Protein aggregation and neurodegenerative disease
暂无分享,去创建一个
[1] Christopher A Ross,et al. The ubiquitin-proteasome pathway in Parkinson's disease and other neurodegenerative diseases. , 2004, Trends in cell biology.
[2] R. Nussbaum,et al. Hereditary Early-Onset Parkinson's Disease Caused by Mutations in PINK1 , 2004, Science.
[3] Francesco Scaravilli,et al. Inhibition of mTOR induces autophagy and reduces toxicity of polyglutamine expansions in fly and mouse models of Huntington disease , 2004, Nature Genetics.
[4] M. Hayden,et al. Inhibition of Calpain Cleavage of Huntingtin Reduces Toxicity , 2004, Journal of Biological Chemistry.
[5] Ronald Wetzel,et al. Eukaryotic proteasomes cannot digest polyglutamine sequences and release them during degradation of polyglutamine-containing proteins. , 2004, Molecular cell.
[6] P. Pandolfi,et al. SUMO Modification of Huntingtin and Huntington's Disease Pathology , 2004, Science.
[7] A. Singleton,et al. The law of mass action applied to neurodegenerative disease: a hypothesis concerning the etiology and pathogenesis of complex diseases. , 2004, Human molecular genetics.
[8] H. Paulson,et al. For Personal Use. Only Reproduce with Permission the Lancet Publishing Group. Molecular Medicine for the Brain: Silencing of Disease Genes with Rna Interference , 2022 .
[9] K. Chung,et al. Phthalocyanine tetrasulfonates affect the amyloid formation and cytotoxicity of α-synuclein , 2004 .
[10] Thomas Scheibel,et al. The elongation of yeast prion fibers involves separable steps of association and conversion. , 2004, Proceedings of the National Academy of Sciences of the United States of America.
[11] Y. Cordeiro,et al. Modulation of Prion Protein Oligomerization, Aggregation, and β-sheet Conversion by 4,4′-Dianilino-1,1′-binaphthyl-5,5′-sulfonate (bis-ANS)* , 2004, Journal of Biological Chemistry.
[12] Takeshi Iwatsubo,et al. Aggresomes Formed by α-Synuclein and Synphilin-1 Are Cytoprotective* , 2004, Journal of Biological Chemistry.
[13] Michel Goedert,et al. Tau protein and neurodegeneration. , 2004, Seminars in cell & developmental biology.
[14] Christopher M Dobson,et al. Principles of protein folding, misfolding and aggregation. , 2004, Seminars in cell & developmental biology.
[15] N. Nukina,et al. Trehalose alleviates polyglutamine-mediated pathology in a mouse model of Huntington disease , 2004, Nature Medicine.
[16] Ying Xu,et al. Mapping abeta amyloid fibril secondary structure using scanning proline mutagenesis. , 2004, Journal of molecular biology.
[17] D. Selkoe. Folding proteins in fatal ways , 2003, Nature.
[18] A. Goldberg,et al. Protein degradation and protection against misfolded or damaged proteins , 2003, Nature.
[19] P. Lansbury,et al. Protofibrils, pores, fibrils, and neurodegeneration: separating the responsible protein aggregates from the innocent bystanders. , 2003, Annual review of neuroscience.
[20] Leslie Michels Thompson,et al. A Rapid Cellular FRET Assay of Polyglutamine Aggregation Identifies a Novel Inhibitor , 2003, Neuron.
[21] J. Buxbaum. Diseases of protein conformation: what do in vitro experiments tell us about in vivo diseases? , 2003, Trends in biochemical sciences.
[22] Janel O. Johnson,et al. α-Synuclein Locus Triplication Causes Parkinson's Disease , 2003, Science.
[23] Aaron Ciechanover,et al. The Ubiquitin Proteasome System in Neurodegenerative Diseases Sometimes the Chicken, Sometimes the Egg , 2003, Neuron.
[24] T. Iwatsubo. Aggregation of α-synuclein in the pathogenesis of Parkinson’s disease , 2003, Journal of Neurology.
[25] Ralf Langen,et al. Structural Organization of α-Synuclein Fibrils Studied by Site-directed Spin Labeling* , 2003, Journal of Biological Chemistry.
