Mutant Huntingtin reduces HSP70 expression through the sequestration of NF‐Y transcription factor
暂无分享,去创建一个
[1] S. Warren,et al. Polyglutamine domain modulates the TBP-TFIIB interaction: implications for its normal function and neurodegeneration , 2007, Nature Neuroscience.
[2] Mauro Delorenzi,et al. Mutant huntingtin's effects on striatal gene expression in mice recapitulate changes observed in human Huntington's disease brain and do not differ with mutant huntingtin length or wild-type huntingtin dosage. , 2007, Human molecular genetics.
[3] I. Kanazawa,et al. The Induction Levels of Heat Shock Protein 70 Differentiate the Vulnerabilities to Mutant Huntingtin among Neuronal Subtypes , 2007, The Journal of Neuroscience.
[4] S. Hersch,et al. Sp1 Is Up-regulated in Cellular and Transgenic Models of Huntington Disease, and Its Reduction Is Neuroprotective* , 2006, Journal of Biological Chemistry.
[5] A. Suzuki,et al. Lgl mediates apical domain disassembly by suppressing the PAR-3-aPKC-PAR-6 complex to orient apical membrane polarity , 2006, Journal of Cell Science.
[6] M. MacDonald,et al. Decreased association of the transcription factor Sp1 with genes downregulated in Huntington's disease , 2006, Neurobiology of Disease.
[7] Richard I. Morimoto,et al. Progressive Disruption of Cellular Protein Folding in Models of Polyglutamine Diseases , 2006, Science.
[8] R. Morimoto,et al. Huntingtin and Mutant SOD1 Form Aggregate Structures with Distinct Molecular Properties in Human Cells* , 2006, Journal of Biological Chemistry.
[9] Y. Kitaura,et al. Active HSF1 Significantly Suppresses Polyglutamine Aggregate Formation in Cellular and Mouse Models* , 2005, Journal of Biological Chemistry.
[10] S. Salzberg,et al. The Transcriptional Landscape of the Mammalian Genome , 2005, Science.
[11] S. Snyder,et al. p53 Mediates Cellular Dysfunction and Behavioral Abnormalities in Huntington’s Disease , 2005, Neuron.
[12] N. Nukina,et al. Decreased expression of hypothalamic neuropeptides in Huntington disease transgenic mice with expanded polyglutamine‐EGFP fluorescent aggregates , 2005, Journal of neurochemistry.
[13] M. Mayer,et al. Hsp70 chaperones: Cellular functions and molecular mechanism , 2005, Cellular and Molecular Life Sciences.
[14] Mehmet Sarikaya,et al. Hsp70 and Hsp40 attenuate formation of spherical and annular polyglutamine oligomers by partitioning monomer , 2004, Nature Structural &Molecular Biology.
[15] G. Bates,et al. Huntingtin and the molecular pathogenesis of Huntington's disease , 2004, EMBO reports.
[16] Y. Kuroiwa,et al. Identification of ubiquitin‐interacting proteins in purified polyglutamine aggregates , 2004, FEBS letters.
[17] Peter Breuer,et al. Cellular toxicity of polyglutamine expansion proteins: mechanism of transcription factor deactivation. , 2004, Molecular cell.
[18] G. Bates,et al. Progressive decrease in chaperone protein levels in a mouse model of Huntington's disease and induction of stress proteins as a therapeutic approach. , 2004, Human molecular genetics.
[19] Xiao-Jiang Li,et al. Huntingtin-protein interactions and the pathogenesis of Huntington's disease. , 2004, Trends in genetics : TIG.
[20] F. Hartl,et al. Roles of molecular chaperones in protein misfolding diseases. , 2004, Seminars in cell & developmental biology.
[21] K. Hoyt,et al. CRE-Mediated Transcription Is Increased in Huntington's Disease Transgenic Mice , 2004, The Journal of Neuroscience.
[22] H. Lehrach,et al. Mutant Huntingtin Promotes the Fibrillogenesis of Wild-type Huntingtin , 2003, Journal of Biological Chemistry.
[23] Erich E Wanker,et al. The hunt for huntingtin function: interaction partners tell many different stories. , 2003, Trends in biochemical sciences.
[24] K. Merienne,et al. Polyglutamine Expansion Induces a Protein-damaging Stress Connecting Heat Shock Protein 70 to the JNK Pathway* , 2003, The Journal of Biological Chemistry.
[25] D. Rubinsztein,et al. Transcriptional abnormalities in Huntington disease. , 2003, Trends in genetics : TIG.
[26] M. MacDonald,et al. Insoluble TATA-binding protein accumulation in Huntington's disease cortex. , 2002, Brain research. Molecular brain research.
[27] F. Hartl,et al. Molecular chaperones as modulators of polyglutamine protein aggregation and toxicity , 2002, Proceedings of the National Academy of Sciences of the United States of America.
[28] J. Olson,et al. Increased huntingtin protein length reduces the number of polyglutamine-induced gene expression changes in mouse models of Huntington's disease. , 2002, Human molecular genetics.
[29] Charles Kooperberg,et al. Dysregulation of gene expression in the R6/2 model of polyglutamine disease: parallel changes in muscle and brain. , 2002, Human molecular genetics.
[30] R. Morimoto,et al. Chaperoning signaling pathways: molecular chaperones as stress-sensing 'heat shock' proteins. , 2002, Journal of cell science.
