Aggregated α-Synuclein Mediates Dopaminergic Neurotoxicity In Vivo
暂无分享,去创建一个
M. Feany | M. Periquet | T. Fulga | M. Schlossmacher | L. Myllykangas | Michael G. Schlossmacher | Liisa Myllykangas | Magali Periquet | Mel B. Feany | Tudor Fulga | Magali Periquet
[1] D. Price,et al. Human alpha-synuclein-harboring familial Parkinson's disease-linked Ala-53 --> Thr mutation causes neurodegenerative disease with alpha-synuclein aggregation in transgenic mice. , 2002, Proceedings of the National Academy of Sciences of the United States of America.
[2] A. Singleton,et al. alpha-Synuclein locus triplication causes Parkinson's disease. , 2003, Science.
[3] R. J. Clem,et al. Prevention of apoptosis by a baculovirus gene during infection of insect cells. , 1991, Science.
[4] P. Lansbury,et al. Zeroing in on the pathogenic form of alpha-synuclein and its mechanism of neurotoxicity in Parkinson's disease. , 2003, Biochemistry.
[5] J. Trojanowski,et al. “Fatal Attractions” of Proteins: A Comprehensive Hypothetical Mechanism Underlying Alzheimer's Disease and Other Neurodegenerative Disorders , 2000, Annals of the New York Academy of Sciences.
[6] M. Ehlers,et al. Learning from NMDA Receptor Trafficking: Clues to the Development and Maturation of Glutamatergic Synapses , 2004, Neurosignals.
[7] P. S. St George-Hyslop,et al. α-Synuclein Membrane Interactions and Lipid Specificity* , 2000, The Journal of Biological Chemistry.
[8] Hideo Fujiwara,et al. Misfolded proteinase K-resistant hyperphosphorylated alpha-synuclein in aged transgenic mice with locomotor deterioration and in human alpha-synucleinopathies. , 2002, The Journal of clinical investigation.
[9] John Q. Trojanowski,et al. Chaperone Suppression of α-Synuclein Toxicity in a Drosophila Model for Parkinson's Disease , 2001, Science.
[10] Robert L. Nussbaum,et al. Mutation in the α-Synuclein Gene Identified in Families with Parkinson's Disease , 1997 .
[11] Karen A. Lewis,et al. A precipitating role for truncated alpha-synuclein and the proteasome in alpha-synuclein aggregation: implications for pathogenesis of Parkinson disease. , 2005, The Journal of biological chemistry.
[12] R. Anthony Crowther,et al. Synthetic filaments assembled from C‐terminally truncated α‐synuclein , 1998 .
[13] L. Petrucelli,et al. α-Synuclein Shares Physical and Functional Homology with 14-3-3 Proteins , 1999, The Journal of Neuroscience.
[14] Bernardino Ghetti,et al. Pathological Changes in Dopaminergic Nerve Cells of the Substantia Nigra and Olfactory Bulb in Mice Transgenic for Truncated Human α-Synuclein(1–120): Implications for Lewy Body Disorders , 2006, The Journal of Neuroscience.
[15] M. Feany,et al. α-Synuclein phosphorylation controls neurotoxicity and inclusion formation in a Drosophila model of Parkinson disease , 2005, Nature Neuroscience.
[16] B. Ghetti,et al. Ubiquitination of α-Synuclein in Lewy Bodies Is a Pathological Event Not Associated with Impairment of Proteasome Function* , 2003, Journal of Biological Chemistry.
[17] J Q Trojanowski,et al. A Hydrophobic Stretch of 12 Amino Acid Residues in the Middle of α-Synuclein Is Essential for Filament Assembly* , 2001, The Journal of Biological Chemistry.
[18] M. Citron,et al. Parkinson's disease-associated alpha-synuclein is more fibrillogenic than beta- and gamma-synuclein and cannot cross-seed its homologs. , 2000, The Journal of biological chemistry.
[19] V. Uversky,et al. Nitration inhibits fibrillation of human alpha-synuclein in vitro by formation of soluble oligomers. , 2003, FEBS letters.
[20] 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.
[21] R. Jakes,et al. Effects of the mutations Ala30 to Pro and Ala53 to Thr on the physical and morphological properties of α‐synuclein protein implicated in Parkinson's disease , 1998, FEBS letters.
