Martin Beckerman - Böcker

The text is aimed at a broad audience of students and other individuals interested in furthering their understanding of how cells regulate and coordinate their core activities. Malfunction in the control layer is responsible for a host of human disorders ranging from neurological disorders to cancers. Most drugs target components in the control layer, and difficulties in drug design are intimately related to the architecture of the control layer. This book will be useful to students and individuals in medicine and pharmacology interested in broadening their understanding of how the control layer works. To further that goal, there are chapters on cancers and apoptosis, and on bacteria and viruses. In those chapters not specifically devoted to pathogens, connections between diseases, drugs and signaling are made. The audience for this book includes students in chemistry, physics and computer science who intend to work in biological and medical physics, and bioinformatics and systems biology. The first five chapters of the book are mainly background and review chapters.Signaling in the immune, endocrine (hormonal) and nervous systems is covered along with cancer, apoptosis and gene regulation.

In today’s world, three great classes of non-infectious diseases – the metabolic syndromes (such as type 2 diabetes and atherosclerosis), the cancers, and the neurodegenerative disorders – have risen to the fore. These diseases, all associated with increasing age of an individual, have proven to be remarkably complex and difficult to treat. This is because, in large measure, when the cellular signaling pathways responsible for maintaining homeostasis and health of the body become dysregulated, they generate equally stable disease states. As a result the body may respond positively to a drug, but only for a while and then revert back to the disease state. Cellular Signaling in Health and Disease summarizes our current understanding of these regulatory networks in the healthy and diseased states, showing which molecular components might be prime targets for drug interventions. This is accomplished by presenting models that explain in mechanistic, molecular detail how a particular part of the cellular signaling web operates properly in health and improperly in disease.The stability of the health- and disease-associated states is dynamic and supported by multiple feedback loops acting positively and negatively along with linkages between pathways. During the past few years an ongoing series of important discoveries have been made that advance our understanding of how the body works and may guide us on how to better deal with these diseases. These include the discovery of chronic inflammation as a causal factor in all of these disease classes, the appearance of reactive oxygen species as a messenger molecule that can act both positively and negatively, the propensity of proteins to misfold into aggregation- and disease-prone forms, and the rise of epigenetics including the emergence of small non-coding RNA with important regulatory functions out of the so-called junk RNA. Chapters are devoted to each of these classes of findings with additional detailsintegrated into the chapters dealing directly with the diseases. The connections responsible for maintaining stability are explored in depth.

Makes connections between diseases, drugs and signaling in those chapters not specifically devoted to pathogens. Reviews background in first 5 chapters then offers chapters on cancers and apoptosis and on bacteria and viruses. Signaling in the immune, endocrine (hormonal) and nervous systems covered along with cancer, apoptosis and gene regulation. Each chapter ends with a problem section to facilitate discussion.

In today’s world, three great classes of non-infectious diseases – the metabolic syndromes (such as type 2 diabetes and atherosclerosis), the cancers, and the neurodegenerative disorders – have risen to the fore. These diseases, all associated with increasing age of an individual, have proven to be remarkably complex and difficult to treat. This is because, in large measure, when the cellular signaling pathways responsible for maintaining homeostasis and health of the body become dysregulated, they generate equally stable disease states. As a result the body may respond positively to a drug, but only for a while and then revert back to the disease state. Cellular Signaling in Health and Disease summarizes our current understanding of these regulatory networks in the healthy and diseased states, showing which molecular components might be prime targets for drug interventions. This is accomplished by presenting models that explain in mechanistic, molecular detail how a particular part of the cellular signaling web operates properly in health and improperly in disease.The stability of the health- and disease-associated states is dynamic and supported by multiple feedback loops acting positively and negatively along with linkages between pathways. During the past few years an ongoing series of important discoveries have been made that advance our understanding of how the body works and may guide us on how to better deal with these diseases. These include the discovery of chronic inflammation as a causal factor in all of these disease classes, the appearance of reactive oxygen species as a messenger molecule that can act both positively and negatively, the propensity of proteins to misfold into aggregation- and disease-prone forms, and the rise of epigenetics including the emergence of small non-coding RNA with important regulatory functions out of the so-called junk RNA. Chapters are devoted to each of these classes of findings with additional detailsintegrated into the chapters dealing directly with the diseases. The connections responsible for maintaining stability are explored in depth.

Starting with protein folding and protein quality control basics, the reader will learn how misfolded proteins can cause diseases ranging from prion diseases to Alzheimer’s disease and Parkinson’s disease to Huntington’s disease, amyotrophic lateral sclerosis and frontotemporal lobar degeneration.