In vivo demonstration that α-synuclein oligomers are toxic
暂无分享,去创建一个
Fred H. Gage | Sebastian Jessberger | Alice Soragni | Beate Winner | Silvia Campioni | Roland Riek | Christos Tzitzilonis | Stefan Aigner | F. Gage | Leah Boyer | A. Consiglio | R. Riek | E. Masliah | B. Winner | S. Maji | Paula Desplats | S. Aigner | S. Jessberger | R. Jappelli | C. Hetzer | T. Loher | M. Vilar | S. Campioni | Christos Tzitzilonis | A. Soragni | H. Mira | E. Pham | Eliezer Masliah | Antonella Consiglio | Roberto Jappelli | Samir K. Maji | Paula A. Desplats | Leah Boyer | Claudia Hetzer | Thomas Loher | Marçal Vilar | Helena Mira | Emiley Pham | Thomas J. Loher
[1] Richard I. Morimoto,et al. Progressive Disruption of Cellular Protein Folding in Models of Polyglutamine Diseases , 2006, Science.
[2] Henning Stahlberg,et al. The fold of α-synuclein fibrils , 2008, Proceedings of the National Academy of Sciences.
[3] P. Lansbury,et al. Fibrils formed in vitro from alpha-synuclein and two mutant forms linked to Parkinson's disease are typical amyloid. , 2000, Biochemistry.
[4] Armin Giese,et al. Different Species of α-Synuclein Oligomers Induce Calcium Influx and Seeding , 2007, The Journal of Neuroscience.
[5] L. Serpell,et al. Fiber diffraction of synthetic alpha-synuclein filaments shows amyloid-like cross-beta conformation. , 2000, Proceedings of the National Academy of Sciences of the United States of America.
[6] Ole Isacson,et al. Dynamic Changes in Presynaptic and Axonal Transport Proteins Combined with Striatal Neuroinflammation Precede Dopaminergic Neuronal Loss in a Rat Model of AAV α-Synucleinopathy , 2009, The Journal of Neuroscience.
[7] M. Polymeropoulos,et al. Mapping of a Gene for Parkinson's Disease to Chromosome 4q21-q23 , 1996, Science.
[8] M. Leist,et al. Requirement of a dopaminergic neuronal phenotype for toxicity of low concentrations of 1-methyl-4-phenylpyridinium to human cells. , 2009, Toxicology and applied pharmacology.
[9] R. Krüger,et al. Ala30Pro mutation in the gene encoding alpha-synuclein in Parkinson's disease. , 1998, Nature genetics.
[10] P. Lansbury,et al. Accelerated Oligomerization by Parkinson's Disease Linked α‐Synuclein Mutants , 2000 .
[11] H. Jäckle,et al. Pre‐fibrillar α‐synuclein variants with impaired β‐structure increase neurotoxicity in Parkinson's disease models , 2009, The EMBO journal.
[12] Thorsten Lührs,et al. Correlation of structural elements and infectivity of the HET-s prion , 2005, Nature.
[13] A. Lees,et al. Ageing and Parkinson's disease: substantia nigra regional selectivity. , 1991, Brain : a journal of neurology.
[14] P. Lansbury,et al. Acceleration of oligomerization, not fibrillization, is a shared property of both alpha-synuclein mutations linked to early-onset Parkinson's disease: implications for pathogenesis and therapy. , 2000, Proceedings of the National Academy of Sciences of the United States of America.
[15] P. Lansbury,et al. Accelerated oligomerization by Parkinson's disease linked alpha-synuclein mutants. , 2000, Annals of the New York Academy of Sciences.
[16] S. Becker,et al. Molecular-level secondary structure, polymorphism, and dynamics of full-length alpha-synuclein fibrils studied by solid-state NMR. , 2005, Proceedings of the National Academy of Sciences of the United States of America.
[17] D. Eliezer,et al. Effects of Parkinson's disease-linked mutations on the structure of lipid-associated α-Synuclein , 2004 .
