Transcriptional activation of REST by Sp1 in Huntington's disease models

In Huntington's disease (HD), mutant huntingtin (mHtt) disrupts the normal transcriptional program of disease neurons by altering the function of several gene expression regulators such as Sp1. REST (Repressor Element-1 Silencing Transcription Factor), a key regulator of neuronal differentiatio...

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Veröffentlicht in:	PloS one 2010-12, Vol.5 (12), p.e14311
Hauptverfasser:	Ravache, Myriam, Weber, Chantal, Mérienne, Karine, Trottier, Yvon
Format:	Artikel
Sprache:	eng
Schlagworte:	Aberration Activation Animal models Animals Binding sites Biochemistry/Transcription and Translation Brain Brain-derived neurotrophic factor Cell Biology/Neuronal and Glial Cell Biology Cell Line, Tumor Cellular biology Differentiation Disease Models, Animal Gene expression Gene regulation Gene silencing Genes Genetic aspects Genetics Genetics and Genomics/Genetics of Disease High definition television Humans Huntingtin Huntingtin Protein Huntington Disease - genetics Huntington Disease - metabolism Huntington's disease Huntingtons disease Life Sciences Lymphatic system Mice Mice, Inbred C57BL Mice, Inbred CBA Mutation Nerve Tissue Proteins - genetics Neurological Disorders Neurons Neurons - metabolism Neurons and Cognition Neuroscience/Neurobiology of Disease and Regeneration Nuclear Proteins - genetics Oxidative stress Pathogenesis Promoter Regions, Genetic Proteins Rats Reporter gene Repressor Proteins - metabolism Rest RNA Serotonin Plasma Membrane Transport Proteins - genetics Sp1 protein Sp1 Transcription Factor - metabolism Transcription (Genetics) Transcription activation Transcription factors Transcriptional Activation Trends
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