Choose an application

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

Dual specificity phosphatases (DUSPs) constitute a heterogeneous group of protein tyrosine phosphatases with the ability to dephosphorylate Ser/Thr and Tyr residues from proteins, as well as from other non-proteinaceous substrates including signaling lipids. DUSPs include, among others, MAP kinase (MAPK) phosphatases (MKPs) and small-size atypical DUSPs. MKPs are enzymes specialized in regulating the activity and subcellular location of MAPKs, whereas the function of small-size atypical DUSPs seems to be more diverse. DUSPs have emerged as key players in the regulation of cell growth, differentiation, stress response, and apoptosis. DUSPs regulate essential physiological processes, including immunity, neurobiology and metabolic homeostasis, and have been implicated in tumorigenesis, pathological inflammation and metabolic disorders. Accordingly, alterations in the expression or function of MKPs and small-size atypical DUSPs have consequences essential to human disease, making these enzymes potential biological markers and therapeutic targets. This Special Issue covers recent advances in the molecular mechanisms and biological functions of MKPs and small-size atypical DUSPs, and their relevance in human disease.

hematopoietic cells --- DEPArray --- n/a --- neuroblastoma --- liver steatosis --- MAPK phosphatase --- DUSP-4 --- granule neurons --- neuronal differentiation --- DUSP10 --- cytokines --- MAPKs --- single cell analysis --- macrophage --- asthma --- E. coli infection --- MAPK --- Cpp1 --- nucleotide receptors --- atypical DUSP --- RSV --- Pmp1 --- cannabinoids --- astrocytes --- sepsis --- influenza --- signaling --- triple-negative breast cancer (TNBC) --- differentiation --- HDAC6 (histone deacetylase isoform 6) --- atypical dual-specificity phosphatases --- microtubules --- respiratory viruses --- MK-STYX (MAPK (mitogen-activated protein kinase) phosphoserine/threonine/tyrosine-binding protein) --- dual-specificity phosphatase --- Msg5 --- TLR signaling --- mitogen-activated protein kinase --- fungal MKPs --- macrophages --- MAP Kinase Phosphatase-2 --- inflammation --- Sdp1 --- circulating tumor cells (CTCs) --- MAP kinases --- MAP kinase phosphatases --- P2X7 --- proliferation --- BDNF --- P2Y13 --- T cell --- hypertriglyceridemia --- integrated omics analysis --- post-translational modification --- rhinovirus --- protein stability --- ubiquitination --- dual-specificity phosphatases --- Mkp-1 --- cancer --- brain metastasis --- HER2 --- COPD --- pseudophosphatase

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)

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.

MAP Kinase Signaling System --- MAP Kinase Kinase Kinases --- Mitogen-Activated Protein Kinase Kinases --- Mitogen-Activated Protein Kinases --- Mitogen-activated protein kinases. --- MAP kinases --- physiology. --- metabolism. --- Protein. --- Stress. --- Mitogen-activated protein kinases --- Intracellular Signaling Peptides and Proteins --- Protein-Serine-Threonine Kinases --- Signal Transduction --- Protein-Tyrosine Kinases --- Proline-Directed Protein Kinases --- Metabolic Networks and Pathways --- Peptides --- Proteins --- Protein Kinases --- Biochemical Processes --- Metabolism --- Cell Physiological Processes --- Biochemical Phenomena --- Phosphotransferases (Alcohol Group Acceptor) --- Amino Acids, Peptides, and Proteins --- Chemical Processes --- Cell Physiological Phenomena --- Metabolic Phenomena --- Chemical Phenomena --- Chemicals and Drugs --- Phosphotransferases --- Phenomena and Processes --- Transferases --- Enzymes --- Enzymes and Coenzymes --- Animal Biochemistry --- Biochemistry --- Biology - General --- Biology --- Human Anatomy & Physiology --- Chemistry --- Health & Biological Sciences --- Physical Sciences & Mathematics --- MAPKs (Enzymes) --- Life sciences. --- Molecular biology. --- Biochemistry. --- Cell biology. --- Life Sciences. --- Biochemistry, general. --- Cell Biology. --- Molecular Medicine. --- Protein kinases --- Cytology. --- Medicine. --- Clinical sciences --- Medical profession --- Human biology --- Life sciences --- Medical sciences --- Pathology --- Physicians --- Cell biology --- Cellular biology --- Cells --- Cytologists --- Biological chemistry --- Chemical composition of organisms --- Organisms --- Physiological chemistry --- Composition --- Health Workforce --- Molecular biochemistry --- Molecular biophysics --- Biophysics --- Biomolecules --- Systems biology --- Medicine --- Biomedical Research. --- Research. --- Biological research --- Biomedical research

Choose an application

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

Arthritis has a high prevalence globally and includes over 100 different types, the most common of which are rheumatoid arthritis, osteoarthritis, psoriatic arthritis, and inflammatory arthritis. The exact etiology of arthritis remains unclear and no cure exists. Anti-inflammatory drugs are commonly used in the treatment of arthritis but are associated with significant side effects. Novel modes of therapy and additional prognostic biomarkers are urgently needed for arthritis patients. This book summarizes and discusses the global picture of the current understanding of arthritis.

