Connecting the dots in Huntington's disease with protein interaction networks
暂无分享,去创建一个
[1] S. Fields,et al. A novel genetic system to detect proteinprotein interactions , 1989, Nature.
[2] Manish S. Shah,et al. A novel gene containing a trinucleotide repeat that is expanded and unstable on Huntington's disease chromosomes , 1993, Cell.
[3] Peer Bork,et al. HEAT repeats in the Huntington's disease protein , 1995, Nature Genetics.
[4] J. Cha,et al. Transcriptional dysregulation in Huntington’s disease , 2000, Trends in Neurosciences.
[5] James R. Knight,et al. A comprehensive analysis of protein–protein interactions in Saccharomyces cerevisiae , 2000, Nature.
[6] H. Zoghbi,et al. Identification of genes that modify ataxin-1-induced neurodegeneration , 2000, Nature.
[7] B. Schwikowski,et al. A network of protein–protein interactions in yeast , 2000, Nature Biotechnology.
[8] T. Ito,et al. Toward a protein-protein interaction map of the budding yeast: A comprehensive system to examine two-hybrid interactions in all possible combinations between the yeast proteins. , 2000, Proceedings of the National Academy of Sciences of the United States of America.
[9] A. F. Neuwald,et al. HEAT repeats associated with condensins, cohesins, and other complexes involved in chromosome-related functions. , 2000, Genome research.
[10] S. Benzer,et al. Genetic suppression of polyglutamine toxicity in Drosophila. , 2000, Science.
[11] R. Lefkowitz,et al. Multiple endocytic pathways of G protein-coupled receptors delineated by GIT1 sensitivity. , 2000, Proceedings of the National Academy of Sciences of the United States of America.
[12] S. Fields. Proteomics in Genomeland , 2001, Science.
[13] David Valle,et al. Human disease genes , 2001, Nature.
[14] S. Fields,et al. Proteomics. Proteomics in genomeland. , 2001, Science.
[15] Elena Cattaneo,et al. Loss of normal huntingtin function: new developments in Huntington's disease research , 2001, Trends in Neurosciences.
[16] D. Housman,et al. Histone deacetylase inhibitors arrest polyglutamine-dependent neurodegeneration in Drosophila , 2001, Nature.
[17] Wolfgang Schmid,et al. Disruption of CREB function in brain leads to neurodegeneration , 2002, Nature Genetics.
[18] D. Rubinsztein,et al. Transcriptional abnormalities in Huntington disease. , 2003, Trends in genetics : TIG.
[19] Martin Drozda,et al. Depletion of wild‐type huntingtin in mouse models of neurologic diseases , 2003, Journal of neurochemistry.
[20] Erich E Wanker,et al. The hunt for huntingtin function: interaction partners tell many different stories. , 2003, Trends in biochemical sciences.
[21] Leslie M Thompson,et al. Suberoylanilide hydroxamic acid, a histone deacetylase inhibitor, ameliorates motor deficits in a mouse model of Huntington's disease , 2003, Proceedings of the National Academy of Sciences of the United States of America.
[22] M. Vidal,et al. Integrating 'omic' information: a bridge between genomics and systems biology. , 2003, Trends in genetics : TIG.
[23] Susan Lindquist,et al. Yeast Genes That Enhance the Toxicity of a Mutant Huntingtin Fragment or α-Synuclein , 2003, Science.
[24] S. Lindquist,et al. Yeast genes that enhance the toxicity of a mutant huntingtin fragment or alpha-synuclein. , 2003, Science.
[25] D. Webb,et al. Synapse formation is regulated by the signaling adaptor GIT1 , 2003, The Journal of cell biology.
[26] Ruth Luthi-Carter,et al. Histone Deacetylase Inhibition by Sodium Butyrate Chemotherapy Ameliorates the Neurodegenerative Phenotype in Huntington's Disease Mice , 2003, The Journal of Neuroscience.
[27] John P. Miller,et al. Using the yeast two-hybrid system to identify interacting proteins. , 2004, Methods in molecular biology.
[28] Alejandro Chavez,et al. Genome-wide RNA interference screen identifies previously undescribed regulators of polyglutamine aggregation. , 2004, Proceedings of the National Academy of Sciences of the United States of America.
[29] H. Lehrach,et al. A protein interaction network links GIT1, an enhancer of huntingtin aggregation, to Huntington's disease. , 2004, Molecular cell.
[30] M. Hayden,et al. Huntingtin Bodies Sequester Vesicle-Associated Proteins by a Polyproline-Dependent Interaction , 2004, The Journal of Neuroscience.
[31] Xiao-Jiang Li,et al. Huntingtin-protein interactions and the pathogenesis of Huntington's disease. , 2004, Trends in genetics : TIG.
[32] Paolo Guidetti,et al. A genomic screen in yeast implicates kynurenine 3-monooxygenase as a therapeutic target for Huntington disease , 2005, Nature Genetics.