T
Thomas Binz
Researcher at Hochschule Hannover
Publications - 109
Citations - 11203
Thomas Binz is an academic researcher from Hochschule Hannover. The author has contributed to research in topics: Synaptobrevin & Synaptic vesicle. The author has an hindex of 50, co-authored 107 publications receiving 10718 citations. Previous affiliations of Thomas Binz include University of Giessen & University of California, Irvine.
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Journal ArticleDOI
A Novel Inhibitor Prevents the Peripheral Neuroparalysis of Botulinum Neurotoxins.
Domenico Azarnia Tehran,Giulia Zanetti,Oneda Leka,Florigio Lista,Silvia Fillo,Thomas Binz,Clifford C. Shone,Ornella Rossetto,Cesare Montecucco,Cristina Paradisi,Andrea Mattarei,Marco Pirazzini +11 more
TL;DR: An optimized procedure to synthesize EGA is proposed and it is shown that, in vitro, it prevents the neurotoxicity of different BoNT serotypes by interfering with their trafficking, which opens the possibility of using EGA as a lead compound to develop novel inhibitors of botulinum neurotoxins.
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Identification of the amino acid residues rendering TI-VAMP insensitive toward botulinum neurotoxin B.
TL;DR: The contribution of each non-conserved amino acid of the whole 34-mer segment to the interaction was investigated employing VAMP-2, and it is found that the eight non- Conserved residues of the 71-80 segment are all necessary for efficient cleavage.
Journal ArticleDOI
Role of the Sec22b-E-Syt complex in neurite growth and ramification.
Alessandra Gallo,Alessandra Gallo,Lydia Danglot,Francesca Giordano,Bailey Hewlett,Thomas Binz,Christian Vannier,Thierry Galli +7 more
TL;DR: The non-fusogenic Sec22b–Stx1 SNARE complex contributes to plasma membrane expansion by interacting with the E-Syt lipid transfer proteins at ER–PM contact sites, and this interaction depends on the longin domain of Sec 22b.
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Botulinum neurotoxin C mutants reveal different effects of syntaxin or SNAP-25 proteolysis on neuromuscular transmission.
Giulia Zanetti,Stefan Sikorra,Andreas Rummel,Nadja Krez,Elisa Duregotti,Samuele Negro,Tina Henke,Ornella Rossetto,Thomas Binz,Marco Pirazzini +9 more
TL;DR: Results indicate that neuroparalysis of BoNT/C at the neuromuscular junction is due to SNAP-25 cleavage, while the proteolysis of syntaxin provides a substantial, but incomplete, neuromUScular impairment.
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Botulinum Neurotoxin G Binds Synaptotagmin-II in a Mode Similar to That of Serotype B: Tyrosine 1186 and Lysine 1191 Cause Its Lower Affinity
TL;DR: The results suggest that synaptotagmin takes the same overall orientation in BoNT/B andBoNT/G governed by the strictly conserved central parts of the toxins' binding site, and the surrounding nonconserved areas differently contribute to receptor binding.