receptor activator of nuclear factor ?B --- infliximab --- tripterine --- triptolide --- osteoblast --- tumor necrosis factor-alpha --- synovial cell --- anti-arthritis --- biosimilars --- Epstein-Barr virus --- cytokines --- SOX9 --- parathyroid hormone --- nitric oxide --- rat --- etanercept --- angiogenesis --- glycosylation --- mitogen activated protein kinase --- Th9 lymphocytes --- rheumatoid arthritis --- IL-6 --- clodronate --- bone erosion --- mesenchymal stem cells --- collagen-induced arthritis --- biological --- gene expression --- inflammatory arthritis --- osteoarthritis --- fraxinellone --- nuclear factor kappa B --- messenger RNA --- inflammation --- miRNA --- disease-modifying --- adipokines --- WNT --- glycoprotein 42 --- miR-199a-5p --- proliferation --- next-generation sequencing --- collagen --- osteoarthritis (OA) --- experimental arthritis --- bone morphogenetic protein --- TNF-? --- computational modeling --- basic research --- osteoclast --- therapeutics --- certolizumab pegol --- chondrocytes --- progenitor cells --- adjuvant arthritis --- adalimumab --- triterpenoid --- sclareol --- TNF? --- fibroblast growth factor 2 --- antibodies --- osteoblasts --- molecular pathology --- Th17 --- immunology --- obesity --- visfatin --- articular cartilage --- autoimmune --- biomarkers --- celastrol --- MAPK --- disease pathways --- IL1? --- arthritis --- bioinformatics --- anticitrullinated peptide antibodies --- drug delivery system --- antagonists --- shared epitope --- pathology --- SMA- and MAD-related protein --- small-molecule inhibitor --- transforming growth factor ? --- mice --- golimumab --- spinal fusion --- antirheumatic drug --- early osteoarthritis --- stem cell --- rheumatoid factor --- therapeutic antibody --- bisphosphonate --- osteoclastogenesis --- interleukin --- spondyloarthropathies --- clinical translation --- therapy --- Traditional Chinese medicine --- chemokines --- structure --- cell signaling --- microRNA

Choose an application

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

Plants possess a rather complex and efficient immune system. During their evolutionary history, plants have developed various defense strategies in order to recognize and distinguishing between self and non-self, and face pathogens and animal pests. Accordingly, to study the plant innate immunity represents a new frontier in the plant pathology and crop protection fields. This book is structured in 6 sections. The first part introduces some basic and general aspects of the plant innate immunity and crop protection. Sections 2–5 focus on fungal and oomycete diseases (section 2), bacterial and phytoplasma diseases (section 3), virus diseases (section 4), and insect pests (section 5), with a number of case studies and plant–pathogen/pest interactions. The last section deals with plant disease detection and control. The book aims to highlight new trends in these relevant areas of plant sciences, providing a global perspective that is useful for future and innovative ideas.

Bakraee --- tomato gray mold --- Citrus sinensis --- CDPKs --- salicylic acid --- calmodulin --- glycerol-3-phosphate --- biotic stress responses --- negative regulator --- rice blast --- metabolomics --- hydroperoxide lyase --- Bromoviridae --- induced defense responses --- leaf transcriptome --- calcium signature --- “Candidatus Liberibacter” --- garden impatiens --- Chilo suppressalis --- plant defence --- plant–virus interactions --- spectral distribution of light --- Magnaporthe oryzae --- plant-virus interaction --- biological control --- ultrastructure --- pathogenicity --- disease resistance --- Potato virus Y --- symbiosis --- N-hydroxypipecolic acid --- VaHAESA --- priming --- plant–microbe interactions --- systemic and local movement --- immunity --- CaWRKY40b --- plant protection products --- hypersensitive response --- cellulose synthase --- herbivore-induced defense response --- Macrosiphum euphorbiae --- RTNLB --- ISR --- RNA silencing --- herbivore-induced plant defenses --- disease management --- sustainable crop protection --- WRKY networks --- Camellia sinensis --- RNA-Seq --- transcriptional modulation --- ETI --- pathogenesis related-protein 2 --- cell wall --- basal defense --- candidate disease resistance gene --- MTI --- grapevine --- defense-related signaling pathways --- wounding --- ethylene --- CMLs --- Prune dwarf virus --- Arabidopsis thaliana --- SAR signalling --- innate immunity --- agrochemicals --- OsGID1 --- Nilaparvata lugens --- tobacco --- tomato leaf mold --- Solanum lycopersicum --- downy mildew --- pipecolic acid --- chemical elicitors --- bismerthiazol --- pre-conditioning --- gibberellin --- “Candidatus Phytoplasma” --- dieback --- CaWRKY22 --- microbiota --- Sogatella furcifera --- PTI --- SAR --- Bacillus subtilis --- PRRs --- aphid resistance --- methyl salicylate --- regurgitant --- Myzus persicae --- Agrobacterium --- Ectropis obliqua --- Capsicum annuum --- polyphenol oxidase --- plant proteases --- plant immunity --- jasmonic acid --- calcium --- light dependent signalling --- Ralstonia solanacearum --- proteomics --- plant defense response --- Arabidopsis --- Lasiodiplodia theobromae --- azelaic acid --- citrus decline disease --- New Guinea impatiens --- replication process --- rice --- mango --- ?-3 fatty acid desaturase --- Ralstonia Solanacearum --- food security --- iTRAQ --- mitogen-activated protein kinase 4