International Review of Cell and Molecular Biology

 
 
Academic Press
  • 1. Auflage
  • |
  • erschienen am 30. September 2016
  • |
  • 440 Seiten
 
E-Book | ePUB mit Adobe DRM | Systemvoraussetzungen
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978-0-12-805220-4 (ISBN)
 

International Review of Cell and Molecular Biology presents comprehensive reviews and current advances in cell and molecular biology, and includes articles that address the structure and control of gene expression, nucleocytoplasmic interactions, control of cell development and differentiation, and cell transformation and growth.

The series has a worldwide readership, maintaining a high standard by publishing invited articles on important and timely topics as authored by prominent cell and molecular biologists.


  • Provides comprehensive reviews and current advances
  • Presents a wide range of perspectives on specific subjects
  • Valuable reference material for advanced undergraduates, graduate students, and professional scientists
1937-6448
  • Englisch
  • San Diego
  • |
  • USA
Elsevier Science
  • 25,52 MB
978-0-12-805220-4 (9780128052204)
0128052201 (0128052201)
weitere Ausgaben werden ermittelt
  • Cover
  • Title Page
  • Copyright Page
  • Contents
  • Contributors
  • Dedication
  • Chapter One - Sensing the Environment Through Sestrins: Implications for Cellular Metabolism
  • Abstract
  • 1 Introduction
  • 2 Regulation and Function of Sestrins
  • 2.1 Regulation of Transcription of the Sestrin Family Members
  • 2.1.1 DNA Damage
  • 2.1.2 Oxidative Stress
  • 2.1.3 Nutrients and Oxygen Deprivation
  • 2.2 Sestrins as Antioxidant Proteins: Old Friends or New Foes?
  • 2.3 Sestrins are Regulators of mTOR
  • 2.3.1 The mTOR Complexes
  • 2.3.2 Regulation of mTORC1
  • 2.3.3 Sestrins Potentiate AMPK Activity
  • 2.3.4 mTORC1 Regulation by the Sestrin-GATOR-Rags Axis
  • 2.3.5 Regulation of the mTORC2-Akt Pathway by Sestrins
  • 2.4 Sestrins and Autophagy
  • 2.4.1 Regulation of Autophagy
  • 2.4.2 Sestrins Promote Autophagy
  • 3 Sestrins are Sensors of Nutrient Availability and are Involved in Regulation of Metabolism
  • 3.1 Hypernutrition and Growth Factors
  • 3.2 Glucose
  • 3.3 Oxygen
  • 3.4 Amino Acids
  • 3.5 Lipids
  • 4 Conclusions and Perspectives
  • Acknowledgments
  • References
  • Chapter Two - Metabolic Regulation of Apoptosis in Cancer
  • Abstract
  • 1 Introduction
  • 2 Overview of Apoptosis Pathways
  • 2.1 Caspases
  • 2.2 Intrinsic and Extrinsic Pathways
  • 2.3 Activation of Initiator Caspases
  • 2.4 Mitochondria Outer Membrane Permeabilization (MOMP)
  • 3 Regulation of Apoptosis Through Glycolytic Pathway
  • 3.1 Hypoxia-Inducible Factor-1
  • 3.2 AKT
  • 3.3 BAD
  • 3.4 NOXA
  • 3.5 Caspase-2
  • 3.6 Cytochrome c
  • 4 p53 and Glucose Metabolism
  • 4.1 GLUT1/GLUT4 and HK2
  • 4.2 TIGAR (TP53-Induced Glycolysis and Apoptosis Regulator)
  • 4.3 Apoptosis-Inducing Factor and Synthesis of Cytochrome c Oxidase 2
  • 4.4 Glucose-6-Phosphate Dehydrogenase
  • 5 Regulation of Apoptosis by Lipid Metabolism
  • 5.1 Introduction of Sphingolipid Pathway
  • 5.2 Pro-apoptotic Functions of Ceramide
  • 5.3 Role of Pathways That Regulate Ceramide Production
  • 5.3.1 Sphingomyelinase (SMase) Pathway
  • 5.3.2 De Novo Synthesis
  • 5.3.3 Salvage Pathway
  • 5.4 Fatty Acids
  • 6 Concluding Remarks
  • Acknowledgments
  • References
  • Chapter Three - A Mechanistic Approach to the Development of Gene Therapy for Chronic Pain