[26] M. Mattson,et al. Good and Bad Amyloid Antibodies , 2003, Science.
[27] R. Heinrikson,et al. Human β-Secretase (BACE) and BACE Inhibitors , 2003 .
[28] V. Uversky,et al. Protein folding revisited. A polypeptide chain at the folding – misfolding – nonfolding cross-roads: which way to go? , 2003, Cellular and Molecular Life Sciences CMLS.
[29] Haibin Xia,et al. Allele-specific silencing of dominant disease genes , 2003, Proceedings of the National Academy of Sciences of the United States of America.
[30] H. Paulson,et al. Protein aggregation and the ubiquitin proteasome pathway: gaining the UPPer hand on neurodegeneration. , 2003, Current opinion in genetics & development.
[31] G. Bates,et al. Huntingtin aggregation and toxicity in Huntington's disease , 2003, The Lancet.
[32] Effat S. Emamian,et al. Serine 776 of Ataxin-1 Is Critical for Polyglutamine-Induced Disease in SCA1 Transgenic Mice , 2003, Neuron.
[33] D. Dash,et al. Role of histidine interruption in mitigating the pathological effects of long polyglutamine stretches in SCA1: A molecular approach , 2003, Protein science : a publication of the Protein Society.
[34] Carl W. Cotman,et al. Common Structure of Soluble Amyloid Oligomers Implies Common Mechanism of Pathogenesis , 2003, Science.
[35] M. Hayden,et al. Nuclear Localization of a Non-caspase Truncation Product of Atrophin-1, with an Expanded Polyglutamine Repeat, Increases Cellular Toxicity* , 2003, The Journal of Biological Chemistry.
[36] F. Cohen,et al. Potent inhibition of scrapie prion replication in cultured cells by bis-acridines , 2003, Proceedings of the National Academy of Sciences of the United States of America.
[37] R. Tycko. Insights into the amyloid folding problem from solid-state NMR. , 2003, Biochemistry.
[38] Matthew P Frosch,et al. The Formation of Highly Soluble Oligomers of α-Synuclein Is Regulated by Fatty Acids and Enhanced in Parkinson's Disease , 2003, Neuron.
[39] Junying Yuan,et al. Pivotal role of oligomerization in expanded polyglutamine neurodegenerative disorders , 2003, Nature.
[40] T. Dawson,et al. Rare genetic mutations shed light on the pathogenesis of Parkinson disease. , 2003, The Journal of clinical investigation.
[41] Claudio Soto,et al. Unfolding the role of protein misfolding in neurodegenerative diseases , 2003, Nature Reviews Neuroscience.
[42] C. Ross,et al. Cell death triggered by polyglutamine-expanded huntingtin in a neuronal cell line is associated with degradation of CREB-binding protein. , 2003, Human molecular genetics.
[43] C. Ross,et al. Polyglutamine fibrillogenesis: The pathway unfolds , 2002, Proceedings of the National Academy of Sciences of the United States of America.
[44] Howard L. Weiner,et al. Inflammation and therapeutic vaccination in CNS diseases , 2002, Nature.
[45] R. Leapman,et al. A structural model for Alzheimer's β-amyloid fibrils based on experimental constraints from solid state NMR , 2002, Proceedings of the National Academy of Sciences of the United States of America.
[46] H. Lehrach,et al. Identification of benzothiazoles as potential polyglutamine aggregation inhibitors of Huntington's disease by using an automated filter retardation assay , 2002, Proceedings of the National Academy of Sciences of the United States of America.
[47] A. Chakrabartty,et al. Oxidation-induced Misfolding and Aggregation of Superoxide Dismutase and Its Implications for Amyotrophic Lateral Sclerosis* , 2002, The Journal of Biological Chemistry.
[48] M. Spillantini,et al. Tau gene mutations: dissecting the pathogenesis of FTDP-17. , 2002, Trends in molecular medicine.
[49] R. Wetzel,et al. Mutational analysis of the structural organization of polyglutamine aggregates , 2002, Proceedings of the National Academy of Sciences of the United States of America.
[50] M. Citron. Alzheimer's disease: treatments in discovery and development , 2002, Nature Neuroscience.
