von HUNDELSHAUSEN LAB
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We are studying effects of chemokines on platelet activity which is related to atherosclerosis and thrombosis.
- We are particularly interested in the fact that chemokines associate with themselves or other soluble mediators to form oligomeric complexes thereby altering the functional behaviour of chemokines.
- Our goal is to elucidate the role of chemokines in atherosclerosis and thrombosis resulting in new targets and novel therapeutics.
LATEST NEWS FROM THE LAB
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Atherosclerotic vascular disease (ASCVD) is a chronic inflammatory disease of the arterial wall and the prerequisite for plaque erosion and rupture, the pathophysiological substrate of acute coronary syndromes and ischemic stroke which account for the major cause of mortality and disability worldwide.
The results of several clinical trials targeting inflammatory mediators including IL-1β prove that targeting inflammation is worthwhile, but needs to be more specific to avoid immunerelated side effects and preserve efficacy so that further research toward immunomodulatory pathways for atherosclerosis/thrombosis is warranted. Chemokines and galectins form heterodimers to modulate inflammation
- Chemokines and galectins are simultaneously upregulated and mediate leukocyte recruitment during inflammation.
Heterodimer by CXCL12-Gal-3 CRD association. (A) The crystal structure of the CXCL12 homodimer (PDB code 4UAI) is shown with one monomer subunit highlighted in green and red. (B) The structure of the Gal-3 CRD (in yellow and red) bound with lactose (in magenta) (PDB code 1A3K) is shown. (C) A model of the heterodimer formed between CXCL12 (green) and Gal-3 (yellow) derived from NMR-directed protein-protein docking, MD simulations and BFE calculations is shown. (D) Spectral expansions of HSQC data of 15N-labelled CXCL12 in the absence (black contours) and presence (red contours) of unlabelled Gal3 CRD are shown. (E) The NMR-based heterodimer model is shown with residues that are most perturbed by interactions between Gal-3 and CXCL12 highlighted in red and orange
Btk is a central signalling molecule in platelets and a potential target in atherothrombosis
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TEAM
GROUP MEMBERS
Philipp von Hundelshausen, MD PhDInstitute DeputyXavier Blanchet, PhDPostdoctoral researcherƒgqlWip jänguyzibvimeävf-YmiRundan Duan, PhDPostdoctoral researcherYa LiPhD studentØg-Vlv;imeävfsmiRui SuPhD studentBfl-RSfvimY ävfemiSabine StreicherTechnicianAlumniVeit Eckardt, former PhD Student
Julian Leberzammer, former MD Student