Our group investigates molecular mechanisms that permit or restrict cell proliferation in mammalian cells. Deregulation of cell proliferation can lead to various human diseases including cancer. We therefore also study how these mechanisms are deregulated during oncogenesis.

Cells decide and commit to divide during a specific window in the mammalian cell cycle or during quiescence. At this time, they are especially responsive to various mitogenic and antimitogenic signals. We study how these diverse signals are integrated and how they impinge on the cell cycle control machinery.

At the core of this machinery is a conserved family of protein kinases called cyclin-dependent kinases (Cdks). Cdk inhibitor proteins bind to these kinases and regulate their catalytic activity.

Current research projects in the lab focus on two main areas: Function and regulation of Cdk- inhibitory proteins and the role of translational control for the decision between cell proliferation and withdrawal from the cell cycle.

The eucaryotic cell division cycle is divided into four phases. DNA replication during S-phase is separated by so-called gap-phases, G1 and G2, from the segregation of the duplicated DNA and other cellular components in mitosis. At the end of M-phase, two daugher cells are generated by cytokinesis.  Until they progress over the restriction point in G1-phase, cells frequently respond to growth or differentiation signals tat can lead to proliferation or growth arrest.