[51] Christopher A. Ross,et al. Huntingtin Spheroids and Protofibrils as Precursors in Polyglutamine Fibrilization* , 2002, The Journal of Biological Chemistry.
[52] Ralf Langen,et al. Structural and Dynamic Features of Alzheimer's Aβ Peptide in Amyloid Fibrils Studied by Site-directed Spin Labeling* , 2002, The Journal of Biological Chemistry.
[53] D. Selkoe. Alzheimer's Disease Is a Synaptic Failure , 2002, Science.
[54] S. Lindquist,et al. Conversion of PrP to a Self-Perpetuating PrPSc-like Conformation in the Cytosol , 2002, Science.
[55] S. Lindquist,et al. Neurotoxicity and Neurodegeneration When PrP Accumulates in the Cytosol , 2002, Science.
[56] K. Lindsten,et al. Aggregate formation inhibits proteasomal degradation of polyglutamine proteins. , 2002, Human molecular genetics.
[57] Blair R. Leavitt,et al. Caspase Cleavage of Mutant Huntingtin Precedes Neurodegeneration in Huntington's Disease , 2002, The Journal of Neuroscience.
[58] R. Wetzel. Ideas of order for amyloid fibril structure. , 2002, Structure.
[59] K. Lindenberg,et al. Proteases acting on mutant huntingtin generate cleaved products that differentially build up cytoplasmic and nuclear inclusions. , 2002, Molecular cell.
[60] J. Hardy,et al. The Amyloid Hypothesis of Alzheimer ’ s Disease : Progress and Problems on the Road to Therapeutics , 2009 .
[61] H. Cai,et al. Genetically engineered mouse models of neurodegenerative diseases , 2002, Nature Neuroscience.
[62] K. Fischbeck,et al. Toxic Proteins in Neurodegenerative Disease , 2002, Science.
[63] Ronald Wetzel,et al. Amyloid-like features of polyglutamine aggregates and their assembly kinetics. , 2002, Biochemistry.
[64] Christopher A. Ross,et al. Lentiviral-Mediated Delivery of Mutant Huntingtin in the Striatum of Rats Induces a Selective Neuropathology Modulated by Polyglutamine Repeat Size, Huntingtin Expression Levels, and Protein Length , 2002, The Journal of Neuroscience.
[65] W. K. Cullen,et al. Naturally secreted oligomers of amyloid β protein potently inhibit hippocampal long-term potentiation in vivo , 2002, Nature.
[66] James C. Sacchettini,et al. Therapeutic strategies for human amyloid diseases , 2002, Nature Reviews Drug Discovery.
[67] R. Wetzel,et al. Conformational Abs recognizing a generic amyloid fibril epitope , 2002, Proceedings of the National Academy of Sciences of the United States of America.
[68] K. Winklhofer,et al. Geldanamycin Restores a Defective Heat Shock Responsein Vivo * , 2001, The Journal of Biological Chemistry.
[69] Peter T. Lansbury,et al. Kinetic Stabilization of the α-Synuclein Protofibril by a Dopamine-α-Synuclein Adduct , 2001, Science.
[70] Piper Pw. The Hsp90 chaperone as a promising drug target. , 2001 .
[71] C. Ross,et al. Expansion explosion: new clues to the pathogenesis of repeat expansion neurodegenerative diseases. , 2001, Trends in Molecular Medicine.
[72] Jeffrey D. Rothstein,et al. From charcot to lou gehrig: deciphering selective motor neuron death in als , 2001, Nature Reviews Neuroscience.
[73] H. Zoghbi,et al. SCA1 molecular genetics: a history of a 13 year collaboration against glutamines. , 2001, Human molecular genetics.
[74] M. Wolfe,et al. A Portrait of Alzheimer Secretases--New Features and Familiar Faces , 2001, Science.
[75] R. Wetzel,et al. Polyglutamine aggregation behavior in vitro supports a recruitment mechanism of cytotoxicity. , 2001, Journal of molecular biology.
[76] P. Lansbury,et al. Vesicle permeabilization by protofibrillar alpha-synuclein: implications for the pathogenesis and treatment of Parkinson's disease. , 2001, Biochemistry.
