Polyglutamine neurodegeneration: protein misfolding revisited
暂无分享,去创建一个
[1] Janghoo Lim,et al. Opposing effects of polyglutamine expansion on native protein complexes contribute to SCA1 , 2008, Nature.
[2] Y. Urade,et al. A toxic monomeric conformer of the polyglutamine protein , 2007, Nature Structural &Molecular Biology.
[3] Harry T Orr,et al. Mutation of the E6-AP Ubiquitin Ligase Reduces Nuclear Inclusion Frequency While Accelerating Polyglutamine-Induced Pathology in SCA1 Mice , 1999, Neuron.
[4] B. Hyman,et al. The Co-chaperone Carboxyl Terminus of Hsp70-interacting Protein (CHIP) Mediates α-Synuclein Degradation Decisions between Proteasomal and Lysosomal Pathways* , 2005, Journal of Biological Chemistry.
[5] Shaomin Li,et al. Amyloid-β protein dimers isolated directly from Alzheimer's brains impair synaptic plasticity and memory , 2008, Nature Medicine.
[6] H. Zoghbi,et al. Glutamine repeats and neurodegeneration. , 2000, Annual review of neuroscience.
[7] R. Morimoto,et al. Polyglutamine Proteins at the Pathogenic Threshold Display Neuron-Specific Aggregation in a Pan-Neuronal Caenorhabditis elegans Model , 2006, The Journal of Neuroscience.
[8] Stephen P Bottomley,et al. Mechanisms of ataxin-3 misfolding and fibril formation: kinetic analysis of a disease-associated polyglutamine protein. , 2007, Journal of molecular biology.
[9] B. Chait,et al. Polyglutamine-expanded ataxin-7 inhibits STAGA histone acetyltransferase activity to produce retinal degeneration. , 2005, Proceedings of the National Academy of Sciences of the United States of America.
[10] Ismael Al-Ramahi,et al. CHIP Protects from the Neurotoxicity of Expanded and Wild-type Ataxin-1 and Promotes Their Ubiquitination and Degradation* , 2006, Journal of Biological Chemistry.
[11] Carol K Hall,et al. Side-chain interactions determine amyloid formation by model polyglutamine peptides in molecular dynamics simulations. , 2006, Biophysical journal.
[12] Osamu Onodera,et al. Soluble polyglutamine oligomers formed prior to inclusion body formation are cytotoxic. , 2008, Human molecular genetics.
[13] Annalisa Pastore,et al. Pathogenic and non-pathogenic polyglutamine tracts have similar structural properties: towards a length-dependent toxicity gradient. , 2007, Journal of molecular biology.
[14] Carri-Lyn R. Mead,et al. CAG-encoded polyglutamine length polymorphism in the human genome , 2007, BMC Genomics.
[15] J. Frydman,et al. The chaperonin TRiC controls polyglutamine aggregation and toxicity through subunit-specific interactions , 2006, Nature Cell Biology.
[16] J. Y. Choi,et al. Co-chaperone CHIP promotes aggregation of ataxin-1 , 2007, Molecular and Cellular Neuroscience.
[17] H. Zoghbi,et al. Glutamine-Expanded Ataxin-7 Alters TFTC/STAGA Recruitment and Chromatin Structure Leading to Photoreceptor Dysfunction , 2006, PLoS biology.
[18] D. Selkoe,et al. Aβ Oligomers – a decade of discovery , 2007, Journal of neurochemistry.
[19] J. Frydman,et al. The Hsp70 and TRiC/CCT Chaperone Systems Cooperate In Vivo To Assemble the Von Hippel-Lindau Tumor Suppressor Complex , 2003, Molecular and Cellular Biology.
[20] S. Warren,et al. Polyglutamine domain modulates the TBP-TFIIB interaction: implications for its normal function and neurodegeneration , 2007, Nature Neuroscience.
[21] Hiroshi Kimura,et al. Cytosolic chaperonin prevents polyglutamine toxicity with altering the aggregation state , 2006, Nature Cell Biology.
[22] H. Ishimoto,et al. Molecular clearance of ataxin‐3 is regulated by a mammalian E4 , 2004, The EMBO journal.
[23] M. Hayden,et al. Absence of behavioral abnormalities and neurodegeneration in vivo despite widespread neuronal huntingtin inclusions. , 2005, Proceedings of the National Academy of Sciences of the United States of America.
[24] Ronald Wetzel,et al. Huntington's disease age-of-onset linked to polyglutamine aggregation nucleation , 2002, Proceedings of the National Academy of Sciences of the United States of America.
[25] K. Kosik,et al. CHIP and HSPs interact with β-APP in a proteasome-dependent manner and influence Aβ metabolism , 2007 .
[26] Huda Y. Zoghbi,et al. Diseases of Unstable Repeat Expansion: Mechanisms and Common Principles , 2005, Nature Reviews Genetics.
[27] A. West,et al. The structure of a polyQ–anti-polyQ complex reveals binding according to a linear lattice model , 2007, Nature Structural &Molecular Biology.
[28] M. Gallagher,et al. A specific amyloid-β protein assembly in the brain impairs memory , 2006, Nature.
[29] Richard I. Morimoto,et al. Progressive Disruption of Cellular Protein Folding in Models of Polyglutamine Diseases , 2006, Science.
[30] A. Pastore,et al. The Interplay between PolyQ and Protein Context Delays Aggregation by Forming a Reservoir of Protofibrils , 2006, PloS one.
[31] G. Sobue,et al. 17-AAG, an Hsp90 inhibitor, ameliorates polyglutamine-mediated motor neuron degeneration , 2005, Nature Medicine.
[32] Steven Finkbeiner,et al. Huntingtin Acts in the Nucleus to Induce Apoptosis but Death Does Not Correlate with the Formation of Intranuclear Inclusions , 1998, Cell.
