<scp>ACKR3</scp> agonism induces heterodimerization with chemokine receptor <scp>CXCR4</scp> and attenuates platelet function
Our results reveal that the formation of platelet ACKR3/CXCR4 heterodimers is dependent on ACKR3 rather than CXCR4. Furthermore, ACKR3 agonism induced heterodimerization is associated with mitigating CXCL12/CXCR4-dependent platelet activation possibly by modulating CXCR4-dependent G protein signalling. Our results indicate possible ACKR3 agonist functions and reinforce the potential therapeutic applications of ACKR3 agonists.
Authors
- Anne‐Katrin Rohlfing (ORCID: https://orcid.org/0000-0001-5469-3648)
- Thanigaimalai Pillaiyar (ORCID: https://orcid.org/0000-0001-5575-8896)
- David Schaale (ORCID: https://orcid.org/0009-0003-9354-0419)
- Stefan Laufer (ORCID: https://orcid.org/0000-0001-6952-1486)
- Zoi Laspa (ORCID: https://orcid.org/0009-0009-4231-6728)
- Tatsiana Castor (ORCID: https://orcid.org/0009-0007-2853-1144)
- Alp Bayrak (ORCID: https://orcid.org/0000-0003-4752-2730)
- Manuel Sigle (ORCID: https://orcid.org/0000-0001-8954-4810)
- Meinrad Gawaz (ORCID: https://orcid.org/0000-0003-1124-9592)
- Valerie Dicenta‐Baunach
Institutions
- University of Tübingen (DE)
Publication Details
- Journal
- European Journal of Clinical Investigation
- Published
- 2024-10-07
- DOI
- https://doi.org/10.1111/eci.14327
- Citations
- 4
- Primary Topic
- Chemokine receptors and signaling
- Type
- article
- Field-Weighted Citation Impact
- 1.13
Funders
- Deutsche Forschungsgemeinschaft
- Deutsche Gesellschaft für Kardiologie-Herz und Kreislaufforschung.