The interest of my laboratory lies in the scientific area of cell signalling via the mitogen-activated protein kinases (MAPKs). More specifically, our aim is to increase our molecular understanding of physiological and pathological processes associated with development and diseases by analysing phenotypic abnormalities caused by the loss of MAPK signalling. The physiological importance of the MAPK cascades has been demonstrated by embryonic death caused by their functional deletion in mice. Consistently, studies using cells derived from these genetically modified animals have provided evidence that MAPK modules regulate numerous cellular functions. For example, we have demonstrated that MEK5/ERK5 is associated with cell proliferation and survival, while JNKs are mainly activated in response to cytokines and extracellular stresses upon phosphorylation by MKK4 and MKK7 and can mediate cell death. In collaboration with the Transgenic Unit, we have developed relevant mouse models of human cancers to examine the requirement of MAPKs in inflammation-driven carcinogenesis. Our most recent work focuses on understanding the mechanisms underlying polarised macrophage activation associated with tumour development and progression.