Endoplasmic Reticulum Stress in Health and Disease [electronic resource] /
Agostinis, Patrizia.editor.
Afshin, Samali.editor.
The Endoplasmic Reticulum (ER) is an organelle with extraordinary signaling and homeostatic functions. It is the organelle responsible for protein folding, maturation, quality control and trafficking of proteins destined for the plasma membrane or for secretion into the extracellular environment. Failure, overloading or malfunctioning of any of the signaling or quality control mechanisms occurring in the ER may provoke a stress condition known as ‘ER stress’. Accumulating evidence indicates that ER stress may dramatically perturb interactions between the cell and its environment, and contribute to the development of human diseases, ranging from metabolic diseases and cancer to neurodegenerative diseases, or impact therapeutic outcome.  This book primarily focuses on the pathophysiology of ER stress.  It introduces the molecular bases of ER stress, the emerging relevance of the ER-mitochondria cross-talk, the signaling pathways engaged and cellular responses to ER stress, including the adaptive Unfolded Protein Response (UPR), autophagy as well as cell death. Next the book addresses the role of ER stress in physiology and in the etiology of relevant pathological conditions, like carcinogenesis and inflammation, neurodegeneration and  metabolic disease. The last chapter describes how ER stress pathways can be targeted for therapeutic benefit.  Altogether, this book will provide the reader with an exhaustive view of ER stress biology and the latest insights in the role of ER stress in relevant human diseases.
Description based upon print version of record.
Preface; Contents; Part I; Cellular Responses to ER Stress; Biology of the Endoplasmic Reticulum; 1 Introduction; 2 Structural Organization of the ER; 2.1 RER and SER; 2.2 Shape; 2.3 Dynamic Structure; 2.4 Association with Other Organelles; 3 ER Function; 3.1 Biosynthesis, Processing and Maturation of Proteins; 3.1.1 Chaperones, Folding Enzymes and Oxidative Protein Folding; 3.1.2 Glycosylation; 3.2 ERAD; 3.3 ER Export and Membrane Trafficking; 3.4 Calcium Storage; 3.5 Drug Detoxification; 3.6 Carbohydrate Metabolism; 3.7 Lipid Biosynthesis; 3.8 The ER Under Stress
3.8.1 Factors that Disrupt Protein Folding Cause ER Stress3.9 ER Stress Responses; 3.10 ER Stress in Physiology and Disease; References; A Tight-Knit Group: Protein Glycosylation, Endoplasmic Reticulum Stress and the Unfolded Protein Response; 1 Introduction; 2 The N-linked Glycosylation Process; 3 The O-linked Glycosylation Process; 4 Protein Glycosylation in Relation to ER Stress and the UPR; 5 Glycosylation, ER Stress and the Biopharmaceutical Industry; 6 Recent Examinations of Glycosylation with Respect to ER Stress and the UPR; 7 Conclusions; References
ER Stress Signaling Pathways in Cell Survival and Death1 Preface; 2 Activation of UPR Signaling Pathways; 2.1 High Order Assembly and Non-canonical Splicing Mediate IRE1 signaling; 2.2 PERK Attenuates Protein Translation and Counters Oxidative Stress; 2.3 Interorganellar Trafficking and Proteolytic Regulation of ATF6; 3 ER Stress: Balancing Between Life and Death; 3.1 Controlling ER-mitochondrial Ca2 + -signaling and Apoptosis
3.1.1 Bcl-2 Proteins at the ER as Gatekeepers of ER Homeostasis and Stress Induced ApoptosisThe Bcl-2 family proteins regulate mitochondrial apoptosis by controlling MOMP and subsequent release of pro-apoptotic proteins, like cytochrome c and apoptosome f3.1.2 MAMs: Specialized Sites Fine-tuningthe ER-mitochondria Crosstalk; 3.2 ER Stress-induced Apoptosis Through the UPR; 3.2.1 PERK-mediated Signaling to Apoptosis; 3.2.2 Fine Tuning of IRE1 Signaling - the UPRosome; 3.2.3 ATF6 Signaling: More than a Just a Prosurvival Pathway?; 4 Concluding Remarks; References
Endoplasmic Reticulum-Mitochondria Connections, Calcium Cross-Talk and Cell Fate: A Closer Inspection1 Background; 1.1 Endoplasmic Reticulum; 1.2 Mitochondria; 2 The ER-mitochondria Connection: The Right Distance; 2.1 The ER-mitochondria Connection in Lipid Transport/Metabolism; 2.2 The ER-mitochondria Connection in Mitochondrial Network Shaping; 2.3 The ER-mitochondria Ca2 +  Cross-talk; 2.3.1 In Cell Bioenergetics and Survival; 2.3.2 In Cell Death; 2.3.3 In ER Stress; 3 Technical Approaches in Studying the ER-mitochondria Relationship; 3.1 The Historical Background
3.1.1 Electron Microscopy
Includes bibliographical references and index.
The Endoplasmic Reticulum (ER) is an organelle with extraordinary signaling and homeostatic functions. It is the organelle responsible for protein folding, maturation, quality control and trafficking of proteins destined for the plasma membrane or for secretion into the extracellular environment. Failure, overloading or malfunctioning of any of the signaling or quality control mechanisms occurring in the ER may provoke a stress condition known as ‘ER stress’. Accumulating evidence indicates that ER stress may dramatically perturb interactions between the cell and its environment, and contribute to the development of human diseases, ranging from metabolic diseases and cancer to neurodegenerative diseases, or impact therapeutic outcome.  This book primarily focuses on the pathophysiology of ER stress.  It introduces the molecular bases of ER stress, the emerging relevance of the ER-mitochondria cross-talk, the signaling pathways engaged and cellular responses to ER stress, including the adaptive Unfolded Protein Response (UPR), autophagy as well as cell death. Next the book addresses the role of ER stress in physiology and in the etiology of relevant pathological conditions, like carcinogenesis and inflammation, neurodegeneration and  metabolic disease. The last chapter describes how ER stress pathways can be targeted for therapeutic benefit.  Altogether, this book will provide the reader with an exhaustive view of ER stress biology and the latest insights in the role of ER stress in relevant human diseases.
Medicine.
Molecular biology.
Cell biology.
Apoptosis.
Cell physiology.
Immunology.
Biomedicine, general.
Molecular Medicine.
Cell Biology.
Apoptosis.
Cell Physiology.
Immunology.