huntington's disease (hd)

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Metabolite Name

1-METHYLADENOSINE (1)
4-ACETAMIDOBUTANOATE (1)
4-QUINOLINECARBOXYLATE (1)
5-HYDROXYTRYPTOPHAN (1)
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N,N,N-TRIMETHYLLYSINE (1)
N-ACETYLALANINE (1)
N-ACETYLPROLINE (1)
O-ACETYLCARNITINE (1)
O-SUCCINYL-HOMOSERINE (1)
OPHTHALMATE (1)
PHENYLACETATE (1)
PHENYLALANINE (1)

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Study type

Transcription profiling by array (55)
RNA-seq of coding RNA (27)
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Lab affiliation

Dept of Experimental Medical Science, Wallenberg Neuroscience Center, Lund University, Sweden (2)
CRG/UPF (1)
Core Unit Proteomics, BIH at Charite and MDC, Robert Roessle Strasse 10, 13125 Berlin (1)
Department for Drug Design and Pharmacology, University of Copenhagen (1)
Department of Biochemistry, The University of Western Ontario, London, Ontario N6A 5C1, Canada. Department of Chemistry, The University of Western Ontario, London, Ontario N6A 5C1, Canada (1)
Department of Biology, Stanford University, USA (1)
Department of Genome Engineering, Institute of Bioorganic Chemistry Polish Academy of Sciences, Poznan, 61-704, Poland (1)
Department of Molecular Biology, Princeton University, USA (1)
Department of Molecular Biology, Princeton University,USA (1)
Dept. Biomedical Sciences, Institute of Neurosciences, School of Medicine and Health Sciences, Universitat de Barcelona, Barcelona, Spain. Institut d’Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Barcelona, Spain (1)
Dept. Biomedical Sciences, Institute of Neurosciences, School of Medicine and Health Sciences, Universitat de Barcelona, Barcelona, Spain. Institut d’Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Barcelona, Spain (1)
EDyP (1)
Evotec (1)
Evotec (München) GmbH Anna-Sigmund-Str. 5 82061 Neuried Germany (1)
Evotec, Martinsried, Germany (1)
Faculty of Health Sciences, Department of Proteomics, The Novo Nordisk Foundation Centre for Protein Research, University of Copenhagen, DK-2200 Copenhagen, Denmark (1)
Institute for Genetics and Cologne Excellence Cluster for Cellular Stress Responses in Aging-Associated Diseases (CECAD) University of Cologne Joseph Stelzmann Strasse 26 50931 Cologne, Germany Phone number: +49 22147884172 Fax number: +49 221 478 84045 E-mail: dvilchez@uni-koeln.de (1)
Institute of Structural and Molecular Biology, University College London, London, United Kingdom (1)
MIRCen, UMR9199, CEA, CNRS, Université Paris-Saclay (1)
Max Planck Institute of Biochemistry, Am Klopferspitz 18, 82152 Martinsried, Germany Department of Proteomics and Signal Transduction (1)
Max Planck Institute, Martinsried, Germany (1)
NNF CPR, Copenhagen Univeristy, Denmark (1)
Professor Cellular Imaging, PI Huntington degradation research groupleader, Department of Medical Biology, Amsterdam UMC location AMC, Amsterdam, The Netherlands (1)
Sherbrooke University, Immunology and cellular biology department, FMSS (1)
University of Cologne, Germany (1)
University of Melbourne, Florey Institute (1)

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HDAC inhibition imparts beneficial transgenerational effects in Huntington's disease mice via altered DNA and histone methylation

Increasing evidence has demonstrated that epigenetic factors can profoundly influence gene expression and, in turn, influence resistance or susceptibility to disease. Epigenetic drugs, such as histone deacetylase (HDAC) inhibitors, are finding their way into clinical practice, although their exact m...