[22] A. Rajput,et al. Prevalence of movement disorders in elderly community residents. , 1994, Neuroepidemiology.
[23] R A Crowther,et al. Synthetic filaments assembled from C-terminally truncated alpha-synuclein. , 1998, FEBS letters.
[24] A Dürr,et al. Causal relation between alpha-synuclein gene duplication and familial Parkinson's disease. , 2004, Lancet.
[25] D. Neill,et al. Aggregates from mutant and wild‐type α‐synuclein proteins and NAC peptide induce apoptotic cell death in human neuroblastoma cells by formation of β‐sheet and amyloid‐like filaments , 1998, FEBS letters.
[26] Olga Pletnikova,et al. Aggregation promoting C-terminal truncation of alpha-synuclein is a normal cellular process and is enhanced by the familial Parkinson's disease-linked mutations. , 2005, Proceedings of the National Academy of Sciences of the United States of America.
[27] Vladimir N Uversky,et al. Conformational behavior of human alpha-synuclein is modulated by familial Parkinson's disease point mutations A30P and A53T. , 2002, Neurotoxicology.
[28] J. Trojanowski,et al. Neuronal alpha-synucleinopathy with severe movement disorder in mice expressing A53T human alpha-synuclein. , 2002, Neuron.
[29] P. S. St George-Hyslop,et al. alpha-Synuclein membrane interactions and lipid specificity. , 2000, The Journal of biological chemistry.
[30] V. Uversky,et al. Nitration inhibits fibrillation of human α‐synuclein in vitro by formation of soluble oligomers , 2003 .
[31] Mark R. Segal,et al. Inclusion body formation reduces levels of mutant huntingtin and the risk of neuronal death , 2004, Nature.
[32] 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.
[33] J. Trojanowski,et al. Oxidative damage linked to neurodegeneration by selective alpha-synuclein nitration in synucleinopathy lesions. , 2000, Science.
[34] P. Axelsen,et al. Role of α-Synuclein Carboxy-Terminus on Fibril Formation in Vitro† , 2003 .
[35] P. Lansbury,et al. The core Alzheimer's peptide NAC forms amyloid fibrils which seed and are seeded by beta-amyloid: is NAC a common trigger or target in neurodegenerative disease? , 1995, Chemistry & biology.
[36] R. Krüger,et al. Ala30Pro mutation in the gene encoding alpha-synuclein in Parkinson's disease. , 1998, Nature genetics.
[37] J. Hirsh,et al. Ectopic G-protein expression in dopamine and serotonin neurons blocks cocaine sensitization in Drosophila melanogaster , 2000, Current Biology.
[38] Peter T. Lansbury,et al. Accelerated in vitro fibril formation by a mutant α-synuclein linked to early-onset Parkinson disease , 1998, Nature Medicine.
[39] T. Iwatsubo,et al. Selective loss of nigral dopamine neurons induced by overexpression of truncated human α-synuclein in mice , 2008, Neurobiology of Aging.
[40] C. Masters,et al. The solubility of α‐synuclein in multiple system atrophy differs from that of dementia with Lewy bodies and Parkinson's disease , 2001 .
[41] Janel O. Johnson,et al. α-Synuclein Locus Triplication Causes Parkinson's Disease , 2003, Science.
[42] J. Hoenicka,et al. The new mutation, E46K, of α‐synuclein causes parkinson and Lewy body dementia , 2004, Annals of neurology.
[43] J. Trojanowski,et al. Mutant and Wild Type Human α-Synucleins Assemble into Elongated Filaments with Distinct Morphologies in Vitro * , 1999, The Journal of Biological Chemistry.
[44] 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.
[45] Hong-Yu Hu,et al. Structural transformation and aggregation of human alpha-synuclein in trifluoroethanol: non-amyloid component sequence is essential and beta-sheet formation is prerequisite to aggregation. , 2002, Biopolymers.
[46] G. Irvine,et al. Identification of the region of non‐Aβ component (NAC) of Alzheimer's disease amyloid responsible for its aggregation and toxicity , 2001, Journal of neurochemistry.
[47] J. Trojanowski,et al. Role of alpha-synuclein carboxy-terminus on fibril formation in vitro. , 2003, Biochemistry.
[48] T. Nagatsu. [Biochemistry of Parkinson's disease]. , 1988, Seikagaku. The Journal of Japanese Biochemical Society.
