What we do and where we go
Our mission is to contribute to a global and better understanding of interactions between biological mechanisms as basis for the development of prophylaxis, diagnosis and therapy of human metabolic diseases.
Large-scale functional genomics
Our group has a long-standing expertise in phenotype-driven, large-scale generation of mouse models by chemical mutagenesis (MEP, Munich ENU Mutagenesis Project).
Metabolic diseases and diabetes research
By in-depth analysis of a new mouse model for osteogenesis imperfecta (OI) we provided for the first time evidence for ER-stress associated apoptosis in osteoblasts as a key component in the pathogenesis of OI (Lisse et al., 2008) but also identified bone-independent cardiopulmonary complications (manuscript in preparation).
Bone related diseases often develop in combination with other defects in multiple sites of the body. The analysis of mouse models that both display pronounced bone phenotypes and altered metabolic parameters allows us to study mutual interactions between bone, fat, pancreas and energy balance in metabolic diseases such as obesity and diabetes. One focus of our research is actual in Delta-Notch signaling and its role in adult tissue homeostasis (e.g. Rubio-Aliaga et al., 2009). Of particular interest are the Delta-like 1 (Dll1) gene, its tissue-specific requirements and its interactions with PDZ-domain containing proteins, which might be of pharmacological relevance.
