Inflammatory processes are driven and controlled by several endogenous mediators that undergo proteolytic conversion from surface-expressed proteins to soluble variants. This process called shedding is one major function of ‘a disintegrin and metalloproteinase (ADAM)’ family members (figure 1). These mediators include cytokines and their receptors (e.g. TNF, TNFR), growth factors (e.g. TGFa, EGF), proteogylcans (e.g. syndecans) as well as junction and adhesion molecules (e.g. JAM-A, VE-cahderin). Rheumatoid arthritis, atherosclerosis, lung inflammation, psoriasis, cancer development/metastasis formation, and Alzheimer’s disease are only a few examples of diseases involving the action of ADAM proteases. However, ADAM proteases are not only implicated in pathology but also contribute to developmental and regenerative processes. Thus, ADAMs can be regarded as valuable drug targets, but the danger of severe side effects, e.g. upon systemic treatment, is obvious.
Based on these aspects, our current research foci are
- the immunological and molecular functions of ADAM proteases in lung and cardiovascular diseases
- sterile inflammation and infection
- the regulation of cell-specific functions
- the assembly and composition of complex membrane structures
with the overall aim of the development of specific treatment options.
Mass spectrometry, FACS, live-cell imaging, viral particles, and infection models are only a few of the used techniques besides common molecular, biochemical and pharmacological methods. Please, have a look on our publications to get deeper insight into our research.
We are always interested in motivated undergraduate students, graduate students and postdocs complementing our team. If you are interested in joining our team, please contact me (daniela.yildiz(at)uks.eu) with your CV, a statement of research interests and contact information for references. I am looking forward to discuss future projects with you!
DFG Gewebespezifische Rolle von ADAM-Proteasen in infektiösen Lungenerkrankungen
DFG YI 176/1-1 (DR 1013/1-1)