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Brain : a Journal of Neurology|October 31, 2012
A point mutation associated with episodic ataxia 6 increases glutamate transporter anion currentsNatalie Winter, Peter Kovermann, Christoph Fahlke
The Journal of Biological Chemistry|May 17, 2011
Substrate-dependent gating of anion channels associated with excitatory amino acid transporter 4Jan-Philipp Machtens, Peter Kovermann, Christoph Fahlke
Channels (Austin, Tex.)|August 19, 2011
Noise analysis to study unitary properties of transporter-associated ion channelsJan-Philipp Machtens, Christoph Fahlke, Peter Kovermann
Frontiers in Cellular Neuroscience|January 28, 2022
Cellular Physiology and Pathophysiology of EAAT Anion ChannelsPeter Kovermann, Miriam Engels, Frank Müller, et al.
Epilepsia|December 28, 2021
Mutations associated with epileptic encephalopathy modify EAAT2 anion channel functionPeter Kovermann, Yulia Kolobkova, Arne Franzen, et al.
The Journal of Biological Chemistry|November 12, 2013
Mutating a conserved proline residue within the trimerization domain modifies Na+ binding to excitatory amino acid transporters and associated conformational changesJasmin Hotzy, Nicole Schneider, Peter Kovermann, et al.
The Journal of Biological Chemistry|June 4, 2010
A conserved aspartate determines pore properties of anion channels associated with excitatory amino acid transporter 4 (EAAT4)Peter Kovermann, Jan-Philipp Machtens, David Ewers, et al.
Human Mutation|August 3, 2020
Functional consequences of SLC1A3 mutations associated with episodic ataxia 6Aparna S Chivukula, Mariia Suslova, Daniel Kortzak, et al.
Frontiers in Physiology|August 4, 2023
Apo state pore opening as functional basis of increased EAAT anion channel activity in episodic ataxia 6Mariia Suslova, Daniel Kortzak, Jan-Philipp Machtens, et al.
Scientific Reports|July 10, 2026
Evolutionary gene number variation and functional diversification of retinal EAATs are reflected in expression pattern adaptationAndré Lehnherr, Peter Kovermann, Christoph Fahlke, et al.
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