Polyglutamine inclusion body toxicity
Author:
Affiliation:
1. Neurology Service & Geriatrics Research, Education, and Clinical Center, Veterans Affairs Ann Arbor Health System, Ann Arbor, MI, and Department of Neurology; University of Michigan; Ann Arbor MI
Funder
National Institute of Neurological Disorders and Stroke
Publisher
Wiley
Subject
Neurology (clinical),Neurology
Link
http://onlinelibrary.wiley.com/wol1/doi/10.1002/mds.27226/fullpdf
Reference4 articles.
1. Inclusion body formation reduces levels of mutant huntingtin and the risk of neuronal death;Arrasate;Nature,2004
2. Huntington aggregates may not predict neuronal death in Huntington's disease;Kuemmerle;Ann Neurol,1999
3. In situ architecture and cellular interactions of PolyQ inclusions;Bäuerlein;Cell,2017
4. Hprt(CAG)146 mice: age of onset of behavioral abnormalities, time course of neuronal intranuclear inclusion accumulation, neurotransmitter marker alterations, mitochondrial function markers, and susceptibility to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine;Tallaksen-Greene;J Comp Neurol,2003
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1. Pathologic changes in neuronal intranuclear inclusion disease are linked to aberrant FUS interaction under hyperosmotic stress;Neurobiology of Disease;2024-01
2. Cryo-electron tomography provides topological insights into mutant huntingtin exon 1 and polyQ aggregates;Communications Biology;2021-07-08
3. Spatiotemporal analysis of soluble aggregates and autophagy markers in the R6/2 mouse model;Scientific Reports;2021-01-08
4. Topological Insights into Mutant Huntingtin Exon 1 and PolyQ Aggregates by Cryo-Electron Tomography;2020-12-09
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