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Your search keyword '"Henkel, Andreas W."' showing total 32 results
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32 results on '"Henkel, Andreas W."'

1. Use-Dependent Inhibition of Synaptic Transmission by the Secretion of Intravesicularly Accumulated Antipsychotic Drugs

Author

Tischbirek, Carsten H., Wenzel, Eva M., Zheng, Fang, Huth, Tobias, Amato, Davide, Trapp, Stefan, Denker, Annette, Welzel, Oliver, Lueke, Katharina, Svetlitchny, Alexei, Rauh, Manfred, Deusser, Janina, Schwab, Annemarie, Rizzoli, Silvio O., Henkel, Andreas W., Müller, Christian P., Alzheimer, Christian, Kornhuber, Johannes, and Groemer, Teja W.

Published
2012
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6. Regulation of transferrin-induced endocytosis by wild-type and C282Y-mutant HFE in transfected HeLa cells

Author

Schwake, Lukas, Henkel, Andreas W., Riedel, Hans D., Schlenker, Thorsten, Both, Matthias, Migala, Andrea, Hadaschik, Boris, Henfling, Nataly, and Stremmel, Wolfgang

Subjects
Endocytosis -- Research, Transferrin -- Physiological aspects, Hemochromatosis -- Physiological aspects, Biological sciences
Abstract

The hereditary hemochromatosis protein HFE is known to complex with the transferrin receptor; however, its function regarding endocytosis of transferrin is unclear. We performed patch-clamp capacitance measurements in transfected HeLa cells carrying wild-type or C282Y-mutant HFE cDNA under the control of a tetracycline-sensitive promoter. Whole cell experiments in cells with suppressed expression of wild-type HFE revealed a decrease in membrane capacitance, reflecting predominance of endocytosis in the presence of transferrin. Cells overexpressing C282Y-mutant HFE displayed less intense capacitance decreases, whereas no significant decrease was observed in cells overexpressing wild-type HFE. The formation of single endocytic vesicles in cells with suppressed expression of wild-type HFE was greatly increased in the presence of transferrin as revealed by cell-attached recordings. According to their calculated diameters, many of these vesicles corresponded to clathrin-coated vesicles. These results suggest that wild-type HFE negatively modulates the endocytic uptake of transferrin. This inhibitory effect is attenuated in cells expressing C282Y-mutant HFE. Time-resolved measurements of cell membrane capacitance provide a powerful tool to study transferrin-induced endocytosis in single cells. hereditary hemochromatosis; transferrin receptor; patch-clamp capacitance measurements

Published
2002

20. Inertia of Synaptic Vesicle Exocytosis

Author

Welzel, Oliver, primary, Groemer, Teja W., additional, Jung, Jasmin, additional, Stroebel, Armin M., additional, Ebert, Katrin, additional, Kornhuber, Johannes, additional, and Henkel, Andreas W., additional

Published
2010
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23. Light-induced exocytosis in cell development and differentiation

Author

Henkel, Andreas W., primary, Upmann, Irene, additional, Bartl, Christina R., additional, Bönsch, Dominikus, additional, Reichardt, Cornelia, additional, Maler, Juan Manuel, additional, Nürnberger, Michael, additional, Umstätter, Richard, additional, Reulbach, Udo, additional, Kornhuber, Johannes, additional, and Wiltfang, Jens, additional

Published
2006
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29. Distinct intracellular vesicle transport mechanisms are selectively modified by spastin and spastin mutations.

Author

Fuerst, Julia C., Henkel, Andreas W., Stroebel, Armin, Welzel, Oliver, Groemer, Teja W., Kornhuber, Johannes, and Bönsch, Dominikus

Subjects
*ENZYME kinetics, *MICROTUBULES, *NEUROBLASTOMA, *GENETIC mutation, *ADENOSINE triphosphatase, *AXONAL transport, *CELL differentiation
Abstract

Spastin is a microtubule severing ATPase that regulates intracellular and axonal transport of vesicles. Intracellular vesicle trafficking was analyzed in differentiated SH-SY5Y-neuroblastoma cells, transfected with spastin wild-type and three spastin mutations (ΔN, K388R, S44L) to investigate spastin-mediated effects on the velocity of vesicles, stained with LysoTracker Red®. The vesicle velocity varied considerably between mutations and detailed analysis revealed up to five distinct velocity classes. Microtubule severing by overexpressed wild-type spastin caused reduced vesicle velocity. S44L and ΔN mutations, which were functionally impaired, showed similar velocities as control cells. K388R-transfected cells exhibited an intermediate velocity profile. The results support the idea that spastin mutations not only alter axonal transport, but in addition regulate intracellular trafficking in the cell soma as well. J. Cell. Physiol. 226: 362-368, 2011. © 2010 Wiley-Liss, Inc. [ABSTRACT FROM AUTHOR]

Published
2011
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32. Dictyostelium myosin IK is involved in the maintenance of cortical tension and affects motility and phagocytosis

Author

Schwarz, Eva C., Neuhaus, Eva M., Kistler, Claudia, Henkel, Andreas W., and Soldati, Thierry

Abstract

Dictyostelium discoideummyosin Ik (MyoK) is a novel type of myosin distinguished by a remarkable architecture. MyoK is related to class I myosins but lacks a cargo-binding tail domain and carries an insertion in a surface loop suggested to modulate motor velocity. This insertion shows similarity to a secondary actin-binding site present in the tail of some class I myosins, and indeed a GST-loop construct binds actin. Probably as a consequence, binding of MyoK to actin was not only ATP-but also salt-dependent. Moreover, as both binding sites reside within its motor domain and carry potential sites of regulation, MyoK might represent a new form of actin crosslinker. MyoK was distributed in the cytoplasm with a significant enrichment in dynamic regions of the cortex. Absence of MyoK resulted in a drop of cortical tension whereas overexpression led to significantly increased tension. Absence and overexpression of MyoK dramatically affected the cortical actin cytoskeleton and resulted in reduced initial rates of phagocytosis. Cells lacking MyoK showed excessive ruffling, mostly in the form of large lamellipodia, accompanied by a thicker basal actin cortex. At early stages of development, aggregation of myoKnull cells was slowed due to reduced motility. Altogether, the data indicate a distinctive role for MyoK in the maintenance and dynamics of the cell cortex.

Published
2000
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