Reference : Chromosomal profiles of gene expression in Huntington's disease.
Scientific journals : Article
Human health sciences : Neurology
http://hdl.handle.net/2268/59364
Chromosomal profiles of gene expression in Huntington's disease.
English
Anderson, Alexander N [Hammersmith Hospital, London > MRC Clinical Sciences Centre > > >]
Roncaroli, Federico [Imperial College London > Department of Clinical Neuroscience > > >]
Hodges, Angela [Institute of Psychiatry, London, UK > MRC Centre for Neurodegeneration Research > > >]
Deprez, Manuel [Université de Liège - ULg > Département des sciences biomédicales et précliniques > Anatomie et cytologie pathologiques >]
Turkheimer, Federico E [Hammersmith Hospital, London > MRC Clinical Sciences Centre > > >]
2008
Brain : A Journal of Neurology
Oxford University Press
131
Pt 2
381-8
Yes (verified by ORBi)
International
0006-8950
1460-2156
Oxford
United Kingdom
[en] Caudate Nucleus/metabolism ; Chromosome Aberrations ; Data Interpretation, Statistical ; Disease Progression ; Female ; Gene Expression Regulation ; Humans ; Huntington Disease/blood/genetics/metabolism ; Male ; Mutation ; Nerve Tissue Proteins/genetics ; Nuclear Proteins/genetics ; Oligonucleotide Array Sequence Analysis/methods ; Transcription, Genetic
[en] Recent studies suggested that Huntington's disease is due to aberrant interactions between mutant huntingtin protein, transcription factors and transcriptional co-activators resulting in widespread transcriptional dysregulation. Mutant huntingtin also interacts with histone acetyltransferases, consequently interfering with the acetylation and deacetylation states of histones. Because histone modifications and chromatin structure coordinate the expression of gene clusters, we have applied a novel mathematical approach, Chromowave, to analyse microarray datasets of brain tissue and whole blood to understand how genomic regions are altered by the effects of mutated huntingtin on chromatin structure. Results show that, in samples of caudate and whole blood from Huntington's disease patients, transcription is indeed deregulated in large genomic regions in coordinated fashion, that transcription in these regions is associated with disease progression and that altered chromosomal clusters in the two tissues are remarkably similar. These findings support the notion of a common genome-wide mechanism of disruption of RNA transcription in the brain and periphery of Huntington's disease patients.
Researchers ; Professionals
http://hdl.handle.net/2268/59364
10.1093/brain/awm312
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