ORGANISM(S): Homo sapiens

2015-04-10 | E-GEOD-67733 | biostudies-arrayexpress

Alterations in the tyrosine and phenylalanine pathways revealed by biochemical profiling in cerebrospinal fluid of Huntington’s disease subjects

Huntington's disease (HD) is a severe neurological disease leading to psychiatric symptoms, motor impairment and cognitive decline. The disease is caused by a CAG expansion in the huntingtin (HTT) gene, but how this translates into the clinical phenotype of HD remains elusive. Using liquid chromatog...

2019-06-21 | MTBLS749 | MetaboLights

mRNA-Seq Expression profiling of human post-mortem BA9 brain tissue for Huntington's Disease and neurologically normal individuals

Huntingtonâ€™s Disease (HD) is a devastating neurodegenerative disorder that is caused by an expanded CAG trinucleotide repeat in the Huntingtin (HTT) gene. Transcriptional dysregulation in the human HD brain has been documented but is incompletely understood. Here we present a genome-wide analysis ...

ORGANISM(S): Homo sapiens

2015-12-08 | E-GEOD-64810 | biostudies-arrayexpress

Depletion of p62 reduces nuclear inclusions and paradoxically ameliorates disease phenotypes in Huntington's model mice

Huntington's disease (HD) is a dominantly inherited genetic disease caused by mutant huntingtin (htt) protein with expanded polyglutamine tracts. A neuropathological hallmark of HD is the presence of neuronal inclusions of mutant htt. p62 is an important regulatory protein in selective autophagy, ...

ORGANISM(S): Mus musculus

2014-10-10 | E-GEOD-62210 | biostudies-arrayexpress

Targeting H3K4 methylation as a therapeutic strategy for Huntington's disease (ChIP-seq)

Transcriptional dysregulation is an early feature of Huntington's disease (HD). We observed gene-specific changes in H3K4me3 at transcriptionally repressed promoters in R6/2 mouse and human HD brain. Genome-wide analysis showed a novel chromatin signature for this mark. Reducing the levels of the H3...

ORGANISM(S): Mus musculus

2013-07-18 | E-GEOD-48960 | biostudies-arrayexpress

The transcriptional modulator H2AFY marks Huntington's disease activity in men and mice

To accelerate the development of disease-modifying therapeutics for Huntington’s disease (HD), a dynamic biomarker of disease activity and treatment response is critically needed. Venous cellular whole blood from 8 patients with Huntington's disease (HD) and 6 control subjects were collected in PAXg...

ORGANISM(S): Homo sapiens

2011-09-01 | E-GEOD-24250 | biostudies-arrayexpress

Targeting H3K4 methylation as a therapeutic strategy for Huntington's disease (RNA-seq)

ORGANISM(S): Mus musculus

2013-07-18 | E-GEOD-48962 | biostudies-arrayexpress

Expression data from of HD-iPSC and CON-iPSC neuron derivatives

Compared the global gene expression profiles of HD- and CON-iPSC-derived neurons We used microarrays to detail the global programme of gene expression for comparing the global gene expression profiles of HD- and CON-iPSC-derived neurons and facilitating studies of medium spiny neurons (MSN)-degenera...

ORGANISM(S): Homo sapiens

2015-09-02 | E-GEOD-59051 | biostudies-arrayexpress

Lymphocyte gene expression data from moderate stage HD patients and controls

Highly quantitative biomarkers of neurodegenerative disease remain an important need in the urgent quest for disease modifying therapies. For Huntington's disease (HD), a genetic test is available (trait marker), but necessary state markers are still in development. In this report, we describe a lar...

ORGANISM(S): Homo sapiens

2007-08-15 | E-GEOD-8762 | biostudies-arrayexpress

Huntington's disease biomarker progression profile identified by transcriptome sequencing in peripheral blood

In this study we investigated the suitability of blood to identify HD transcriptomic biomarkers, validated the outcome in an independent cohort and derived a first empiric panel of biomarkers capable of predicting HD motor scores. Finally we examined whether patient gene expression profiles could pr...

ORGANISM(S): Homo sapiens

2015-02-02 | E-GEOD-51799 | biostudies-arrayexpress

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