[49] E. Masliah,et al. alpha-Synuclein is phosphorylated in synucleinopathy lesions. , 2002, Nature cell biology.
[50] M. Citron,et al. Parkinson's Disease-associated α-Synuclein Is More Fibrillogenic than β- and γ-Synuclein and Cannot Cross-seed Its Homologs* , 2000, The Journal of Biological Chemistry.
[51] J Q Trojanowski,et al. Aggregation of alpha-synuclein in Lewy bodies of sporadic Parkinson's disease and dementia with Lewy bodies. , 1998, The American journal of pathology.
[52] P. Axelsen,et al. The E46K mutation in alpha-synuclein increases amyloid fibril formation. , 2005, The Journal of biological chemistry.
[53] Philip J. Thomas,et al. A Precipitating Role for Truncated α-Synuclein and the Proteasome in α-Synuclein Aggregation , 2005, Journal of Biological Chemistry.
[54] Paul H. Axelsen,et al. The E46K Mutation in α-Synuclein Increases Amyloid Fibril Formation* , 2005, Journal of Biological Chemistry.
[55] R. Barbour,et al. Phosphorylation of Ser-129 Is the Dominant Pathological Modification of α-Synuclein in Familial and Sporadic Lewy Body Disease* , 2006, Journal of Biological Chemistry.
[56] J. Trojanowski,et al. Chaperone suppression of alpha-synuclein toxicity in a Drosophila model for Parkinson's disease. , 2002, Science.
[57] J. Trojanowski,et al. Neuronal α-Synucleinopathy with Severe Movement Disorder in Mice Expressing A53T Human α-Synuclein , 2002, Neuron.
[58] E. Masliah,et al. α-Synuclein is phosphorylated in synucleinopathy lesions , 2002, Nature Cell Biology.
[59] J. Trojanowski,et al. Misfolded proteinase K-resistant hyperphosphorylated alpha-synuclein in aged transgenic mice with locomotor deterioration and in human alpha-synucleinopathies. , 2002, The Journal of clinical investigation.
[60] M. Feany,et al. Alpha-synuclein phosphorylation controls neurotoxicity and inclusion formation in a Drosophila model of Parkinson disease. , 2005, Nature neuroscience.
[61] P. Auluck,et al. Mechanisms of Suppression of α-Synuclein Neurotoxicity by Geldanamycin in Drosophila* , 2005, Journal of Biological Chemistry.
[62] Isao Nishimura,et al. Parkin Suppresses Dopaminergic Neuron-Selective Neurotoxicity Induced by Pael-R in Drosophila , 2003, Neuron.
[63] M. Citron,et al. Both Familial Parkinson’s Disease Mutations Accelerate α-Synuclein Aggregation* , 1999, The Journal of Biological Chemistry.
[64] W. Bender,et al. A Drosophila model of Parkinson's disease , 2000, Nature.
[65] V. Uversky,et al. Methionine oxidation, a-synuclein and Parkinson's disease , 2005 .
[66] Hamid Mirzaei,et al. Identification of rotenone-induced modifications in alpha-synuclein using affinity pull-down and tandem mass spectrometry. , 2006, Analytical chemistry.
[67] M. Zigmond,et al. A Role for α-Synuclein in the Regulation of Dopamine Biosynthesis , 2002, The Journal of Neuroscience.
[68] A Dürr,et al. Causal relation between α-synuclein locus duplication as a cause of familial Parkinson's disease , 2004, The Lancet.
[69] Gerald M. Rubin,et al. Drosophila homologs of baculovirus inhibitor of apoptosis proteins function to block cell death , 1995, Cell.
[70] G. Mardon,et al. Whole‐mount analysis reveals normal numbers of dopaminergic neurons following misexpression of α‐Synuclein in Drosophila , 2005, Genesis.
[71] V. Uversky,et al. Methionine oxidation, alpha-synuclein and Parkinson's disease. , 2005, Biochimica et biophysica acta.
[72] Nancy A. Jenkins,et al. Human α-synuclein-harboring familial Parkinson's disease-linked Ala-53 → Thr mutation causes neurodegenerative disease with α-synuclein aggregation in transgenic mice , 2002, Proceedings of the National Academy of Sciences of the United States of America.