MAPK Kinase Kinase Regulation of SAPK/JNK Pathways -- Alternative p38 MAPK Pathways -- The regulation of stress-activated MAP kinase signalling by protein phosphatases -- Transcriptional regulation by the p38 MAPK signaling pathway in mammalian cells -- Regulation of gene expression in response to osmostress by the yeast stress-activated protein kinase Hog1 -- Regulation of Tumorigenesis by p38? MAP Kinase -- Control of Cell Cycle by SAPKs in Budding and Fission Yeast -- Hog1-mediated Metabolic Adjustments Following Hyperosmotic Shock in the Yeast Saccharomyces cerevisiae -- Control of mRNA Stability by SAPKs -- Intrinsically Active (MKK-Independent) Variants of SAPKs - How do They Work? -- Regulation of MAPK Signaling in Yeast -- Modeling the Dynamics of Stress Activated Protein Kinases (SAPK) in Cellular Stress Response -- Stress-activated Protein Kinase Signaling in Drosophila -- Protein Kinases as Substrates for SAPKs -- Functions of stress-activated MAP kinases in the immune response -- Stress-activated MAP Kinases in Chromatin and Transcriptional Complexes -- SAPK and Translational Control. To maximize the probability of survival, cells need to coordinate their intracellular activities in response to changes in the extracellular environment. MAP kinase cascades play an important role in the transduction of signals inside eukaryotic cells. In particular, stress stimuli result in the rapid activation of a highly conserved group of MAP kinases, known as SAPKs (Stress-Activated Protein Kinases). These kinases coordinate the generation of adaptive responses that are essential for cell survival, which include the modulation of several aspects of cell physiology from metabolism to gene expression. In this book, leading researchers in the field discuss the state-of-the-art of many aspects of SAPK signalling in various systems from yeast to mammals. These include various chapters on regulatory mechanisms as well as the contribution of the SAPK signalling pathways to processes such as gene expression, metabolism, cell cycle regulation, immune responses and tumorigenesis.