Nuclear localization of ataxin-3 is required for the manifestation of symptoms in SCA3: in vivo evidence (Q28585964)

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2 January 2020

title

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

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GOA release 2020-03-11

author

Hartwig Wolburg

12

0 references

Lukas Rüttiger

5

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Marlies Knipper

9

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Olaf Riess

14

object named as

Olaf Riess

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author name string

Ulrike Bichelmeier

1

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Thorsten Schmidt

2

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Jeannette Hübener

3

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Jana Boy

4

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Karina Häbig

6

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Sven Poths

7

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Michael Bonin

8

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Johannes Wilbertz

11

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Franco Laccone

13

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Lukas Rüttiger

5

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Marlies Knipper

9

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Werner J Schmidt

10

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Hartwig Wolburg

12

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language of work or name

English

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publication date

1 July 2007

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2 January 2020

published in

Journal of Neuroscience

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volume

27

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page(s)

7418-7428

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issue

28

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Heterogeneous intracellular localization and expression of ataxin-3.

2 January 2020

cites work

1 reference

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Mice transgenic for an expanded CAG repeat in the Huntington's disease gene develop diabetes

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Brain neurotransmitter deficits in mice transgenic for the Huntington's disease mutation

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Abundant expression and cytoplasmic aggregations of [alpha]1A voltage-dependent calcium channel protein associated with neurodegeneration in spinocerebellar ataxia type 6

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

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Nuclear targeting of mutant Huntingtin increases toxicity

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Characterization of the rat spinocerebellar ataxia type 3 gene.

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Nuclear localization or inclusion body formation of ataxin-2 are not necessary for SCA2 pathogenesis in mouse or human

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SCA17, a novel autosomal dominant cerebellar ataxia caused by an expanded polyglutamine in TATA-binding protein

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Spinocerebellar ataxias in the Netherlands: prevalence and age at onset variance analysis.

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Protein surveillance machinery in brains with spinocerebellar ataxia type 3: redistribution and differential recruitment of 26S proteasome subunits and chaperones to neuronal intranuclear inclusions

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YAC transgenic mice carrying pathological alleles of the MJD1 locus exhibit a mild and slowly progressive cerebellar deficit.

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Time course of polyglutamine aggregate body formation and cell death: enhanced growth in nucleus and an interval for cell death.

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A fast polymerase chain reaction-mediated strategy for introducing repeat expansions into CAG-repeat containing genes.

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Lack of Bdnf and TrkB signalling in the postnatal cochlea leads to a spatial reshaping of innervation along the tonotopic axis and hearing loss

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Microtubule destabilization and nuclear entry are sequential steps leading to toxicity in Huntington's disease

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The polyglutamine neurodegenerative protein ataxin-3 binds polyubiquitylated proteins and has ubiquitin protease activity

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Transgenic mice expressing mutant A53T human alpha-synuclein show neuronal dysfunction in the absence of aggregate formation.

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Functional recovery of locus coeruleus noradrenergic neurons after DSP-4 lesion: effects on dopamine levels and neuroleptic induced-parkinsonian symptoms in rats

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Paroxetine retards disease onset and progression in Huntingtin mutant mice

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Autosomal dominant cerebellar ataxias: clinical features, genetics, and pathogenesis

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Under stress, the absence of intermediate filaments from Müller cells in the retina has structural and functional consequences

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Structural and functional analysis of ataxin-2 and ataxin-3.

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Differential roles of fibroblast growth factor-2 during development and maintenance of auditory sensory epithelia.

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12 December 2020

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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12 December 2020

The R6/2 transgenic mouse model of Huntington's disease develops diabetes due to deficient beta-cell mass and exocytosis

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EMPReSS: European mouse phenotyping resource for standardized screens

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The neuroprotective efficacy of alpha-crystallin against acute inflammation in mice

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

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12 December 2020

A semiautomated analysis method for catecholamines, indoleamines, and some prominent metabolites in microdissected regions of the nervous system: an isocratic HPLC technique employing coulometric detection and minimal sample preparation.

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12 December 2020

Striatal dopamine and homovanillic acid in Huntington's Disease

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Cleavage of Structural Proteins during the Assembly of the Head of Bacteriophage T4

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A short amino acid sequence able to specify nuclear location

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Identification of a signal for rapid export of proteins from the nucleus

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Expression analysis of the ataxin-1 protein in tissues from normal and spinocerebellar ataxia type 1 individuals

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CAG expansions in a novel gene for Machado-Joseph disease at chromosome 14q32.1

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A clinical and pathologic study of a large Japanese family with Machado-Joseph disease tightly linked to the DNA markers on chromosome 14q

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Spinocerebellar ataxia 3 and Machado-Joseph disease: clinical, molecular, and neuropathological features.

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Expanded polyglutamine in the Machado-Joseph disease protein induces cell death in vitro and in vivo

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

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Brain MRI, lumbar CSF monoamine concentrations, and clinical descriptors of patients with spinocerebellar ataxia mutations

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Characterisation of two promoters for prion protein (PrP) gene expression in neuronal cells.

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Machado-Joseph disease gene product is a cytoplasmic protein widely expressed in brain

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Machado-Joseph disease gene products carrying different carboxyl termini

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Intranuclear inclusions of expanded polyglutamine protein in spinocerebellar ataxia type 3.

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Aggregation of huntingtin in neuronal intranuclear inclusions and dystrophic neurites in brain

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Spinocerebellar ataxia type 2. Genotype and phenotype in German kindreds.

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Behavioral and functional analysis of mouse phenotype: SHIRPA, a proposed protocol for comprehensive phenotype assessment

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Truncated N-terminal fragments of huntingtin with expanded glutamine repeats form nuclear and cytoplasmic aggregates in cell culture.

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Ataxin-3 is transported into the nucleus and associates with the nuclear matrix

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

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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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In vitro evidence for both the nucleus and cytoplasm as subcellular sites of pathogenesis in Huntington's disease.

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10.1523/JNEUROSCI.4540-06.2007

Identifiers

DOI

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Consolidated OpenCitations Corpus – April 2017

570964

https://www.ebi.ac.uk/europepmc/webservices/rest/search?query=EXT_ID:17626202%20AND%20SRC:MED&resulttype=core&format=json

2 January 2020

570964

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Consolidated OpenCitations Corpus – April 2017

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https://www.ebi.ac.uk/europepmc/webservices/rest/search?query=EXT_ID:17626202%20AND%20SRC:MED&resulttype=core&format=json

2 January 2020

2 references

Consolidated OpenCitations Corpus – April 2017

570964