[33] Dan Garza,et al. HDAC6 rescues neurodegeneration and provides an essential link between autophagy and the UPS , 2007, Nature.
[34] Wen-Lang Lin,et al. Deletion of the Ubiquitin Ligase CHIP Leads to the Accumulation, But Not the Aggregation, of Both Endogenous Phospho- and Caspase-3-Cleaved Tau Species , 2006, The Journal of Neuroscience.
[35] Amit Mishra,et al. E6-AP Promotes Misfolded Polyglutamine Proteins for Proteasomal Degradation and Suppresses Polyglutamine Protein Aggregation and Toxicity* , 2008, Journal of Biological Chemistry.
[36] Ehud Cohen,et al. Opposing Activities Protect Against Age-Onset Proteotoxicity , 2006, Science.
[37] Cynthia Kenyon,et al. Regulation of Aging and Age-Related Disease by DAF-16 and Heat-Shock Factor , 2003, Science.
[38] 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.
[39] 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.
[40] N. Bonini,et al. RNA toxicity is a component of ataxin-3 degeneration in Drosophila , 2008, Nature.
[41] Ronald Wetzel,et al. Amyloid-like features of polyglutamine aggregates and their assembly kinetics. , 2002, Biochemistry.
[42] Janghoo Lim,et al. ATAXIN-1 Interacts with the Repressor Capicua in Its Native Complex to Cause SCA1 Neuropathology , 2006, Cell.
[43] Carl W. Cotman,et al. Common Structure of Soluble Amyloid Oligomers Implies Common Mechanism of Pathogenesis , 2003, Science.
[44] D. Merry,et al. Soluble Androgen Receptor Oligomers Underlie Pathology in a Mouse Model of Spinobulbar Muscular Atrophy* , 2007, Journal of Biological Chemistry.
[45] A. Hart,et al. Autophagy Genes Protect Against Disease Caused by Polyglutamine Expansion Proteins in Caenorhabditis elegans , 2007, Autophagy.
[46] Richard I. Morimoto,et al. Adapting Proteostasis for Disease Intervention , 2008, Science.
[47] H. Paulson,et al. CHIP Suppresses Polyglutamine Aggregation and Toxicity In Vitro and In Vivo , 2005, The Journal of Neuroscience.
[48] Mark R. Segal,et al. Inclusion body formation reduces levels of mutant huntingtin and the risk of neuronal death , 2004, Nature.
[49] Peter Breuer,et al. Cellular toxicity of polyglutamine expansion proteins: mechanism of transcription factor deactivation. , 2004, Molecular cell.
[50] Nancy M Bonini,et al. Genome-Wide Screen for Modifiers of Ataxin-3 Neurodegeneration in Drosophila , 2007, PLoS genetics.
[51] J. Olson,et al. Huntingtin Interacting Proteins Are Genetic Modifiers of Neurodegeneration , 2007, PLoS genetics.
[52] G. Bates,et al. Sensitive biochemical aggregate detection reveals aggregation onset before symptom development in cellular and murine models of Huntington’s disease , 2007, Journal of neurochemistry.
[53] Howard Schulman,et al. Global changes to the ubiquitin system in Huntington's disease , 2007, Nature.
[54] Richard I. Morimoto,et al. The threshold for polyglutamine-expansion protein aggregation and cellular toxicity is dynamic and influenced by aging in Caenorhabditis elegans , 2002, Proceedings of the National Academy of Sciences of the United States of America.
[55] F. Hartl,et al. Chaperonin TRiC promotes the assembly of polyQ expansion proteins into nontoxic oligomers. , 2006, Molecular cell.
[56] L. Ukani,et al. Comparative analysis of genetic modifiers in Drosophila points to common and distinct mechanisms of pathogenesis among polyglutamine diseases. , 2008, Human molecular genetics.
[57] Elizabeth Head,et al. Fibril specific, conformation dependent antibodies recognize a generic epitope common to amyloid fibrils and fibrillar oligomers that is absent in prefibrillar oligomers , 2007, Molecular Neurodegeneration.
[58] H. Paulson,et al. Spinocerebellar Ataxia Type 3 (SCA3): Thalamic Neurodegeneration Occurs Independently from Thalamic Ataxin‐3 Immunopositive Neuronal Intranuclear Inclusions , 2006, Brain pathology.
[59] N. Thakor,et al. Parkin Facilitates the Elimination of Expanded Polyglutamine Proteins and Leads to Preservation of Proteasome Function* , 2003, Journal of Biological Chemistry.
[60] J. Lucas,et al. Full Motor Recovery Despite Striatal Neuron Loss and Formation of Irreversible Amyloid-Like Inclusions in a Conditional Mouse Model of Huntington's Disease , 2005, The Journal of Neuroscience.
[61] S. Plassmann,et al. An arginine/lysine‐rich motif is crucial for VCP/p97‐mediated modulation of ataxin‐3 fibrillogenesis , 2006, The EMBO journal.
[62] P. Muchowski,et al. Modulation of neurodegeneration by molecular chaperones , 2005, Nature Reviews Neuroscience.
[63] Tian Xu,et al. Drosophila Atrophin Homolog Functions as a Transcriptional Corepressor in Multiple Developmental Processes , 2002, Cell.
[64] Keiji Tanaka,et al. Co-chaperone CHIP Associates with Expanded Polyglutamine Protein and Promotes Their Degradation by Proteasomes* , 2005, Journal of Biological Chemistry.
[65] Fumiaki Tanaka,et al. CHIP Overexpression Reduces Mutant Androgen Receptor Protein and Ameliorates Phenotypes of the Spinal and Bulbar Muscular Atrophy Transgenic Mouse Model , 2007, The Journal of Neuroscience.