Rebekka Schlatter

TL;DR: A large-scale literature-based Boolean model of the central intrinsic and extrinsic apoptosis pathways as well as pathways connected with them is built and gives new insights into the complex interplay of pro- and antiapoptotic factors and can be easily expanded to other signaling pathways.

TL;DR: A network model for apoptosis and crosstalk in hepatocytes shows four different system states and reproduces a number of different conditions around apoptosis including effects of different growth substrates and viral infections.

TL;DR: In this article, the authors discuss model combination approaches for Boolean models and propose modelling standards for combining Boolean models as a prerequisite for smooth model integration, and demonstrate the coupling of two logical models on two different examples concerning cellular interactions in the liver.

TL;DR: It is reported that TNF α sensitizes primary murine hepatocytes cultured on collagen to Fas ligand (FasL)–induced apoptosis and the mechanism of TNFα‐induced sensitization is supported by a mathematical model that correctly reproduces the biological findings.

TL;DR: A mathematical model reproduces the complex interplay regulating the phosphorylation status of JNK and generation of ROS and delivers insight in the dynamical interplay between the TNFα and FasL pathways, NF-κB and ROS.