[18] P. Aebischer,et al. α-Synucleinopathy and selective dopaminergic neuron loss in a rat lentiviral-based model of Parkinson's disease , 2002, Proceedings of the National Academy of Sciences of the United States of America.
[19] Jeannie Chen,et al. Investigation of alpha-synuclein fibril structure by site-directed spin labeling. , 2007, The Journal of biological chemistry.
[20] Jeannie Chen,et al. Investigation of α-Synuclein Fibril Structure by Site-directed Spin Labeling* , 2007, Journal of Biological Chemistry.
[21] A. Jonas,et al. Stabilization of α-Synuclein Secondary Structure upon Binding to Synthetic Membranes* , 1998, The Journal of Biological Chemistry.
[22] J. Hoenicka,et al. The new mutation, E46K, of α‐synuclein causes parkinson and Lewy body dementia , 2004, Annals of neurology.
[23] R. Riek,et al. 3D structure of Alzheimer's amyloid-β(1–42) fibrils , 2005 .
[24] 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.
[25] P. Lansbury,et al. Protofibrils, pores, fibrils, and neurodegeneration: separating the responsible protein aggregates from the innocent bystanders. , 2003, Annual review of neuroscience.
[26] J Q Trojanowski,et al. Axon pathology in Parkinson's disease and Lewy body dementia hippocampus contains alpha-, beta-, and gamma-synuclein. , 1999, Proceedings of the National Academy of Sciences of the United States of America.
[27] Carl W. Cotman,et al. Common Structure of Soluble Amyloid Oligomers Implies Common Mechanism of Pathogenesis , 2003, Science.
[28] Michel Goedert,et al. Alpha-synuclein and neurodegenerative diseases , 2001, Nature Reviews Neuroscience.
[29] Ralf Langen,et al. Structural Organization of α-Synuclein Fibrils Studied by Site-directed Spin Labeling* , 2003, Journal of Biological Chemistry.
[30] J. Ridet,et al. alpha -Synucleinopathy and selective dopaminergic neuron loss in a rat lentiviral-based model of Parkinson's disease. , 2002, Proceedings of the National Academy of Sciences of the United States of America.
[31] P. Lansbury,et al. Vesicle permeabilization by protofibrillar alpha-synuclein: implications for the pathogenesis and treatment of Parkinson's disease. , 2001, Biochemistry.
[32] 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.
[33] Seung-Jae Lee,et al. Controlling the mass action of α‐synuclein in Parkinson’s disease , 2008, Journal of neurochemistry.
[34] Armin Giese,et al. Different species of alpha-synuclein oligomers induce calcium influx and seeding. , 2007, The Journal of neuroscience : the official journal of the Society for Neuroscience.
[35] Janel O. Johnson,et al. α-Synuclein Locus Triplication Causes Parkinson's Disease , 2003, Science.
[36] D. Eliezer,et al. Effects of Parkinson's disease-linked mutations on the structure of lipid-associated alpha-synuclein. , 2004, Biochemistry.
[37] R. Riek,et al. 3D structure of Alzheimer's amyloid-beta(1-42) fibrils. , 2005, Proceedings of the National Academy of Sciences of the United States of America.
[38] A. Singleton,et al. alpha-Synuclein locus triplication causes Parkinson's disease. , 2003, Science.
[39] M. Ntzouni,et al. Cell-Produced α-Synuclein Is Secreted in a Calcium-Dependent Manner by Exosomes and Impacts Neuronal Survival , 2010, The Journal of Neuroscience.
[40] Peter T. Lansbury,et al. Accelerated in vitro fibril formation by a mutant α-synuclein linked to early-onset Parkinson disease , 1998, Nature Medicine.
[41] E. Masliah,et al. Mechanisms of Hybrid Oligomer Formation in the Pathogenesis of Combined Alzheimer's and Parkinson's Diseases , 2008, PloS one.