  • Abstract
  • 1 Introduction
  • 2 Basics of Gene Therapy
  • 2.1 Gene Transfer Mechanisms
  • 2.2 Various Viral Vectors and Their Characteristics
  • 3 Physiological Mechanisms of Nociception/Pain
  • 3.1 Detection and Transmission of Nociceptive Signals Through the Nervous System
  • 3.1.1 From the Periphery to the SC
  • 3.1.2 Transmission at the First Relay, the SC
  • 3.1.3 Ascending Pathways and the Supraspinal Processing of Pain
  • 3.2 The Modulatory Systems of Pain Transmission
  • 3.2.1 Spinal Control of Pain, or the Gate-Control Theory
  • 3.2.2 Supraspinal Control of Pain, or the Descending Inhibitory Pathway
  • 4 Chronic Neuropathic Pain
  • 4.1 Anatomical, Cellular, and Molecular Basis of Neuropathic Pain
  • 4.2 Gene Therapy for Neuropathic Pain
  • 4.3 Perspectives on Gene Therapy for Neuropathic Pain
  • 5 Chronic Nociceptive or Inflammatory Pain
  • 5.1 Anatomical, Cellular, and Molecular Basis of Inflammatory Pain
  • 5.2 Gene Therapy for Chronic Inflammatory Pain
  • 5.3 Perspectives on Gene Therapy for Inflammatory Pain
  • 6 Chronic Mixed Pain (Cancer), Opioid Analgesia, and Gene Therapy
  • 6.1 Improving Long-Term Opioid Analgesia in Chronic Pain by Targeting Opioid Receptors via Gene Therapy
  • 6.2 Reducing Opioid Tolerance in Chronic Pain by Targeting Inflammatory Factors via Gene Therapy
  • 7 Conclusions
  • Acknowledgments
  • References
  • Chapter Four - Roles and Regulation of Epithelial Splicing Regulatory Proteins 1 and 2 in Epithelial-Mesenchymal Transition
  • Abstract
  • 1 Introduction
  • 2 Epithelial-Mesenchymal Transition Program
  • 3 Alternative Splicing in EMT
  • 3.1 Alternative Splicing of Pre-mRNA
  • 3.2 Identification of Epithelial Splicing Regulatory Proteins
  • 3.3 Cell and Tissue Specificity of ESRP Expression and Function
  • 3.4 Targets of ESRPs
  • 3.5 Phenotypical Consequences of ESRP Activity
  • 3.5.1 Epithelial Splice Variants of Cell-Adhesion Proteins
  • 3.5.1.1 p120-Catenin
  • 3.5.1.2 CD44
  • 3.5.1.3 Integrin-a6
  • 3.5.2 Epithelial Splice Variants of Proteins Affecting Migration and Invasion
  • 3.5.2.1 MENA
  • 3.5.2.2 Exo70
  • 4 ESRPs as Regulators of EMT
  • 5 Regulation of ESRP Expression and Function
  • 6 Linking ESRPs to Carcinogenesis
  • 7 Concluding Remarks
  • References
  • Chapter Five - Orchestrating Lymphocyte Polarity in Cognate Immune Cell-Cell Interactions
  • Abstract
  • 1 Introduction
  • 2 Membrane Microdomains and Nanoclusters Orchestrate Cell-Cell Contacts
  • 2.1 T Cell-APC Contact: Initiating Immune Synapse
  • 2.2 Intracellular Traffic of TCR/CD3, LAT, and Lck
  • 2.3 Negative Regulatory Signals
  • 2.4 Intraflagellar Transport System
  • 3 Centrosome as Organelle-Organizing Center
  • 4 Endoplasmic Reticulum and Golgi Apparatus
  • 5 Multivesicular Bodies in Secretion, Recycling, and Renewal of Immune Synapse Components
  • 6 Lysosomes and Autophagy: More Than Degradation
  • 7 Mitochondria: Powering Immune Synapse
  • 7.1 Mitochondria Translocation to Immune Synapse
  • 7.2 Calcium Buffering During T-Cell Activation: Local Control at Immune Synapse
  • 7.3 ATP Reservoirs for Signaling
  • 8 Lytic Granules: Polarizing Killing Machinery
  • 9 Asymmetric Cell Division: Versus Clonal Expansion
  • 9.1 Nucleus Regulation: INSIDE OUT
  • 9.2 Nuclear Pores and Nucleoskeleton
  • 9.3 Asymmetric Cell Division: Versus Clonal Expansion
  • 9.4 Asymmetric Cell Division and Cell Fate
  • 9.5 Clonal T-Cell Expansion
