Protein Kinase-mediated Decisions Between Life and Death (Advances in Experimental Medicine and Biology, 1275)

Protein phosphorylation via protein kinases is an inevitable process that alters physiological and pathological functions of the cells. Thus, protein kinases play key roles in the regulation of cell life or death decisions. Protein kinases are frequently a driving factor in a variety of human diseases including aging and cellular senescence, immune system and endothelial dysfunctions, cancers, insulin resistance, cholestasis and neurodegenerative diseases, as well as bacterial resistance in persistent infections. Recent developments in quantitative proteomics provide important opinions on kinase inhibitor selectivity and their modes of action in the biological context. Protein Kinase-mediated Decisions Between Life and Death aims to have the reader catch insights about up-to-date opinions on “Protein Kinases” related pathways that threaten human health and life. As “Protein Kinases” are related to many health problems, clinicians, basic science researchers and students need this information. Chapter “Signal Transduction in Immune Cells and Protein Kinases” is available open access under a Creative Commons Attribution 4.0 International License via link.springer.com. Contents Contributors 1: Protein Kinase-Mediated Decision Between the Life and Death 1 Introduction 2 Cross-Talk Between Cell-Death Morphologies and Protein Kinases 3 Determination of Cell Life via Tumor Necrosis Factor-α-Protein Kinase Cross-Talk 4 Conclusion References 2: Aging and Protein Kinases 1 Introduction 2 DNA Damage, DNA Repair Pathways and Protein Kinases 3 Calorie Restriction and Aging 4 Telomeres and Aging 5 MicroRNAs, Protein Kinases and Aging 6 Managing Energy Homeostasis and Resistance to Stress in Aging 7 Conclusion References 3: The Connection Between Cell Fate and Telomere 1 Introduction 2 “Hayflick Limit” Setting Factors 3 Shelterin Complex in Protection of Telomere 4 Telomere Damage 5 Non-homologous End-Joining Pathways at Telomeres 6 Conclusion References 4: Dark-Side of Exosomes 1 Introduction 2 Structure and Functions of the Exosomes 3 The Next Cell Hypothesis 4 Exosomes and Cell Death 5 Exosomes and Tumor Growth 6 Adipose Tissue and Exosomes 7 Exosomes and Inflammation 8 Conclusion References 5: Signal Transduction in Immune Cells and Protein Kinases 1 Introduction 1.1 PKCs Traits 2 Toll-Like Receptor Signaling in the Innate System 2.1 PKC Isoforms Involved in TLR Signaling 2.1.1 PKC-α 2.1.2 PKC-δ 2.1.3 PKC-ε 2.1.4 PKC-ζ 3 PKCs in T-Cell Receptor Signaling 3.1 PKCs Families 3.1.1 PKCθ 3.1.2 PKC-α 3.1.3 PKCδ 4 B-Cell Receptor Signaling 4.1 PKCs Role in BCR Signaling Events 5 Conclusion References 6: Role of Protein Kinase C in Immune Cell Activation and Its Implication Chemical-Induced Immunotoxicity 1 Introduction 2 PKC: From Discovery to Its Role in Cell Homeostasis and Activation 3 PKC Expression in Immune Cells and Its Functions 3.1 Innate Immunity 3.2 Acquired Immunity 3.2.1 T Cells 3.2.2 B Cells 4 Role of PKC in Chemical-Induced Immunotoxicity 4.1 Chemical Allergens 4.2 Endocrine Disruptors 5 Conclusions References 7: Combined Toxicity of Metal Nanoparticles: Comparison of Individual and Mixture Particles Effect 1 Introduction 2 Endothelial Transport of NPs 3 Protein Kinase Mediated Toxicity of NPs 4 Toxicity of Diesel Emission Particles 5 Conclusion References 8: Protein Kinases Signaling in Pancreatic Beta-cells Death and Type 2 Diabetes 1 Introduction 2 Glucose Homeostasis and β-Cells in T2D 3 Human Islet Amyloid Polypeptide in T2D 4 β-Cell, ER Stress and Protein Kinases 5 β-Cell Differentiation and Dedifferentiation in T2D 6 Conclusion References 9: Bile Acid Toxicity and Protein Kinases 1 Introduction 2 Bile Acid Biosynthesis and Transporters 3 Protein Kinases-Bile Acids Crosstalk 4 Bile Acids and Cell Death 5 Bile Acid-Induced Hepatic Inflammation 6 Bile Acid-Induced Apoptosis 7 Antiapoptotic Effect of Bile Acids 8 Bile Acid-Induced Necroptosis and Necrosis 9 Conclusion References 10: N-Methyl-D-Aspartate Receptor Signaling-Protein