Thermoregulatory and metabolic defects in Huntington's disease transgenic mice implicate PGC-1α in Huntington's disease neurodegeneration
- 1 November 2006
- journal article
- Published by Elsevier in Cell Metabolism
- Vol. 4 (5) , 349-362
- https://doi.org/10.1016/j.cmet.2006.10.004
Abstract
No abstract availableKeywords
Funding Information
- Hereditary Disease Foundation
- American Foundation for Aging Research (AG00057)
- National Institutes of Health (DK063986, DK17047, NS050352)
This publication has 58 references indexed in Scilit:
- The orphan nuclear receptor SHP regulates PGC-1α expression and energy production in brown adipocytesCell Metabolism, 2005
- HD CAG repeat implicates a dominant property of huntingtin in mitochondrial energy metabolismHuman Molecular Genetics, 2005
- PGC-1α Deficiency Causes Multi-System Energy Metabolic Derangements: Muscle Dysfunction, Abnormal Weight Control and Hepatic SteatosisPLoS Biology, 2005
- Use of within-array replicate spots for assessing differential expression in microarray experimentsBioinformatics, 2005
- Statistical significance for genomewide studiesProceedings of the National Academy of Sciences, 2003
- PGC-1α-responsive genes involved in oxidative phosphorylation are coordinately downregulated in human diabetesNature Genetics, 2003
- Regulatory Motifs for CREB-binding Protein and Nfe2l2 Transcription Factors in the Upstream Enhancer of the Mitochondrial Uncoupling Protein 1 GeneJournal of Biological Chemistry, 2002
- Exon 1 of the HD Gene with an Expanded CAG Repeat Is Sufficient to Cause a Progressive Neurological Phenotype in Transgenic MiceCell, 1996
- A huntingtin-associated protein enriched in brain with implications for pathologyNature, 1995
- Oligonucleotides with fluorescent dyes at opposite ends provide a quenched probe system useful for detecting PCR product and nucleic acid hybridization.Genome Research, 1995