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FEBS Letters|April 11, 2018
Refolding of helical soluble α-synuclein through transient interaction with lipid interfacesMatteo Rovere, John B Sanderson, Luis Fonseca-Ornelas, et al.
Proceedings of the National Academy of Sciences of the United States of America|July 9, 2015
KTKEGV repeat motifs are key mediators of normal α-synuclein tetramerization: Their mutation causes excess monomers and neurotoxicityUlf Dettmer, Andrew J Newman, Victoria E von Saucken, et al.
The Journal of Biological Chemistry|June 20, 2014
Soluble, prefibrillar α-synuclein oligomers promote complex I-dependent, Ca2+-induced mitochondrial dysfunctionEric S Luth, Irina G Stavrovskaya, Tim Bartels, et al.
Biophysical Journal|October 7, 2010
The N-terminus of the intrinsically disordered protein α-synuclein triggers membrane binding and helix foldingTim Bartels, Logan S Ahlstrom, Avigdor Leftin, et al.
The Journal of Physiology|November 12, 2024
Acute introduction of monomeric or multimeric α-synuclein induces distinct impacts on synaptic vesicle trafficking at lamprey giant synapsesCristina Román-Vendrell, Jaqulin N Wallace, Aurelia Hays Watson, et al.
NPJ Parkinson'S Disease|March 1, 2026
Higher-molecular-weight a-synuclein oligomers are increased in the brain cytosol of patients with dementia with Lewy bodiesEmil Gregersen, Mia R Antorini, Lasse Reimer, et al.
Frontiers in Neuroscience|February 22, 2021
Effects of Excess Brain-Derived Human α-Synuclein on Synaptic Vesicle TraffickingCristina Román-Vendrell, Audrey T Medeiros, John B Sanderson, et al.
Neuron|April 2, 2014
Soluble Aβ oligomers are rapidly sequestered from brain ISF in vivo and bind GM1 ganglioside on cellular membranesSoyon Hong, Beth L Ostaszewski, Ting Yang, et al.
The Journal of Biological Chemistry|May 4, 2019
E46K-like α-synuclein mutants increase lipid interactions and disrupt membrane selectivityMatteo Rovere, Alex E Powers, Haiyang Jiang, et al.
Nature Communications|June 17, 2015
Parkinson-causing α-synuclein missense mutations shift native tetramers to monomers as a mechanism for disease initiationUlf Dettmer, Andrew J Newman, Frank Soldner, et al.
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