  • 10 Concluding Remarks
  • Acknowledgments
  • References
  • Chapter Six - The Process of Cornification Evolved From the Initial Keratinization in the Epidermis and Epidermal Derivatives of Vertebrates: A New Synthesis and the Case of Sauropsids
  • Abstract
  • 1 Introduction
  • 2 Keratinization and Cornification are Continuous but not Equivalent Process
  • 2.1 Keratinization Indicates Accumulation of IF-Keratins
  • 2.2 Cornification Indicates the Addition of Specialized Proteins to IF-Keratins
  • 3 Anamniote Epidermis Keratinizes While Cornification Occurs in few Body Regions
  • 3.1 Epidermis in Fish and Amphibians
  • 3.2 Skin Appendages in Anamniotes
  • 4 Formation of the Corneous Layer in Amniotes
  • 4.1 Epidermis in Amniotes
  • 4.2 Skin Appendages in Amniotes
  • 5 Increase of Protein Types in Amniote Epidermis Compared to Anamniotes
  • 5.1 Fish and Amphibians
  • 5.2 Amniotes (Sauropsids and Mammals)
  • 6 Alpha and Beta-Keratinization Indicate Prevalence of Corneous Proteins Containing Alpha-Helix or Beta-Sheets, not of Keratins
  • 7 Differences Between IF-Alpha/Beta-Keratins and Sauropsid Beta-Keratins Indicate the Latter are Corneous Beta-Proteins
  • 8 The Process of Cornification in Sauropsids
  • 8.1 Cornification of Scales in Turtles, Crocodilians, and Lepidosaurians
  • 8.2 Cornification in Claws and Ramphothecas (Beaks)
  • 8.3 Cornification of Feathers
  • 9 Evolution of the Process of Cornification in the Epidermis and Skin Appendages: A New Synthesis
  • 9.1 From the Cytoskeleton to the Keratin Basal Framework of Keratinocytes
  • 9.2 Addition of Corneous Proteins to the Keratin Framework
  • 9.3 The Case of Sauropsid Cornification
  • 10 Concluding Remarks and Future Directions
  • Acknowledgements
  • References
  • Chapter Seven - The Calcium-Sensing Receptor in Health and Disease
  • Abstract
  • 1 Structure and Physiological Functions of the CaSR
  • 1.1 Structure of the CaSR
  • 1.2 Signaling Pathways of the CaSR
  • 1.3 CaSR Ligands and Biased Agonism
  • 1.4 CaSR and Extracellular Ca2+ Homeostasis
  • 2 Monitoring CaSR Activity in Living Cells
  • 3 CaSR in Endocrine Pathology
  • 4 CaSR in Cardiovascular Physiopathology
  • 5 CaSR in Asthma
  • 6 CaSR in Alzheimer's Disease
  • 7 CaSR in Cancer
  • 7.1 CaSR in Cancer Development and Progression
  • 7.2 CaSR in Parathyroid Cancer
  • 7.3 CaSR and Neuroblastoma
  • 7.4 CaSR in Colorectal Cancer
  • 7.5 CaSR in Breast Cancer
  • Acknowledgments
  • References
  • Chapter Eight - Molecular Interactions Between Flowering Time and Abiotic Stress Pathways
  • Abstract
  • 1 Introduction
  • 2 Developmental and Seasonal Control of Flowering Time
  • 3 Key Molecular Regulators of Flowering Time
  • 4 Abiotic Stresses Affecting Flowering Time
  • 4.1 Temperature
  • 4.2 Drought and ABA
  • 4.3 Salinity
  • 4.4 Nutrients
  • 5 Stress-Signal Integration by Major Flowering Time Regulators
  • 5.1 FLC Integrating Cold and ABA Into Autonomous and Vernalization Pathways
  • 5.2 CO Integrating Light Signaling and Photoperiod Pathways With Salt and Cold Stresses
  • 5.3 DELLAs Integrating GA Regulation of Flowering With Salt and Cold Stresses
  • 5.4 GI Integrating Photoperiod With Drought, Cold, and Salt Stresses
  • 6 Role of GI in Influencing Flowering Time and Circadian Clock Components
  • 7 Conclusions
  • Acknowledgments
  • References
  • Index
  • Back cover

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