A YAC mouse model for Huntington's disease with full-length mutant huntingtin, cytoplasmic toxicity, and selective striatal neurodegeneration. (Q45298582)

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scientific article published in May 1999

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English	A YAC mouse model for Huntington's disease with full-length mutant huntingtin, cytoplasmic toxicity, and selective striatal neurodegeneration.	scientific article published in May 1999

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scholarly article

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10 December 2019

A YAC mouse model for Huntington's disease with full-length mutant huntingtin, cytoplasmic toxicity, and selective striatal neurodegeneration (English)

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10 December 2019

Huntington's disease

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Michael R. Hayden

19

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10 December 2019

Roshni Singaraja

6

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10 December 2019

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10 December 2019

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J G Hodgson

1

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10 December 2019

N Agopyan

2

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10 December 2019

C A Gutekunst

3

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10 December 2019

B R Leavitt

4

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10 December 2019

F LePiane

5

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10 December 2019

D J Smith

7

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10 December 2019

N Bissada

8

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10 December 2019

K McCutcheon

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10 December 2019

J Nasir

10

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10 December 2019

L Jamot

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10 December 2019

X J Li

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10 December 2019

M E Stevens

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10 December 2019

J C Roder

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10 December 2019

A G Phillips

16

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10 December 2019

E M Rubin

17

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10 December 2019

S M Hersch

18

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10 December 2019

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1 May 1999

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10 December 2019

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10 December 2019

23

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10 December 2019

1

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10 December 2019

181-192

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10 December 2019

Alternative excitotoxic hypotheses

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Dentatorubral and pallidoluysian atrophy (DRPLA). Clinical and neuropathological findings in genetically confirmed North American and European pedigrees

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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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Huntingtin is a cytoplasmic protein associated with vesicles in human and rat brain neurons

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Selective sparing of a class of striatal neurons in Huntington's disease

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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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Human huntingtin derived from YAC transgenes compensates for loss of murine huntingtin by rescue of the embryonic lethal phenotype

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Length of huntingtin and its polyglutamine tract influences localization and frequency of intracellular aggregates

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Selective impairment of learning and blockade of long-term potentiation by an N-methyl-D-aspartate receptor antagonist, AP5

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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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