Choose an application

• Reference Manager
• EndNote
• RefWorks (Direct export to RefWorks)

Cellular Responses to Stress brings together a group of scientists who work on different but interrelated aspects of cellular stress responses. The book provides state-of-the-art information on the wide spectrum of ways in which cells can respond to different forms of stress induced by chemicals, oxidants, and DNA-damaging agents. Mechanisms are described that involve altered uptake and efflux of chemical agents, intracellular detoxification, and DNA damage responses. Many of these changes trigger a cascade of reactions mediated by stress-activated signaling pathways, which have the capacity to determine whether a cell will survive or die. The spectrum of topics covered in this book aims to provide a broad overview of our current knowledge of the different forms of adaptive response systems.It is hoped that this text will stimulate further research to establish the relative cellular role of specific response pathways and will enable us to gain a deeper understanding of the mechanisms that allow cells to live or die. This book will be valued by university researchers at all levels, industrial scientists in the pharmaceutical and biotechnology industries, and clinical researchers.Originally published in 1999.The Princeton Legacy Library uses the latest print-on-demand technology to again make available previously out-of-print books from the distinguished backlist of Princeton University Press. These editions preserve the original texts of these important books while presenting them in durable paperback and hardcover editions. The goal of the Princeton Legacy Library is to vastly increase access to the rich scholarly heritage found in the thousands of books published by Princeton University Press since its founding in 1905.

Stress (Physiology) --- Cell metabolism --- Cellular control mechanisms --- Cells --- Metabolism --- Regulation --- AMPK. --- ASK1. --- Actin. --- Activation. --- Angiogenesis. --- Antibody. --- Antigen. --- Apoptosis. --- Autoimmunity. --- Autophosphorylation. --- C-Fos. --- C-Jun N-terminal kinases. --- C-terminus. --- Cell Cycle Arrest. --- Cell Line, Transformed. --- Cell cycle. --- Cell membrane. --- Cell migration. --- Cell surface receptor. --- Cellular differentiation. --- Cellular stress response. --- Conformational change. --- Cytochrome P450. --- Cytokine receptor. --- Cytokine. --- Cytotoxicity. --- DNA-PKcs. --- Drug metabolism. --- Ectopic expression. --- Effector (biology). --- Endonuclease. --- Enzyme. --- Epidermal growth factor receptor. --- Epidermal growth factor. --- Extracellular signal–regulated kinases. --- Fibroblast growth factor. --- Gene expression. --- Gene therapy. --- Gene. --- Germinal center. --- Glutathione S-transferase. --- HMG-CoA reductase. --- Heat shock. --- Histidine kinase. --- Hormone-sensitive lipase. --- Hsp27. --- Immortalised cell line. --- Immunodeficiency. --- Immunoglobulins. --- Immunoprecipitation. --- In vitro. --- Inducer. --- Inflammation. --- Jurkat cells. --- Kinase. --- Lymphotoxin. --- Macrophage colony-stimulating factor. --- Mechanism of action. --- Mechanistic target of rapamycin. --- Metabolism. --- Mitogen-activated protein kinase kinase. --- Mitogen-activated protein kinase. --- Mitogen. --- Mitosis. --- Model organism. --- Neuropeptide. --- Neurotoxin. --- Osmotic shock. --- Oxidative phosphorylation. --- Oxidative stress. --- P38 mitogen-activated protein kinases. --- Pathogenesis. --- Peptide. --- Peroxidase. --- Phosphatase. --- Phosphoinositide 3-kinase. --- Phosphorylation cascade. --- Phosphorylation. --- Post-translational modification. --- Protease. --- Protein kinase. --- Protein phosphorylation. --- Protein synthesis inhibitor. --- Protein. --- Proteolysis. --- RNA interference. --- Receptor (biochemistry). --- Receptor tyrosine kinase. --- Repressor. --- Response element. --- Signal transduction. --- Ternary Complex Factors. --- Thrombin. --- Transcription factor. --- Transcriptional regulation. --- Transfection. --- Transposable element. --- Tumor necrosis factor superfamily. --- Turgor pressure. --- Vascular endothelial growth factor.

Choose an application

• Reference Manager
• EndNote
• RefWorks (Direct export to RefWorks)

Pure sciences. Natural sciences (general)