Silvia Weis
University of Mainz
11 Papers
110 Citations
Silvia Weis is an academic researcher from University of Mainz. The author has contributed to research in topics: Cytolysin & Streptolysin. The author has an hindex of 11, co-authored 11 publications. Previous affiliations of Silvia Weis include Newcastle University.
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Papers
Pore-forming toxins activate MAPK p38 by causing loss of cellular potassium.
Nicole Kloft,Tim Busch,Claudia Neukirch,Silvia Weis,Fatima Boukhallouk,Wiesia Bobkiewicz,Ingo Cibis,Sucharit Bhakdi,Matthias Husmann +8 more
TL;DR: It is proposed that PFT trigger the p38 MAPK-pathway by causing loss of cellular K+, likely to be the critical parameter.
93
Binding of Escherichia coli hemolysin and activation of the target cells is not receptor-dependent.
Angela Valeva,Ivan Walev,Helene Kemmer,Silvia Weis,Isabel Siegel,Fatima Boukhallouk,Trudy M. Wassenaar,Triantafyllos Chavakis,Sucharit Bhakdi +8 more
TL;DR: It is concluded that HlyA binds nonspecifically to target cells and a receptor is involved neither in causing hemolysis nor in triggering cellular reactions.
60
Streptolysin O: inhibition of the conformational change during membrane binding of the monomer prevents oligomerization and pore formation.
TL;DR: Findings corroborate the contention that the target membrane acts as an allosteric effector to activate the oligomerizing and pore-forming capability of streptolysin O.
45
A cellular metalloproteinase activates Vibrio cholerae pro-cytolysin.
Angela Valeva,Ivan Walev,Silvia Weis,Fatima Boukhallouk,Trudy M. Wassenaar,Kristina Endres,Falk Fahrenholz,Sucharit Bhakdi,Alexander Zitzer +8 more
TL;DR: ADAM-17 is identified as a potent activator of pro-VCC, the first evidence for processing by a cellular metalloproteinase, in Vibrio cholerae.
42
Modulation of translation and induction of autophagy by bacterial exoproducts.
Gisela von Hoven,Nicole Kloft,Claudia Neukirch,Sabrina Ebinger,Wiesia Bobkiewicz,Silvia Weis,Klaus Boller,Kim D. Janda,Matthias Husmann +8 more
TL;DR: The output of this response, that is, transient metabolic reprogramming is an essential part of a defense program which enables cells to survive attack by a pore-forming agent, and nutrient/energy sensors serve as sentinels of plasma membrane integrity.