AP-1: a central switch converting extracellular signals into genetic responses. Extracellular signals acting through upstream protein kinase cascades affect the activity of the transcription factor AP-1, a dimeric complex composed of members of the Jun, Fos and ATF protein families. Functional analyses of AP-1 members were performed using genetically modified mouse models as well as cell- and organ cultures derived thereof.

Our research aims at understanding molecular principles of signal transduction pathways elicited by extracellular signals to control essential genetic programs in cell physiology and pathology. Work is focused on the identification and regulation of components of such signalling cascades with a great deal of attention to the receiving ends, -nuclear transcription factors-, as well as the subordinated sets of target genes.

Our special interest is devoted to the transcription factor AP-1 representing the sum of dimeric protein complexes composed of members of the Fos, Jun and ATF protein families. AP-1 mediates gene regulation in response to a plethora of physiological and pathological stimuli, including cytokines, growth factors, stress signals, bacterial and viral infections as well as oncogenic stimuli. Using genetically modified animal models, in vitro organ systems, and genome-wide expression analyses, we are studying the function of individual AP-1 members, identify specific target genes, and analyse how the individual AP-1 subunits themselves are regulated within the context of a complex dynamic network of signalling pathways. We have been able to show that AP-1 members are involved in numerous biological processes including proliferation, cell death transformation and dissemination of, tumour cells. By defining critical genetic programs and elucidating the function of individual genes involved in these processes our final aim is to identify novel diagnostic markers for cancer cells, and to develop novel therapies in collaboration with clinical partners.

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