Author

D. Schaale

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

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Cell Biology· 1 Physiology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 2 Research Focus:host-pathogen & immune response· 2 Organism:human· 2 Assay:flow cytometry· 1

Frequent Co-Authors

A. Bayrak· 2 shared A.-K. Rohlfing· 2 shared M. Sigle· 2 shared S. Laufer· 2 shared T. Castor· 2 shared T. Pillaiyar· 2 shared V. Dicenta-Baunach· 2 shared Z. Laspa· 2 shared

Activity by Year

2024-2025 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 45 mutual co-author links

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2 shared papersPhysiology

A. Bayrak

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2 papers

Recent·Most cited

ACKR3 agonism induces heterodimerization with chemokine receptor CXCR4 and attenuates platelet function

V. Dicenta-Baunach, Z. Laspa, D. Schaale, M. Sigle, A. Bayrak, T. Castor, T. Pillaiyar, S. Laufer, M. P. Gawaz, A.-K. Rohlfing

This study shows that ACKR3 agonism promotes heterodimerization with CXCR4 in platelets, reducing platelet activation and thrombus formation by modulating CXCR4 signaling.

European Journal of Clinical Investigation · Jan 1, 2025Peer-reviewedPhysiology

Hemin-induced platelet activation is regulated via ACKR3 chemokine surface receptor - implications for passivation of vulnerable atherosclerotic plaque

Z. Laspa, V. Dicenta-Baunach, D. Schaale, M. Sigle, R. Hochuli, T. Castor, A. Bayrak, T. Harm, K. A. L. Mueller, T. Pillaiyar, S. Laufer, A.-K. Rohlfing, M. Gawaz

This study shows hemin activates platelets and promotes thrombosis, which can be inhibited by ACKR3 agonists, suggesting a potential therapeutic strategy for atherosclerotic plaque vulnerability.

bioRxiv · May 13, 2024 · PreprintCell Biology