Signal Transduction And Human Disease

This book uniquely relates the broad impact of signal transduction research on the understanding and treatment of human disease. There have been significant advances in the area of signaling in disease processes, yet no resource presently connects these advances with understanding of disease processes and applications for novel therapeutics. Given the emphasis on translational research and biological relevance in biotechnology, and, conversely, the importance of molecular approaches for clinical research, it is evident that a single resource bridging signaling research and human disease will be invaluable.

Providing an overview of recent developments in the field of signal transduction, this volume emphasizes direct clinical significance. As such, topics like nuclear receptors, apoptosis, growth factors, cell cycles and cancer are examined.

Signal transduction is any process by which a cell converts one kind of signal or stimulus into another. Processes referred to as signal transduction often involve a sequence of biochemical reactions inside the cell, which are carried out by enzymes and linked through second messengers. In many transduction processes, an increasing number of enzymes and other molecules become engaged in the events that proceed from the initial stimulus. Responses of cells to environmental signals, toxins and stressors have profound implications for diverse aspects of human health and disease including development, cystic fibrosis, diabetes, asthma, heart, auto-immune diseases and cancer. The delineation of the signal transduction pathways affected in these and other complex human diseases are likely to present new avenues for therapeutic intervention and understanding of human disease mechanisms. This book presents the latest research in the field.

Signal transduction is any process by which a cell converts one kind of signal or stimulus into another. Processes referred to as signal transduction often involve a sequence of biochemical reactions inside the cell, which are carried out by enzymes and linked through second messengers. In many transduction processes, an increasing number of enzymes and other molecules become engaged in the events that proceed from the initial stimulus. Responses of cells to environmental signals, toxins and stressors have profound implications for diverse aspects of human health and disease including development, cystic fibrosis, diabetes, asthma, heart, autoimmune diseases and cancer. The delineation of the signal transduction pathways affected in these and other complex human diseases are likely to present new avenues for therapeutic intervention and understanding of human disease mechanisms.

Signal transduction is any process by which a cell converts one kind of signal or stimulus into another. Processes referred to as signal transduction often involve a sequence of biochemical reactions inside the cell, which are carried out by enzymes and linked through second messengers. In many transduction processes, an increasing number of enzymes and other molecules become engaged in the events that proceed from the initial stimulus. Responses of cells to environmental signals, toxins and stressors have profound implications for diverse aspects of human health and disease including development, cystic fibrosis, diabetes, asthma, heart, autoimmune diseases and cancer. The delineation of the signal transduction pathways affected in these and other complex human diseases are likely to present new avenues for therapeutic intervention and understanding of human disease mechanisms.

Mitogen-activated protein kinases (MAPK) are a large family of enzymes that function as signal transducers to regulate a diverse range of physiological responses. However, signaling via extracellular signal-regulated kinase (ERK), c-Jun amino terminal kinase (JNK), and p38 MAPK also underpin many disease processes. This Special Issue provides new insights into how MAPK signaling contributes to specific pathological processes across a range of conditions, including disorders of lung development, type 2 diabetes, proliferative skin diseases, cardiovascular diseases, and neurological diseases.

Caveolae (latin for little caves) are small structures found at the surface of cells. They are responsible for the regulation of important metabolic pathway. As a consequence, they may play a critical role in several human diseases such as atherosclerosis, cancer, diabetes, and muscular dystrophies. This book analyzes the role and function of caveolae in these aspects and serves as the first textbook currently available on caveolae/caveolin.

This volume focuses on the relationship between the regulation of signal transduction and disease mechanisms, and discusses how the dysregulation of intracellular signals cause diseases, cell death, carcinogenesis, and other disorders. Growth, survival, transformation, and metabolic activities at the cellular level are regulated by various intracellular signal transduction pathways. Sources that stimulate intracellular signals include intracellular stresses and signal regulators/modulators, as well as extracellular growth factors. Recent studies on signal transduction analysis using animal and human cell lines have revealed how the intracellular signals are regulated and why their dysregulation leads to pathological states such as tumorigenesis, metabolic diseases, cell death, and so on. This book highlights several important key molecules and intracellular signaling pathways such as microRNA, the TGF-beta signaling pathway, the Wnt signaling pathway and MET signaling pathway as topical and highly relevant issues in human cell research related to signal transduction. In addition to assessing the pathogenic role of these signaling pathways, it focuses on the molecular design of small molecule regulators/inhibitors of said pathways, one of the most important approaches in this area. This book offers a valuable guide, helping not only research scientists but also clinicians to understand how the dysregulation of intracellular signals leads to diseases.