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Article

SCA1-like disease in mice expressing wild-type ataxin-1 with a serine to aspartic acid replacement at residue 776.

Neuron - 23 Sept 2010

Duvick Lisa, Barnes Justin, Ebner Blake, Agrawal Smita, Andresen Michael, Lim Janghoo, Giesler Glenn J, Zoghbi Huda Y, Orr Harry T

Abstract excerpt

Glutamine tract expansion triggers nine neurodegenerative diseases by conferring toxic properties to the mutant protein. In SCA1, phosphorylation of ATXN1 at Ser776 is thought to be key for pathogenesis. Here, we show that replacing Ser776 with a phosphomimicking Asp converted ATXN1 with a wild-t...

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Identifiers

PMID: 20869591
DOI: 10.1016/j.neuron.2010.08.022
PMCID: PMC2946945

Genes

ATXN1

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 2 Sept 2026. Prepared record publication-20869591-2026-09-02.2. Manifest publication-graph-cohort-2026-09-02.2.

Source receipt: PubMed via Helena Literature Corpus, retrieved 2 Sept 2026.

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SCA1-like disease in mice expressing wild-type ataxin-1 with a serine to aspartic acid replacement at residue 776.PMID 20869591Read ↗

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