Study of epigenetic programming of inflammation. Controlled inducible expression of inflammation responsive genes is essential during immune responses and immune homeostasis. In contrast, deregulated chronic inflammatory conditions in various cell types frequently result in cancer, cardiovascular or neurological disease. Selectivity, strength and time dependency of gene expression largely depends on activation and interaction of transcription factors/cofactors (i.e. NFkB, AP1, Sp1, HDAC, HMT, dnmt, etc.) and their posttranslational modifications with the chromatin environment. Furthermore, chromatin regulation (nucleosome dynamics, histone modifications), noncoding RNAs and epigenetic modifications (DNA methylation of CpG motifs) integrate various input signals (infection, inflammation, stress, metabolism, nutrition) which are ultimately recorded and imprinted into the epigenome.
Identifying specific protein interactions and signaling functions in relation to epigenetic marks in in different in vitro/ in vivo cell models, representative for cancer, cardiovascular or neuroimmunological disease, is an absolute requirement for translational approaches aiming at identifying small inhibitor molecules (for example derived from medicinal plants) for preventive or therapeutic applications.