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Your search keyword '"Höltje, Markus"' showing total 3 results
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3 results on '"Höltje, Markus"'

1. A Therapeutic Non-self-reactive SARS-CoV-2 Antibody Protects from Lung Pathology in a COVID-19 Hamster Model

Author

Kreye, Jakob, primary, Reincke, S. Momsen, additional, Kornau, Hans-Christian, additional, Sánchez-Sendin, Elisa, additional, Corman, Victor Max, additional, Liu, Hejun, additional, Yuan, Meng, additional, Wu, Nicholas C., additional, Zhu, Xueyong, additional, Lee, Chang-Chun D., additional, Trimpert, Jakob, additional, Höltje, Markus, additional, Dietert, Kristina, additional, Stöffler, Laura, additional, von Wardenburg, Niels, additional, van Hoof, Scott, additional, Homeyer, Marie A., additional, Hoffmann, Julius, additional, Abdelgawad, Azza, additional, Gruber, Achim D., additional, Bertzbach, Luca D., additional, Vladimirova, Daria, additional, Li, Lucie Y., additional, Barthel, Paula Charlotte, additional, Skriner, Karl, additional, Hocke, Andreas C., additional, Hippenstiel, Stefan, additional, Witzenrath, Martin, additional, Suttorp, Norbert, additional, Kurth, Florian, additional, Franke, Christiana, additional, Endres, Matthias, additional, Schmitz, Dietmar, additional, Jeworowski, Lara Maria, additional, Richter, Anja, additional, Schmidt, Marie Luisa, additional, Schwarz, Tatjana, additional, Müller, Marcel Alexander, additional, Drosten, Christian, additional, Wendisch, Daniel, additional, Sander, Leif E., additional, Osterrieder, Nikolaus, additional, Wilson, Ian A., additional, and Prüss, Harald, additional

Published
2020
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3. Serotonylation of small GTPases is a signal transduction pathway that triggers platelet alpha-granule release.

Author

Walther DJ, Peter JU, Winter S, Höltje M, Paulmann N, Grohmann M, Vowinckel J, Alamo-Bethencourt V, Wilhelm CS, Ahnert-Hilger G, and Bader M

Subjects
Animals, Bleeding Time, Blood Coagulation drug effects, Blood Coagulation physiology, Blood Platelets drug effects, Blood Platelets metabolism, Calcium Signaling drug effects, Calcium Signaling physiology, Cell Adhesion drug effects, Cell Adhesion genetics, Cell Aggregation drug effects, Cell Aggregation genetics, Cytoplasm metabolism, Exocytosis drug effects, Exocytosis physiology, Factor VIII metabolism, Humans, Mice, Mice, Knockout, Molecular Sequence Data, Secretory Vesicles drug effects, Secretory Vesicles metabolism, Sequence Homology, Amino Acid, Serotonin metabolism, Serotonin pharmacology, Signal Transduction drug effects, Signal Transduction physiology, Thromboembolism enzymology, Thromboembolism genetics, Transglutaminases metabolism, Tryptophan Hydroxylase genetics, von Willebrand Factor metabolism, Blood Platelets enzymology, GTP Phosphohydrolases metabolism, Secretory Vesicles enzymology, Serotonin deficiency, Tryptophan Hydroxylase deficiency
Abstract

Serotonin is a neurotransmitter in the central nervous system. In the periphery, serotonin functions as a ubiquitous hormone involved in vasoconstriction and platelet function. Serotonin is synthesized independently in peripheral tissues and neurons by two different rate-limiting tryptophan hydroxylase (TPH) isoenzymes. Here, we show that mice selectively deficient in peripheral TPH and serotonin exhibit impaired hemostasis, resulting in a reduced risk of thrombosis and thromboembolism, although the ultrastructure of the platelets is not affected. While the aggregation of serotonin-deficient platelets in vitro is apparently normal, their adhesion in vivo is reduced due to a blunted secretion of adhesive alpha-granular proteins. In elucidating the mechanism further, we demonstrate that serotonin is transamidated to small GTPases by transglutaminases during activation and aggregation of platelets, rendering these GTPases constitutively active. Our data provides evidence for a receptor-independent signaling mechanism, termed herein as "serotonylation," which leads to alpha-granule exocytosis from platelets.

Published
2003
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