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International review of cell and molecular biology. Vol. 326 /

International Review of Cell and Molecular Biology presents current advances and comprehensive reviews in cell biology--both plant and animal. Articles address structure and control of gene expression, nucleocytoplasmic interactions, control of cell development and differentiation, and cell transfor...

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Bibliographic Details
Corporate Author: ScienceDirect (Online service)
Other Authors: Jeon, Kwang W., Galluzzi, Lorenzo
Format: eBook
Language:English
Published: Amsterdam ; Boston : Elsevier : Academic Press, 2016.
Edition:1st ed.
Subjects:
Cells.
Molecular biology.
Cells
Molecular Biology
Cellules.
Biologie moléculaire.
molecular biology.
MEDICAL > Anatomy.
SCIENCE > Life Sciences > Human Anatomy & Physiology.
SCIENCE > Life Sciences > Biology.
Molecular biology
Electronic books.
Online Access:Connect to the full text of this electronic book
Table of Contents:
  • Cover
  • Title page
  • Copyright Page
  • Contents
  • Contributors
  • Chapter One
  • Compartmentalization and Regulation of Sulfate Assimilation Pathways in Plants
  • Abstract
  • 1 Introduction
  • 2 Sulfate Transport Systems
  • 2.1 Molecular Cloning of Sulfate Transporter
  • 2.2 Sulfate Uptake in Roots
  • 2.2.1 Transporters for Sulfate Uptake in Roots
  • 2.2.2 Regulation of Sulfate Uptake
  • 2.3 Sulfate Distribution in Plants
  • 2.3.1 Root-to-Shoot Transport of Sulfate
  • 2.3.2 Source-to-Sink Transport of Sulfate and Sulfur Metabolites
  • 2.3.3 Intracellular Transport of Sulfate
  • 3 Sulfate Assimilation
  • 3.1 Metabolic Pathway Compartmentalization and Regulation
  • 3.1.1 APS and PAPS Biosynthetic Pathways
  • 3.1.2 Sulfur Metabolic Flux Partitioning and Regulation
  • 3.2 Plastid-Cytosol Metabolic Pathway Integration
  • 3.2.1 PAPS Transport and Metabolism
  • 3.2.2 Synergy in Metabolic Flux Regulation
  • 4 Conclusions and Future Perspectives
  • Acknowledgments
  • References
  • Chapter Two
  • Insight Into the Role of Long Noncoding RNA in Cancer Development and Progression
  • Abstract
  • 1 Introduction
  • 1.1 Molecular Mechanisms of lncRNA
  • 1.2 Cancer-Associated Signaling Pathways
  • 2 Roles of lncRNA During Cancer Development
  • 2.1 Chromosomal Instability
  • 2.2 DNA Damage Response
  • 2.3 Virus-Induced Carcinogenesis
  • 2.4 Carcinogen Stimulation
  • 3 Cancer Cell Survival
  • 3.1 Cancer Metabolism
  • 3.2 Radiation and Oxidative Stress
  • 3.3 Hypoxia
  • 4 LncRNA in Cancer Stem Cell
  • 4.1 Stemness Features
  • 4.2 Renewal
  • 4.3 Transformation of Cancer Stem Cell
  • 5 Insight of Novel lncRNA Roles in Cancer
  • 5.1 Immunity
  • 5.2 Cancer Microenvironment
  • 6 Diagnostic and Prognostic Value of lncRNAs
  • 7 Concluding Remarks
  • Acknowledgment
  • References
  • Chapter Three
  • Endogenous Mechanisms of Cardiac Regeneration
  • Abstract
  • 1 Introduction.
  • 2 Endogenous Cellular Sources for Cardiac Regeneration
  • 2.1 Cardiac Stem and Progenitor Cells
  • 2.1.1 Identification of Cardiac Stem and Progenitor Cells
  • 2.1.2 Regenerative Capacity of c-Kit+ Cardiac Stem Cells
  • 2.1.3 Genetic Fate-Mapping of Endogenous Cardiac Stem Cells
  • 2.2 Cardiomyocytes
  • 2.2.1 Adult Zebrafish Cardiomyocytes
  • 2.2.2 Proliferative Capacity of Mouse Cardiomyocytes
  • 2.2.3 Evidence for Cardiomyocyte Renewal in Adult Humans
  • 2.3 Transdifferentiation
  • 2.3.1 Epicardial to Myocardial Transdifferentiation
  • 2.3.2 Atrial-to-Ventricular Muscle Lineage Conversion
  • 2.3.3 Contributions by Noncardiac Stem Cells
  • 3 Molecular Mechanisms Limiting Cardiac Regeneration
  • 3.1 Postnatal Changes Inducing Cardiomyocyte Cell Cycle Arrest
  • 3.1.1 Postnatal Induction of Global DNA Methylation
  • 3.1.2 Cell Cycle Regulation by Transcription Factor Meis1
  • 3.1.3 Loss of Centrosome Integrity and Cell Cycle Arrest
  • 3.2 miRNAs That Suppress Cardiomyocyte Proliferation
  • 3.2.1 miR-15 Family
  • 3.2.2 miR-133 Family
  • 3.2.3 miR-99/100 Family
  • 3.3 Myocardial Functions of the Hippo Signaling Pathway
  • 3.3.1 Hippo Pathway Signal Transduction Cascade
  • 3.3.2 Hippo Pathway and Cardiomyocyte Proliferation
  • 3.3.3 Hippo Pathway and Cardiac Regeneration
  • 3.3.4 Post transcriptional Regulation of Myocardial Hippo Signaling
  • 3.4 Environmental O2 and Cardiac Regenerative Capacity
  • 3.4.1 Cell Cycle Arrest by Reactive Oxygen Species-Mediated DNA Damage Responses
  • 3.4.2 Cardiomyocyte Renewal by Hypoxic Cardiomyocytes
  • 3.4.3 Hypoxia, Mechanical Unloading, and Cardiomyocyte Proliferation
  • 4 Molecular Mechanisms Stimulating Cardiac Regeneration
  • 4.1 Inflammatory Signals Inducing Cardiomyocyte Proliferation
  • 4.1.1 The Hydrogen Peroxide Pathway
  • 4.1.2 Jak1/Stat3 Pathway
  • 4.1.3 NF-?B Signaling Pathway.