Kinases Crosstalk in Cerebral Ischemia 1 Introduction 2 NMDA-Mediated Excitotoxicity and Protein Kinases 3 NMDA and PSD-95 Crosstalk in Cerebral Stroke 4 Protein S-Nitrosylation 5 Death-Associated Protein Kinase and Stroke 6 Cyclin-Dependent Kinase 5 7 Endoplasmic Reticulum Stress-Induced Cell Death 8 Hyperhomocysteinemia and Stroke 9 Ephrin-B-Dependent Amplification of NMDA-Evoked Neuronal Excitotoxicity 10 Lysosomal Membrane Permeabilization and Stroke 11 Conclusion, and Future Perspectives in Therapeutic Interventions References 11: Alzheimer’s Disease and Protein Kinases 1 Introduction 2 Abeta Hypothesis in Alzheimer’s Disease 3 Abeta Toxicity on N-Methyl-D-Aspartate Receptor in Alzheimer’s Disease 4 Neuroinflammation in Alzheimer’s Disease 5 Oxidative Stress and Alzheimer’s Disease 6 Alzheimer’s Disease and mTOR Pathway 7 Synaptic Activity in Alzheimer’s Disease 8 Glucose Metabolism, Insulin Resistance and Alzheimer’s Disease 9 Clinical Perspective 10 Conclusion References 12: Bacterial Protein Kinases 1 Introduction 2 Histidine Kinases and Two Component Systems 3 Bacterial Tyrosine Kinases 4 PEP Group Translocation – Phosphotransferase System – PTS 5 Serine/Threonine Kinase 6 Conclusion References 13: Indoleamine 2,3-Dioxygenase Activity-Induced Acceleration of Tumor Growth, and Protein Kinases-Related Novel Therapeutics Regimens 1 Introduction 2 IDO1 Activity in Cancer Progression 3 IDO Immunostaining Is a Reliable Guide in Complementary Cancer Therapy 4 IDO1-Protein Kinases Crosstalk in Inhibition of Cancer Progression 5 Combination Therapy with IDO Inhibitors 6 Conclusion References 14: A Crosstalk Between Dual-Specific Phosphatases and Dual-Specific Protein Kinases Can Be A Potential Therapeutic Target for Anti-cancer Therapy 1 Introduction 2 Protein Kinases 2.1 mTOR Inhibitors 2.2 CDK Inhibitors 2.3 CLK and DYRK1A/B Inhibitors 2.4 MAPK/ERK/MEK Inhibitors 2.5 AKT Kinase Inhibitors 3 Lipid Kinases 4 Protein Phosphatases 4.1 Dual-Specificity Phosphatases (DUSPs)/MAPK Phosphatases (MKP) 5 Conclusion References 15: Protein Kinases in Hematological Disorders 1 Introduction and the Family of Protein Kinases 1.1 MAPK Signal Transduction Pathway 1.2 Ras/Raf/MEK/ERK Signal Transduction Pathway 1.3 PI-3 Kinase/Protein Kinase B Signal Transduction Pathway 1.4 Cytoplasmic (Non-receptor) Tyrosine Kinases Signal Transduction Pathway 1.5 STAT Proteins and Signal Transduction Pathway 2 Protein Kinases in Hematological Neoplastic Disorders 3 Protein Kinases in CML 4 Protein Kinases in Malignant Myeloid Neoplasms 5 Protein Kinases in Malignant Lymphoid Neoplasms 6 Conclusions, Future Hypotheses and Perspectives References 16: Metabolic Stress and Immunity: Nutrient-Sensing Kinases and Tryptophan Metabolism 1 Introduction 1.1 Nutrient Sensing and Strategies to Cope with Starvation 2 Tryptophan Breakdown, a Metabolic Checkpoint for Immunoregulation 3 Tryptophan Deficiency and GCN2 Signaling 4 Tryptophan Metabolism and mTOR 5 Conclusion References Correction to: Signal Transduction in Immune Cells and Protein Kinases Index "Protein phosphorylation via protein kinases is an inevitable process that alters physiological and pathological functions of the cells. Thus, protein kinases play key roles in the regulation of cell life or death decisions. Protein kinases are frequently a driving factor in a variety of human diseases including aging and cellular senescence, immune system and endothelial dysfunctions, cancers, insulin resistance, cholestasis and neurodegenerative diseases, as well as bacterial resistance in persistent infections. Recent developments in quantitative proteomics provide important opinions on kinase inhibitor selectivity and their modes of action in the biological context. Protein Kinase-mediated Decisions Between Life and Death aims to have the reader catch insights about up-to-date opinions on “Protein Kinases” related pathways that threaten human health and life. As "Protein Kinases" are related to many health problems, clinicians, basic science researchers and students need this information."--Page 4 de la couverture