JAK tyrosine kinases and STAT transcription factors constitute a signaling pathway, which is activated by cytokines. By activating gene transcription it regulates essential biological responses to environmental cues. The Jak-Stat pathway is involved in the regulation of cell development, differentiation, proliferation and apoptosis. Improper function may contribute to hematopoietic malignancies and cancer. This book provides comprehensive insights into the latest basic and clinical developments in the field. The first part reviews recent findings and new technologies pertaining to basics of Jak-Stat function. The second part describes the evolution of Jak-Stat signaling and the role of the pathway in invertebrate organisms. The third part focuses on Jak-Stat signaling in hematopoietic cells under both physiological and pathophysiological conditions. Finally, chapters in the fourth section describe the relationship of Jak-Stat signaling to various states of disease, particularly infection, leukemias and solid cancers. The book is intended for all scientists in molecular biology, biochemistry and cell biology dealing with biomedical issues.
Thomas Decker obtained a masters degree in Biology and, in 1986, his PhD at the Albert-Ludwig University of Freiburg, Both his PhD project and his subsequent postdoctoral research at the Rockefeller University, New York, USA, concerned the immunological activity and molecular biology of interferons. This line of research led to intensive investigation of Jak-Stat signal transduction which continued duing subsequent group leader positions and professorships at the Fraunhofer Society, Hannover, Germany, the Karolinska Institute, Stockholm, Sweden and, finally, the University of Vienna where he currently holds the position of a full professor of immunobiology. Work in Decker’s laboratory revolves around interferons, the Jak-Stat signalling pathway and mechanisms of gene activation in bacterial infections.
Mathias Müller studied veterinary medicine at the Ludwig-Maximilians University Munich (Germany) and completed his PhD thesis at the Gene Center Munich. During a postdoctoral fellowship at the ICRF (Imperial Cancer Research Fund, London UK; now CRUK, Cancer Research UK) he entered the field of interferon signal transduction and participated in the pioneering studies that led to the identification of the biological roles of Jaks and Stats by genetic complementation of cytokine signalling defective mutant cell lines. In 1998 he was appointed Full Professor of Veterinary Biotechnology and Molecular Genetics at the University of Veterinary Medicine Vienna. His laboratory focuses on the use of transgenic models for studying JAK–STAT signalling networks.
