A glutaminyl cyclase-catalyzed α-synuclein modification identified in human synucleinopathies

Parkinson’s disease (PD) is a progressive neurodegenerative disorder that is neuropathologically characterized by degeneration of dopaminergic neurons of the substantia nigra (SN) and formation of Lewy bodies and Lewy neurites composed of aggregated α-synuclein. Proteolysis of α-synuclein by matrix...

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Veröffentlicht in:	Acta neuropathologica Jg. 142; H. 3; S. 399 - 421
Hauptverfasser:	Hartlage-Rübsamen, Maike, Bluhm, Alexandra, Moceri, Sandra, Machner, Lisa, Köppen, Janett, Schenk, Mathias, Hilbrich, Isabel, Holzer, Max, Weidenfeller, Martin, Richter, Franziska, Coras, Roland, Serrano, Geidy E., Beach, Thomas G., Schilling, Stephan, von Hörsten, Stephan, Xiang, Wei, Schulze, Anja, Roßner, Steffen
Format:	Journal Article
Sprache:	Englisch
Veröffentlicht:	Berlin/Heidelberg Springer Berlin Heidelberg 01.09.2021 Springer Nature B.V
Schlagworte:	alpha-Synuclein - metabolism Alzheimer's disease Aminoacyltransferases - metabolism Animals Axons Brain - pathology Cell size Cell Survival Cell viability Chromatography, Gel Dementia disorders Dopamine receptors Dopaminergic Neurons - metabolism Electron microscopy Epitopes Fibrils Glutamine Glutamine - metabolism Humans Kinetics Lewy bodies Lewy Body Disease - genetics Lewy Body Disease - metabolism Mass spectroscopy Matrix metalloproteinase Medicine Medicine & Public Health Mice Mice, Transgenic Movement disorders N-Terminus Neurodegeneration Neurodegenerative diseases Neurons Neurosciences Neurotoxicity Original Paper Parkinson Disease - genetics Parkinson Disease - metabolism Parkinson's disease Pathology Protein interaction Protein Processing, Post-Translational Proteolysis Sambucus nigra - cytology Sambucus nigra - metabolism Substantia nigra Synuclein Synucleinopathies - genetics Transgenic mice Post-translational modification α-Synuclein Glutaminyl cyclase Animal models Substantia nigra Parkinson’s disease Dementia with Lewy bodies
ISSN:	0001-6322, 1432-0533, 1432-0533
Online-Zugang:	Volltext
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