(Q48574817)

12 February 2018

title

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

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12 February 2018

author name string

J M Ordway

1

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12 February 2018

S Tallaksen-Greene

2

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12 February 2018

C A Gutekunst

3

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12 February 2018

E M Bernstein

4

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12 February 2018

J A Cearley

5

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12 February 2018

H W Wiener

6

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12 February 2018

L S Dure

7

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12 February 2018

R Lindsey

8

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12 February 2018

S M Hersch

9

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12 February 2018

R S Jope

10

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12 February 2018

R L Albin

11

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12 February 2018

P J Detloff

12

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12 February 2018

language of work or name

English

0 references

publication date

1 December 1997

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12 February 2018

published in

Cell

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12 February 2018

volume

91

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12 February 2018

page(s)

753-763

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12 February 2018

issue

6

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12 February 2018

Trinucleotide repeats in neurologic diseases: an hypothesis concerning the pathogenesis of Huntington's disease, Kennedy's disease, and spinocerebellar ataxia type I.

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Cloning of the SCA7 gene reveals a highly unstable CAG repeat expansion

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

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

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

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Brain purines in a genetic mouse model of Lesch-Nyhan disease

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Dopamine deficiency in a genetic mouse model of Lesch-Nyhan disease

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Evidence for a repressive function of the long polyglutamine tract in the human androgen receptor: possible pathogenetic relevance for the (CAG)n-expanded neuronopathies

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Monoclonal antibodies directed against the amino-terminal domain of human TBP cross-react with TBP from other species.

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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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The cerebellar leucine-rich acidic nuclear protein interacts with ataxin-1

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Derivation of completely cell culture-derived mice from early-passage embryonic stem cells

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Huntington disease: new insights into the relationship between CAG expansion and disease

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In vitro synthesis and cloning of long CAG repeats

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When more is less: pathogenesis of glutamine repeat neurodegenerative diseases

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Huntingtin-encoded polyglutamine expansions form amyloid-like protein aggregates in vitro and in vivo

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Polyglutamine expansion as a pathological epitope in Huntington's disease and four dominant cerebellar ataxias

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Neuropathological classification of Huntington's disease

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Mouse models of hypoxanthine phosphoribosyltransferase deficiency

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7 January 2021

Autosomal dominant cerebellar ataxia (SCA6) associated with small polyglutamine expansions in the alpha 1A-voltage-dependent calcium channel

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7 January 2021

The expanding world of ataxins

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7 January 2021

Amphetamine-induced behavioral phenotype in a hypoxanthine-guanine phosphoribosyltransferase-deficient mouse model of Lesch-Nyhan syndrome

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Identifiers

DOI

1 reference

12 February 2018

PubMed ID

9413985

1 reference

12 February 2018