal transduction pathways.

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Human receptor for activated protein kinase C1 associates with polyglutamine aggregates and modulates polyglutamine toxicity.

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The carboxy-terminal region of the human immunodeficiency virus type 1 protein Rev has multiple roles in mediating CRM1-related Rev functions

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Chromatin immunoprecipitation for determining the association of proteins with specific genomic sequences in vivo

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