Deletion of the triplet repeat encoding polyglutamine within the mouse Huntington's disease gene results in subtle behavioral/motor phenotypes in vivo and elevated levels of ATP with cellular senescence in vitro
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Huntingtin has a membrane association signal that can modulate huntingtin aggregation, nuclear entry and toxicityHuntington's disease: the past, present, and future search for disease modifiers.Unbiased gene expression analysis implicates the huntingtin polyglutamine tract in extra-mitochondrial energy metabolismFunctional characterization of rare FOXP2 variants in neurodevelopmental disorder.Generation and Characterization of Knock-in Mouse Models Expressing Versions of Huntingtin with Either an N17 or a Combined PolyQ and Proline-Rich Region Deletion.HCN channels expressed in the inner ear are necessary for normal balance function.Deletion of the huntingtin proline-rich region does not significantly affect normal huntingtin function in miceDeletion of the huntingtin polyglutamine stretch enhances neuronal autophagy and longevity in mice.LRRK2 knockout mice have an intact dopaminergic system but display alterations in exploratory and motor co-ordination behaviors.Huntingtin facilitates polycomb repressive complex 2.Huntington's disease: revisiting the aggregation hypothesis in polyglutamine neurodegenerative diseases.Striatal neurons expressing full-length mutant huntingtin exhibit decreased N-cadherin and altered neuritogenesis.HD CAG-correlated gene expression changes support a simple dominant gain of function.Neurodegenerative processes in Huntington's disease.Is Huntington's a glutamine storage disease?Animal models of Huntington's disease: implications in uncovering pathogenic mechanisms and developing therapies.Multiple pathways contribute to the pathogenesis of Huntington disease.Therapeutic perspectives for the treatment of Huntington's disease: treating the whole bodyMolecular mechanisms and potential therapeutical targets in Huntington's disease.Huntington's disease, calcium, and mitochondria.The biological function of the Huntingtin protein and its relevance to Huntington's Disease pathologyAn in vitro perspective on the molecular mechanisms underlying mutant huntingtin protein toxicityHuntingtin gene repeat size variations affect risk of lifetime depression.
P2860
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P2860
Deletion of the triplet repeat encoding polyglutamine within the mouse Huntington's disease gene results in subtle behavioral/motor phenotypes in vivo and elevated levels of ATP with cellular senescence in vitro
description
2006 թուականի Փետրուարին հրատարակուած գիտական յօդուած
@hyw
2006 թվականի փետրվարին հրատարակված գիտական հոդված
@hy
artículu científicu espublizáu en 2006
@ast
im Februar 2006 veröffentlichter wissenschaftlicher Artikel
@de
scientific journal article
@en
vedecký článok (publikovaný 2006/02/15)
@sk
vědecký článek publikovaný v roce 2006
@cs
wetenschappelijk artikel (gepubliceerd op 2006/02/15)
@nl
наукова стаття, опублікована в лютому 2006
@uk
مقالة علمية (نشرت في 15-2-2006)
@ar
name
Deletion of the triplet repeat ...... h cellular senescence in vitro
@ast
Deletion of the triplet repeat ...... h cellular senescence in vitro
@en
Deletion of the triplet repeat ...... h cellular senescence in vitro
@nl
type
label
Deletion of the triplet repeat ...... h cellular senescence in vitro
@ast
Deletion of the triplet repeat ...... h cellular senescence in vitro
@en
Deletion of the triplet repeat ...... h cellular senescence in vitro
@nl
prefLabel
Deletion of the triplet repeat ...... h cellular senescence in vitro
@ast
Deletion of the triplet repeat ...... h cellular senescence in vitro
@en
Deletion of the triplet repeat ...... h cellular senescence in vitro
@nl
P2860
P356
P1476
Deletion of the triplet repeat ...... h cellular senescence in vitro
@en
P2093
Erin B. D. Clabough
Scott O. Zeitlin
P2860
P304
P356
10.1093/HMG/DDI477
P577
2006-02-15T00:00:00Z