[31] Dimitri Krainc,et al. Sp1 and TAFII130 Transcriptional Activity Disrupted in Early Huntington's Disease , 2002, Science.
[32] Zhao-Xue Yu,et al. Huntingtin inclusions do not deplete polyglutamine-containing transcription factors in HD mice. , 2002, Human molecular genetics.
[33] He Li,et al. Interaction of Huntington Disease Protein with Transcriptional Activator Sp1 , 2002, Molecular and Cellular Biology.
[34] Shihua Li,et al. Chaperone Suppression of Cellular Toxicity of Huntingtin Is Independent of Polyglutamine Aggregation* , 2001, The Journal of Biological Chemistry.
[35] R. Mantovani,et al. HSP-CBF Is an NF-Y-dependent Coactivator of the Heat Shock Promoters CCAAT Boxes* , 2001, The Journal of Biological Chemistry.
[36] F. Gage,et al. Identities of Sequestered Proteins in Aggregates from Cells with Induced Polyglutamine Expression , 2001, The Journal of cell biology.
[37] C A Ross,et al. Interference by Huntingtin and Atrophin-1 with CBP-Mediated Transcription Leading to Cellular Toxicity , 2001, Science.
[38] M. Hayden,et al. The Gln-Ala repeat transcriptional activator CA150 interacts with huntingtin: neuropathologic and genetic evidence for a role in Huntington's disease pathogenesis. , 2001, Proceedings of the National Academy of Sciences of the United States of America.
[39] H. Paulson,et al. Mechanisms of chaperone suppression of polyglutamine disease: selectivity, synergy and modulation of protein solubility in Drosophila. , 2000, Human molecular genetics.
[40] J. Cha,et al. Transcriptional dysregulation in Huntington’s disease , 2000, Trends in Neurosciences.
[41] N. Nukina,et al. Polyglutamine length-dependent interaction of Hsp40 and Hsp70 family chaperones with truncated N-terminal huntingtin: their role in suppression of aggregation and cellular toxicity. , 2000, Human molecular genetics.
[42] I. Kanazawa,et al. Ataxin-3, the MJD1 gene product, interacts with the two human homologs of yeast DNA repair protein RAD23, HHR23A and HHR23B. , 2000, Human molecular genetics.
[43] E. Wanker,et al. Hsp70 and hsp40 chaperones can inhibit self-assembly of polyglutamine proteins into amyloid-like fibrils. , 2000, Proceedings of the National Academy of Sciences of the United States of America.
[44] D. Housman,et al. The Huntington's disease protein interacts with p53 and CREB-binding protein and represses transcription. , 2000, Proceedings of the National Academy of Sciences of the United States of America.
[45] S. Benzer,et al. Genetic suppression of polyglutamine toxicity in Drosophila. , 2000, Science.
[46] R. Mantovani,et al. The molecular biology of the CCAAT-binding factor NF-Y. , 1999, Gene.
[47] A. Wolffe,et al. Xenopus NF‐Y pre‐sets chromatin to potentiate p300 and acetylation‐responsive transcription from the Xenopus hsp70 promoter in vivo , 1998, The EMBO journal.
[48] B. Crombrugghe,et al. Role of the CCAAT-binding protein CBF/NF-Y in transcription. , 1998, Trends in biochemical sciences.
[49] K. Ohtsuka,et al. Characterization of HSE sequences in human Hsp40 gene: structural and promoter analysis. , 1998, Biochimica et biophysica acta.
[50] Hans Lehrach,et al. Huntingtin-Encoded Polyglutamine Expansions Form Amyloid-like Protein Aggregates In Vitro and In Vivo , 1997, Cell.
[51] Mark Turmaine,et al. Formation of Neuronal Intranuclear Inclusions Underlies the Neurological Dysfunction in Mice Transgenic for the HD Mutation , 1997, Cell.
[52] M. Fiorenza,et al. Developmental activation of an episomic hsp70 gene promoter in two-cell mouse embryos by transcription factor Sp1. , 1997, Nucleic acids research.
[53] S. W. Davies,et al. Exon 1 of the HD Gene with an Expanded CAG Repeat Is Sufficient to Cause a Progressive Neurological Phenotype in Transgenic Mice , 1996, Cell.
[54] Manish S. Shah,et al. A novel gene containing a trinucleotide repeat that is expanded and unstable on Huntington's disease chromosomes , 1993, Cell.
[55] W. D. Morgan,et al. Transcription factor Sp1 binds to and activates a human hsp70 gene promoter , 1989, Molecular and cellular biology.
[56] R. Morimoto,et al. Coordinate changes in heat shock element-binding activity and HSP70 gene transcription rates in human cells. , 1988, Molecular and cellular biology.
[57] R. Kingston,et al. Multiple basal elements of a human hsp70 promoter function differently in human and rodent cell lines , 1987, Molecular and cellular biology.
[58] R. Tjian,et al. Two transcriptional activators, CCAAT-box-binding transcription factor and heat shock transcription factor, interact with a human hsp70 gene promoter , 1987, Molecular and cellular biology.
[59] R. Kingston,et al. Human HSP70 promoter contains at least two distinct regulatory domains. , 1986, Proceedings of the National Academy of Sciences of the United States of America.
[60] I. Guzhova,et al. Hsp70 chaperone as a survival factor in cell pathology. , 2006, International review of cytology.