  • 4.2 Mechanisms Promoting Cardiomyocyte Dedifferentiation
  • 4.2.1 Reexpression of Cardiogenic Transcription Factors
  • 4.2.2 Oncostatin M Signaling Pathway
  • 4.3 Signaling Pathways Promoting Cardiomyocyte Proliferation
  • 4.3.1 Neuregulin 1 Pathway in the Mouse Heart
  • 4.3.2 Nrg1 Pathway in Zebrafish Heart
  • 4.3.3 Thyroid Hormone Pathway in the Preadolescent Mouse Heart
  • 5 Nonmyocyte Regulation of Cardiac Regeneration
  • 5.1 Roles of Epicardial and Endocardial Cells
  • 5.1.1 Proregenerative Factors Produced by Epicardial and Endocardial Cells
  • 5.1.2 Epicardial Regulation of Cardiomyocyte Migration
  • 5.1.3 Epicardial Regulation of Vasculature Regeneration
  • 5.2 New Mechanisms of Cardiac Regeneration Mediated by Nonmyocytes
  • 5.2.1 Epicardial Reconstitution of Follistatin-Like 1
  • 5.2.2 Epicardial Regeneration Directed by the Bulbous Arteriosus
  • 5.2.3 Proregenerative Roles of Macrophages
  • 5.2.4 Nerve Control of Neonatal Mouse Heart Regeneration
  • 6 Summary and Prospects
  • Acknowledgments
  • References
  • Chapter Four
  • NF-?B signaling as a driver of ageing
  • Abstract
  • 1 Introduction
  • 2 NF-?B Signaling Pathway
  • 2.1 IKK Complex
  • 2.2 I?B Proteins
  • 2.3 NF-?B Transcription Factors
  • 2.4 Canonical and Noncanonical Signaling
  • 3 NF-?B Activation in Ageing
  • 4 Monitoring NF-?B Activity During Ageing
  • 5 NF-?B Signaling in Ageing
  • 5.1 NF-?B Lessons From Progeroid Animal Models
  • 5.1.1 Sirt6-Deficient Mice
  • 5.1.2 Ercc1-Deficient Mice
  • 5.1.3 Zmpste24-Deficiency and LmnaG609G Mice
  • 5.1.4 Nfkb1-Deficient Mice
  • 5.2 NF-?B Secretory Phenotype
  • 5.3 NF-?B and Apoptosis
  • 5.4 NF-?B and Cellular Senescence
  • 5.5 NF-?B and Telomeres
  • 5.6 Immunosenescence
  • 5.7 NF-?B Crosstalk with Other Ageing Regulators
  • 5.7.1 Sirtuins
  • 5.7.2 Insulin-IGF-1 signaling
  • 5.7.3 mTOR
  • 5.7.4 FoxO (DAF-16)
  • 5.7.5 p53.