[77] S. Prusiner,et al. Shattuck lecture--neurodegenerative diseases and prions. , 2001, The New England journal of medicine.
[78] C. Finch,et al. Targeting small Aβ oligomers: the solution to an Alzheimer's disease conundrum? , 2001, Trends in Neurosciences.
[79] C A Ross,et al. Interference by Huntingtin and Atrophin-1 with CBP-Mediated Transcription Leading to Cellular Toxicity , 2001, Science.
[80] S. Lindquist,et al. Investigating protein conformation-based inheritance and disease in yeast. , 2001, Philosophical transactions of the Royal Society of London. Series B, Biological sciences.
[81] J. Frydman,et al. Molecular chaperones and the art of recognizing a lost cause , 2001, Nature Cell Biology.
[82] R. Kopito,et al. Impairment of the ubiquitin-proteasome system by protein aggregation. , 2001, Science.
[83] P. Piper. The Hsp90 chaperone as a promising drug target. , 2001, Current opinion in investigational drugs.
[84] R. Kopito,et al. Aggresomes, inclusion bodies and protein aggregation. , 2000, Trends in cell biology.
[85] J. Trojanowski,et al. Oxidative damage linked to neurodegeneration by selective alpha-synuclein nitration in synucleinopathy lesions. , 2000, Science.
[86] R. Leapman,et al. Amyloid Fibril Formation by Aβ16-22, a Seven-Residue Fragment of the Alzheimer's β-Amyloid Peptide, and Structural Characterization by Solid State NMR† , 2000 .
[87] D. F. Andrews,et al. A one-hit model of cell death in inherited neuronal degenerations , 2000, Nature.
[88] R A Houghten,et al. Inhibition of beta-amyloid-induced neurotoxicity by imidazopyridoindoles derived from a synthetic combinatorial library. , 2000, Journal of structural biology.
[89] J. Dubochet,et al. Self-assembly of beta-amyloid 42 is retarded by small molecular ligands at the stage of structural intermediates. , 2000, Journal of structural biology.
[90] J. M. Smith,et al. Direct visualisation of the beta-sheet structure of synthetic Alzheimer's amyloid. , 2000, Journal of molecular biology.
[91] René Hen,et al. Reversal of Neuropathology and Motor Dysfunction in a Conditional Model of Huntington's Disease , 2000, Cell.
[92] T. Benzinger,et al. Two-Dimensional Structure of β-Amyloid(10−35) Fibrils† , 2000 .
[93] L. Meijer,et al. Constitutive Phosphorylation of the Parkinson's Disease Associated α-Synuclein* , 2000, The Journal of Biological Chemistry.
[94] S. Hersch,et al. Huntingtin aggregates may not predict neuronal death in Huntington's disease , 1999 .
[95] C. Masters,et al. Soluble pool of Aβ amyloid as a determinant of severity of neurodegeneration in Alzheimer's disease , 1999, Annals of neurology.
[96] D. Housman,et al. Insoluble detergent-resistant aggregates form between pathological and nonpathological lengths of polyglutamine in mammalian cells. , 1999, Proceedings of the National Academy of Sciences of the United States of America.
[97] L. Lue,et al. Soluble Amyloid β Peptide Concentration as a Predictor of Synaptic Change in Alzheimer’s Disease , 1999 .
[98] C. Ross,et al. Nuclear Targeting of Mutant Huntingtin Increases Toxicity , 1999, Molecular and Cellular Neuroscience.
[99] Peter T. Lansbury,et al. Assembly of Aβ Amyloid Protofibrils: An in Vitro Model for a Possible Early Event in Alzheimer's Disease† , 1999 .
[100] G P Bates,et al. Self-assembly of polyglutamine-containing huntingtin fragments into amyloid-like fibrils: implications for Huntington's disease pathology. , 1999, Proceedings of the National Academy of Sciences of the United States of America.
[101] Claire-Anne Gutekunst,et al. Nuclear and Neuropil Aggregates in Huntington’s Disease: Relationship to Neuropathology , 1999, The Journal of Neuroscience.
[102] S. Hersch,et al. Huntington aggregates may not predict neuronal death in Huntington's disease. , 1999, Annals of neurology.
