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Apoptosis by Y. Kuchino

Apoptosis plays a central role in the regulation of cell proliferation. Disruption of this control mechanism may cause serious human diseases such as encephalomyelitis and cancer. Thus, understanding of the molecular mechanisms of apoptotic cell death should lead to fundamental advances in the therapy of these diseases.

Product Details

ISBN-13: 9783642798528
Publisher: Springer Berlin Heidelberg
Publication date: 12/14/2011
Series: Progress in Molecular and Subcellular Biology Series , #16
Edition description: Softcover reprint of the original 1st ed. 1996
Pages: 149
Product dimensions: 6.10(w) x 9.25(h) x 0.01(d)

Table of Contents

An Endonuclease Responsible for Apoptosis.- 1 Introduction.- 2 Results.- 3 Discussion.- References.- Cytopathic Feline Leukemia Viruses Cause Apoptosis in Hemolymphatic Cells.- Abstract.- 1 Introduction.- 2 Cytopathic Infections with FeLV-C in Vivo and Direct Induction of Apoptosis in T4 Cells by FeLV-C.- 3 Killing of Lymphocytes by FeLV-FAIDS/p61C and Associated Variants.- 4 FeLV-C-Related Nonregenerative Anemia: Potential Role for Apoptosis.- 5 FeLV Genes Important in Cytopathicity/Apoptosis Induction.- 5.1 General Remarks.- 5.2 T-Cell Killing.- 5.3 Erythroid Aplasias.- 6 Speculative Relationship to Endogenous Virus Recombinants and Importance Across Evolution.- 7 Regions of FeLV p15E Important in Immunosuppression.- 8 Other Types of Cytopathic Disease Seen in Viremic Cats Which Could Have an Apoptotic Basis.- 8.1 Enteritis.- 8.2 Infertility and Abortion.- 8.3 Neurologic Syndrome.- 9 So How Does FeLV Cause Apoptosis?.- 10 Other Retroviruses and Animal Viruses as Potential Causes of Apoptosis.- 10.1 Retroviruses that Behave as Superantigens.- 10.2 HIV and Other Lentiviruses.- 10.3 Chicken Anemia Virus.- References.- Neurotoxicity in Rat Cortical Cells Caused by N-Methyl-D-Aspartate (NMDA) and gp120 of HIV-1: Induction and Pharmacological Intervention.- Abstract.- 1 Introduction.- 2 Induction of Apoptosis in Rat Cortical Cells by HIV-1 gp120 or NMDA In Vitro.- 2.1 DNA Fragmentation and Cell Morphology After gp120 Treatment.- 2.2 Induction of Apoptosis in Cortical Cell Cultures by HIV-1 Particles.- 2.3 Increased Release of Arachidonic Acid from Neurons After Incubation with gp120.- 2.4 Inhibition of Arachidonic Acid Release by Phospholipase A2 Inhibitor.- 2.5 Induction of Apoptosis in Cortical Cell Cultures of NMDA.- 2.6 Influence of NMDA Antagonists on Arachidonic Acid Release.- 2.7 Arachidonic Acid Augments the NMDA-Caused DNA Fragmentation.- 3 Prevention of Apoptosis in Cortical Cells In Vitro by Memantine and Flupirtine.- 3.1 Memantine.- 3.2 Flupirtine.- 3.2.1 Prevention of NMDA or HIV-gp120-Induced Apoptosis in Cortical Cells by Flupirtine.- 3.2.2 Cytoprotective Effect of Flupirtine on Untreated Rat Cortical Cells.- 4 Conclusion.- 4.1 Cell Biological Findings.- 4.2 Pharmacological Interventions.- References.- Apoptosis of Mature T Lymphocytes: Putative Role in the Regulation of Cellular Immune Responses and in the Pathogenesis of HIV Infection.- Abstract.- 1 Apoptosis of Immature T Lymphocytes.- 2 Apoptosis of Mature T Lymphocytes.- 3 Apoptosis of T Lymphocytes Induced by Superantigens and Conventional Antigen.- 4 Apoptosis of Mature T Lymphocytes In Vivo and Ex Vivo.- 5 Role of T-Cell Apoptosis in HIV Pathogenesis.- 6 Concluding Remarks.- References.- bcl-2: Antidote for Cell Death.- Abstract.- 1 Introduction.- 2 Structure and Expression of the bcl-2 Gene.- 3 Biological Function of bcl-2: Apoptotic Death-Sparing Activity.- 4 Role of bcl-2 in the Immune System.- 4.1 bcl-2 in Lymphocyte Selection.- 4.2 Production of Autoimmune Disease.- 5 Role of bcl-2 in Neuronal Tissue.- 6 Role of bcl-2 in Lymphomagenesis.- 7 Role of bcl-2 in Other Systems.- 7.1 Virus Persistent Infection.- 7.2 Epithelial Cells.- 7.3 Morphogenesis.- 8 Analysis of bcl-2-Deficient Mice.- 9 Subcellular Localization of bcl-2: Multiple Membrane Locations.- 10 Biochemical Function of bcl-2 Protein.- 11 bcl-2 Related Genes and bcl-2 Associated Proteins.- 12 Epilogue.- References.- Apoptosis Mediated by the Fas System.- Abstract.- 1 Introduction.- 2 Fas, a Receptor for a Death Factor.- 2.1 Molecular Properties of Fas.- 2.2 Expression of Fas.- 3 Mutation in the Fas Gene of lpr-Mice.- 3.1 Chromosomal Gene for Fas.- 3.2 Insertion of an Early Transposable Element in Intron of Fas Gene in lpr-Mice.- 3.3 A Point Mutation in the Fas Gene of lprcg Mice.- 4 Fas-Mediated Apoptosis.- 4.1 Apoptosis In Vitro.- 4.2 Apoptosis In Vivo.- 4.3 Activation of Fas to Induce Apoptotic Signal.- 4.4 Apoptotic Signal Mediated by Fas.- 5 Fas Ligand, a Death Factor.- 5.1 Identification and Purification of Fas Ligand.- 5.2 Molecular Properties of the Fas Ligand.- 5.3 Expression of the Fas Ligand.- 6 Physiological Roles of the Fas System.- 6.1 Involvement of the Fas System in Development of T-Cells.- 6.2 Involvement of the Fas System in CTL-Mediated Cytotoxicity.- 6.3 Pathological Tissue Damage Caused by the Fas System.- 7 Perspectives.- References.- Myc-Mediated Apoptosis.- Abstract.- 1 Introduction.- 2 c-Myc-Mediated Apoptosis.- 3 s-Myc-Mediated Apoptosis.- 3.1 Structural Feature of the s-myc Gene.- 3.2 Structural Feature and Biological Functions of the s-Myc Protein.- 3.3 Expression of the s-myc Gene.- 3.4 s-Myc-Mediated Apoptosis.- 4 Escape from Myc-Induced Apoptotic Cell Death.- 5 Conclusions.- References.- Clusterin: A Role in Cell Survival in the Face of Apoptosis?.- Abstract.- 1 Introduction.- 2 Clusterin-a Widely Expressed Multifunctional Protein.- 3 Clusterin Gene Expression in Apoptotic Epithelial Tissues.- 4 Clusterin Gene Expression in the Thymus.- 5 Clusterin Gene Expression in Retinitis Pigmentosa (RP) Retina.- 6 Clusterin Expression During Degenerative Processes in the Brain.- 7 Conclusions and Perspectives.- References.

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