  • 5.7.6 Wnt Signaling
  • 5.7.7 PARP-1
  • 5.7.8 Longevity Assurance Proteins
  • 5.7.9 Klotho
  • 5.8 NF-?B and Metabolism
  • 5.9 NF-?B in Age-Associated Pathologies
  • 5.10 NF-?B in Cell Reprogramming and Stem Cells Biology
  • 5.11 Fat Inflammatory Paradox
  • 5.12 NF-?B and Microbiota
  • 6 NF-?B and Cancer
  • 7 NF-?B as a Biomarker of Ageing
  • 8 Rejuvenation Approaches Based on NF-?B Inhibition
  • 9 Conclusions
  • Acknowledgments
  • References
  • Chapter Five
  • Metabolic and Signaling Functions of Cancer Cell-Derived Extracellular Vesicles
  • Abstract
  • 1 Introduction
  • 1.1 Extracellular Vesicles
  • 1.2 Exosome Biogenesis
  • 1.3 Molecular Content of Exosomes
  • 1.4 Uptake of Exosomes
  • 1.5 Functional Properties of the Exosomes
  • 1.6 Cancer Cell-Derived Exosomes
  • 2 Cellular metabolism and exosomes
  • 2.1 Introduction
  • 2.2 The Role of Cancer Cell Metabolism on Exosome Secretion
  • 2.3 Exosomes as Carriers of Metabolites
  • 2.4 Extracellular Vesicles Possess Intrinsic Catalytic Activity
  • 2.5 Role of Cancer Cell Metabolism on Extracellular Vesicle Uptake
  • 2.6 Effect of Exosomes on the Metabolism of the Recipient Cells
  • 3 Future perspectives and directions
  • References
  • Chapter Six
  • Mutually Supportive Mechanisms of Inflammation and Vascular Remodeling
  • Abstract
  • 1 Introduction
  • 2 Inflammation Promotes Angiogenesis and Vascular Remodeling
  • 2.1 Biochemical and Environmental Factors
  • 2.1.1 Hypoxia
  • 2.1.2 Growth Factors
  • 2.1.3 Angiopoietin/Tie-2 System
  • 2.1.4 Chemokines and Cytokines
  • 2.1.5 Matrix Metalloproteinases
  • 2.1.6 Heparan Sulfate Proteoglycans and Syndecans
  • 2.2 Proangiogenic Leukocytes
  • 2.2.1 Monocytes and Macrophages
  • 2.2.2 Neutrophils
  • 2.2.3 Eosinophils, Basophils, and Mast Cells
  • 3 Inflammatory Angiogenesis and Disease Progression
  • 3.1 Atherosclerotic Plaque-Associated Neovascularization.
  • 3.2 Arthritis and Angiogenesis
  • 3.3 Tumor-Associated Angiogenesis
  • 4 Postischemic Revascularization
  • 4.1 Inflammation in Ischemic Tissues
  • 4.2 Collateral Artery Remodeling
  • 4.3 Therapeutic Revascularization
  • 5 Angiogenesis Supports Chronic Inflammation
  • 5.1 Vasa Vasorum and Atherosclerotic Plaque Progression
  • 5.2 Leukocytes are Delivered to Inflamed Joints by Angiogenic Vessels
  • 5.3 Recruitment of Tumor-Associated Leukocytes Via Tumor Vasculature
  • 6 Conclusions
  • Acknowledgments
  • References
  • Chapter Seven
  • Pharmacological Actions of Glucagon-Like Peptide-1, Gastric Inhibitory Polypeptide, and Glucagon
  • Abstract
  • 1 Introduction
  • 2 Glucagon-Like Peptide-1
  • 2.1 Therapeutic Potency
  • 2.1.1 Type-2 Diabetes Mellitus
  • 2.1.1.1 GLP-1R Agonists
  • 2.1.1.1.1 Short-Acting GLP-1R Agonists
  • 2.1.1.1.1.1 Exenatide-Twice Daily
  • 2.1.1.1.1.2 Lixisenatide
  • 2.1.1.1.2 Continuous-Acting GLP-1R Agonists
  • 2.1.1.1.2.1 Liraglutide
  • 2.1.1.1.2.2 Exenatide-Once Weekly
  • 2.1.1.1.2.3 Albiglutide
  • 2.1.1.1.2.4 Other GLP-1R Agonists
  • 2.1.1.2 DPP-4 Inhibitors
  • 2.1.1.2.1 Sitagliptin
  • 2.1.1.2.2 Saxagliptin
  • 2.1.1.2.3 Vildagliptin
  • 2.1.1.2.4 Linagliptin
  • 2.1.2 Weight Reduction and Energy Intake
  • 2.1.3 Pancreatic ß-Cell Pathogenesis
  • 2.1.4 Renal Impairment
  • 2.1.5 Cardiovascular Effect
  • 2.1.6 Other Actions
  • 2.2 Safety and Tolerability Concerns
  • 2.2.1 Pancreatitis
  • 2.2.2 Cancer Risk
  • 2.2.3 Hypoglycemia
  • 2.2.4 Nausea
  • 2.2.5 Hypersensitivity Reactions
  • 2.3 Conclusions
  • 3 GIP
  • 3.1 Therapeutic Potential
  • 3.1.1 Type-2 Diabetes
  • 3.1.1.1 GIPR Agonists
  • 3.1.1.1.1 GIP Analog (D-GIP1-30)
  • 3.1.1.1.2 N-AcGIP(LysPAL16) and N-AcGIP(LysPAL37)
  • 3.1.1.2 DPP-4 Inhibitors
  • 3.1.1.3 GIP Antagonist
  • 3.1.1.3.1 (Pro3) GIP
  • 3.1.1.3.2 GIP6-30amide
  • 3.1.1.3.3 GIP-Oxyntomodulin Hybrid Peptide
  • 3.2 Conclusions.