Raised calcium promotes α-synuclein aggregate formation
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[1] Jason T Giurleo,et al. In vitro formation of amyloid from alpha-synuclein is dominated by reactions at hydrophobic interfaces. , 2010, Journal of the American Chemical Society.
[2] Yves Engelborghs,et al. Early aggregation steps in alpha-synuclein as measured by FCS and FRET: evidence for a contagious conformational change. , 2010, Biophysical journal.
[3] V. Subramaniam,et al. A stable lipid-induced aggregate of alpha-synuclein. , 2010, Journal of the American Chemical Society.
[4] J. Rochet,et al. Adsorption of alpha-synuclein on lipid bilayers: modulating the structure and stability of protein assemblies. , 2010, The journal of physical chemistry. B.
[5] Carol D. Hicks,et al. Brain-Permeable Small-Molecule Inhibitors of Hsp90 Prevent α-Synuclein Oligomer Formation and Rescue α-Synuclein-Induced Toxicity , 2010, Journal of Pharmacology and Experimental Therapeutics.
[6] J. Olzmann,et al. Parkin-mediated ubiquitin signalling in aggresome formation and autophagy. , 2010, Biochemical Society transactions.
[7] D. Surmeier,et al. Calcium, cellular aging, and selective neuronal vulnerability in Parkinson's disease. , 2010, Cell calcium.
[8] R. Nicoll,et al. Increased Expression of α-Synuclein Reduces Neurotransmitter Release by Inhibiting Synaptic Vesicle Reclustering after Endocytosis , 2010, Neuron.
[9] G. Wenning,et al. Multiple system atrophy: an update , 2009, The Lancet Neurology.
[10] M. Dallas,et al. α‐Synuclein modulation of Ca2+ signaling in human neuroblastoma (SH‐SY5Y) cells , 2009, Journal of neurochemistry.
[11] Enikö Kövari,et al. Proteomics in human Parkinson's disease research. , 2009, Journal of proteomics.
[12] Michael Wolff,et al. Seeding induced by α‐synuclein oligomers provides evidence for spreading of α‐synuclein pathology , 2009, Journal of neurochemistry.
[13] Vladimir N Uversky,et al. Biophysics of Parkinson's disease: structure and aggregation of alpha-synuclein. , 2009, Current protein & peptide science.
[14] K. Jellinger,et al. Formation and development of Lewy pathology: a critical update , 2009, Journal of Neurology.
[15] V. Uversky. Intrinsic Disorder in Proteins Associated with Neurodegenerative Diseases , 2009 .
[16] A. Brice,et al. Parkinson's disease: from monogenic forms to genetic susceptibility factors. , 2009, Human molecular genetics.
[17] Jason D. Perlmutter,et al. Curvature dynamics of alpha-synuclein familial Parkinson disease mutants: molecular simulations of the micelle- and bilayer-bound forms. , 2009, The Journal of biological chemistry.
[18] M. Cookson. α-Synuclein and neuronal cell death , 2009, Molecular Neurodegeneration.
[19] Seung-Jae Lee,et al. Controlling the mass action of α‐synuclein in Parkinson’s disease , 2008, Journal of neurochemistry.
[20] C. Griesinger,et al. Site-specific interactions of Cu(II) with alpha and beta-synuclein: bridging the molecular gap between metal binding and aggregation. , 2008, Journal of the American Chemical Society.
[21] T. Lazaridis,et al. Membrane‐bound structure and energetics of α‐synuclein , 2008 .
[22] Armin Giese,et al. Different Species of α-Synuclein Oligomers Induce Calcium Influx and Seeding , 2007, The Journal of Neuroscience.
[23] M. Mattson,et al. Calcium and neurodegeneration , 2007, Aging cell.
[24] Julia Thom Oxford,et al. Calpain-Cleavage of α-Synuclein : Connecting Proteolytic Processing to Disease-Linked Aggregation , 2007 .
[25] V. Uversky,et al. Conformational properties of the SDS-bound state of alpha-synuclein probed by limited proteolysis: unexpected rigidity of the acidic C-terminal tail. , 2006, Biochemistry.
[26] A. Young,et al. Pharmacological promotion of inclusion formation: a therapeutic approach for Huntington's and Parkinson's diseases. , 2006, Proceedings of the National Academy of Sciences of the United States of America.
[27] C. Shults. Lewy bodies. , 2006, Proceedings of the National Academy of Sciences of the United States of America.
[28] X. Shen,et al. SUMO-1 marks subdomains within glial cytoplasmic inclusions of multiple system atrophy , 2005, Neuroscience Letters.
[29] C. Dobson,et al. Mapping long-range interactions in alpha-synuclein using spin-label NMR and ensemble molecular dynamics simulations. , 2005, Journal of the American Chemical Society.
[30] N. Voelcker,et al. Calcium(II) selectively induces α‐synuclein annular oligomers via interaction with the C‐terminal domain , 2004, Protein science : a publication of the Protein Society.
[31] M. Chesselet,et al. Alpha-synuclein and transgenic mouse models , 2004, Neurobiology of Disease.
[32] P. Lansbury,et al. Zeroing in on the pathogenic form of alpha-synuclein and its mechanism of neurotoxicity in Parkinson's disease. , 2003, Biochemistry.
[33] P. Lansbury,et al. Alpha-synuclein, especially the Parkinson's disease-associated mutants, forms pore-like annular and tubular protofibrils. , 2002, Journal of molecular biology.
[34] Sebastian Doniach,et al. Biophysical Properties of the Synucleins and Their Propensities to Fibrillate , 2002, The Journal of Biological Chemistry.
[35] H. Vorum,et al. Ca2+ Binding to α-Synuclein Regulates Ligand Binding and Oligomerization* , 2001, The Journal of Biological Chemistry.
[36] B. Hyman,et al. α-Synuclein–enhanced green fluorescent protein fusion proteins form proteasome sensitive inclusions in primary neurons , 2001, Neuroscience.
[37] D. Eliezer,et al. Conformational properties of alpha-synuclein in its free and lipid-associated states. , 2001, Journal of molecular biology.
[38] P. Lansbury,et al. Accelerated Oligomerization by Parkinson's Disease Linked α‐Synuclein Mutants , 2000 .
[39] W. Bender,et al. A Drosophila model of Parkinson's disease , 2000, Nature.
[40] Robert L. Nussbaum,et al. Mutation in the α-Synuclein Gene Identified in Families with Parkinson's Disease , 1997 .
[41] P. Mcgeer,et al. Relative sparing in Parkinson's disease of substantia nigra dopamine neurons containing calbindin-D28K , 1990, Brain Research.
[42] T. Dawson,et al. The role of parkin in familial and sporadic Parkinson's disease , 2010, Movement disorders : official journal of the Movement Disorder Society.
[43] N. Voelcker,et al. Annular alpha-synuclein oligomers are potentially toxic agents in alpha-synucleinopathy. Hypothesis , 2009, Neurotoxicity Research.