It is currently becoming clear that most cell-fate decisions in mammalian cells are not controlled by one single pathway alone. Rather, the combinatorial, and quantitatively different activation of signalling pathways seems to determine the cellular response.

It is currently not clear, which systems approaches will be applicable to understand how these decisions are made. We develop and apply several modelling methods on large-scale data sets of the activity of signalling proteins and the phenotypic response. These models are of different nature, including logical and statistical models, and simplified ODE models. Applying these different approaches will help us to understand which modelling method can be scaled up to problems that involve a large part of the cellular signalling network.

Experimentally, we generate large-scale datasets using microarrays and PosphoPlex measurements on cancer cells that we perturbe with different targeted inhibitors.

Funding: BMBF through FORSYS-Partner and ColoNET.