[103] M. MacDonald,et al. Amyloid Formation by Mutant Huntingtin: Threshold, Progressivity and Recruitment of Normal Polyglutamine Proteins , 1998, Somatic cell and molecular genetics.
[104] T. Benzinger,et al. Propagating structure of Alzheimer’s β-amyloid(10–35) is parallel β-sheet with residues in exact register , 1998 .
[105] 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.
[106] L. Bruijn,et al. Aggregation and motor neuron toxicity of an ALS-linked SOD1 mutant independent from wild-type SOD1. , 1998, Science.
[107] T. Morgan,et al. Diffusible, nonfibrillar ligands derived from Abeta1-42 are potent central nervous system neurotoxins. , 1998, Proceedings of the National Academy of Sciences of the United States of America.
[108] C. Blake,et al. From the globular to the fibrous state: protein structure and structural conversion in amyloid formation , 1998, Quarterly Reviews of Biophysics.
[109] S. W. Davies,et al. Intranuclear Neuronal Inclusions in Huntington's Disease and Dentatorubral and Pallidoluysian Atrophy: Correlation between the Density of Inclusions andIT15CAG Triplet Repeat Length , 1998, Neurobiology of Disease.
[110] P. Lansbury,et al. Atomic force microscopic imaging of seeded fibril formation and fibril branching by the Alzheimer's disease amyloid-beta protein. , 1997, Chemistry & biology.
[111] P. Lansbury. Structural Neurology: Are Seeds at the Root of Neuronal Degeneration? , 1997, Neuron.
[112] S. W. Davies,et al. Aggregation of huntingtin in neuronal intranuclear inclusions and dystrophic neurites in brain. , 1997, Science.
[113] D. Walsh,et al. Amyloid beta-protein fibrillogenesis. Detection of a protofibrillar intermediate. , 1997, The Journal of biological chemistry.
[114] M. L. Schmidt,et al. α-Synuclein in Lewy bodies , 1997, Nature.
[115] Mark Turmaine,et al. Formation of Neuronal Intranuclear Inclusions Underlies the Neurological Dysfunction in Mice Transgenic for the HD Mutation , 1997, Cell.
[116] P. Lansbury,et al. Models of amyloid seeding in Alzheimer's disease and scrapie: mechanistic truths and physiological consequences of the time-dependent solubility of amyloid proteins. , 1997, Annual review of biochemistry.
[117] D. Davies,et al. The Interaction of an Epidermal Growth Factor/Transforming Growth Factor α Tail Chimera with the Human Epidermal Growth Factor Receptor Reveals Unexpected Complexities* , 1996, The Journal of Biological Chemistry.
[118] J. Trojanowski,et al. Purification and characterization of Lewy bodies from the brains of patients with diffuse Lewy body disease. , 1996, The American journal of pathology.
[119] L. Forno,et al. Neuropathology of Parkinson's Disease , 1996, Journal of neuropathology and experimental neurology.
[120] M. Hurle,et al. Selective Inhibition of A Fibril Formation , 1996, The Journal of Biological Chemistry.
[121] C A Ross,et al. When more is less: Pathogenesis of glutamine repeat neurodegenerative diseases , 1995, Neuron.
[122] C. Glabe,et al. Surfactant properties of Alzheimer's A beta peptides and the mechanism of amyloid aggregation. , 1994, The Journal of biological chemistry.
[123] D. Salmon,et al. Physical basis of cognitive alterations in alzheimer's disease: Synapse loss is the major correlate of cognitive impairment , 1991, Annals of neurology.
[124] C. Sikström,et al. Population Studies in Northern Sweden , 1988 .
[125] D. Benson,et al. Alzheimer's disease and Parkinson's disease , 1988, Neurology.
[126] J. B. Martin,et al. Clinical and neuropathologic assessment of severity in Huntington's disease , 1988, Neurology.
[127] R. Ferrante,et al. Neuropathological Classification of Huntington's Disease , 1985, Journal of neuropathology and experimental neurology.
[128] G. Glenner,et al. X-RAY DIFFRACTION STUDIES ON AMYLOID FILAMENTS , 1968, The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society.