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Mechanisms of Lymphocyte Activation and Immune Regulation VI

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Cover of 'Mechanisms of Lymphocyte Activation and Immune Regulation VI'

Table of Contents

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    Book Overview
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    Chapter 1 Apoptosis/Programmed Cell Death
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    Chapter 2 Apoptosis and Its Regulation
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    Chapter 3 Mechanisms for Recognition and Phagocytosis of Apoptotic Lymphocytes by Macrophages
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    Chapter 4 Cytotoxic Lymphocyte Killing Enters the Ice Age
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    Chapter 5 Cross-talk between ceramide and PKC activity in the control of apoptosis in WEHI-231.
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    Chapter 6 Cell Cycle Control of T Cell Apoptosis Induced by Activation Through the T Cell Antigen Receptor
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    Chapter 7 Role of antibody signaling in inducing tumor dormancy.
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    Chapter 8 Regulation of lymphoid apoptosis by Bcl-2 and Bcl-XL.
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    Chapter 9 The Epstein-Barr virus gene BHRF1, a homologue of the cellular oncogene Bcl-2, inhibits apoptosis induced by gamma radiation and chemotherapeutic drugs.
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    Chapter 10 Structure—Function Analysis of Bcl-2 Family Proteins
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    Chapter 11 Role of Ice-Proteases in Apoptosis
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    Chapter 12 Fas-mediated apoptosis.
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    Chapter 13 Fas Splicing Variants and their Effect on Apoptosis
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    Chapter 14 The Role of FasL and TNF in the Homeostatic Regulation of Immune Responses
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    Chapter 15 Signals for survival and apoptosis in normal and neoplastic B lymphocytes.
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    Chapter 16 Regulation of B Cell Apoptosis
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    Chapter 17 Apoptotic Cell Death in the Chicken Bursa of Fabricius
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    Chapter 18 Generation and Regulation of B Cell Autoreactivity Arising in the Periphery
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    Chapter 19 Inducible Resistance to Fas-Mediated Apoptosis in Primary B Lymphocytes
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    Chapter 20 The thymus and T cell death.
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    Chapter 21 Genetic Regulation of Apoptosis in the Mouse Thymus
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    Chapter 22 Regulation of T Cell Activation by CD28 and CTLA4
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    Chapter 23 Granzyme B-Induced Apoptosis
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    Chapter 24 Mature T Lymphocyte Apoptosis in the Healthy and Diseased Immune System
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    Chapter 25 Autoimmunity Due to Defective NUR77, Fas, and TNF-RI Apoptosis
Attention for Chapter 9: The Epstein-Barr virus gene BHRF1, a homologue of the cellular oncogene Bcl-2, inhibits apoptosis induced by gamma radiation and chemotherapeutic drugs.
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Chapter title
The Epstein-Barr virus gene BHRF1, a homologue of the cellular oncogene Bcl-2, inhibits apoptosis induced by gamma radiation and chemotherapeutic drugs.
Chapter number 9
Book title
Mechanisms of Lymphocyte Activation and Immune Regulation VI
Published in
Advances in experimental medicine and biology, January 1996
DOI 10.1007/978-1-4899-0274-0_9
Pubmed ID
Book ISBNs
978-1-4899-0276-4, 978-1-4899-0274-0
Authors

McCarthy, N J, Hazlewood, S A, Huen, D S, Rickinson, A B, Williams, G T, McCarthy, N. J., Hazlewood, S. A., Huen, D. S., Rickinson, A. B., Williams, G. T.

Abstract

Analysis of apoptosis, active and controllable cell death, has demonstrated that the size of a cell population can be regulated by changes in the cell death rate as well as in the rates of proliferation and differentiation. Factors which alter the rate of cell death, such as expression of the proto-oncogene bcl-2, can therefore directly affect the number of cells within a population. Bcl-2 has been shown to suppress apoptosis in response to a variety of stimuli and to act as a complementary survival signal for the random acquisition of other oncogenic mutations, such as deregulated c-myc. The Epstein Barr virus (EBV) gene BHRF1 was the first of a family of bcl-2 homologues now being identified. BHRF1 and bcl-2 share 25% primary amino acid sequence homology. Here we show that gamma radiation and several cytotoxic anticancer agents induce apoptosis in Burkitt's lymphoma (BL) cell lines, as has been found in several other systems. Using gene transfection studies we have also shown that expression of either BHRF1 or bcl-2 in BL cell lines significantly suppresses apoptosis in response to a variety of anticancer treatment. This has confirmed that BHRF1 is functionally homologous to bcl-2 in B-cells and suggests that BHRF1 may act to prevent apoptosis during EBV infection, maximising virus particle production, as has been suggested for other human and insect viral genes. Suppression of chemotherapeutic drug induced cell death by bcl-2 and BHRF1 as demonstrated in this cell system, results in resistance to a variety of different agents and may represent an alternative mechanism by which multidrug resistance arises during chemotherapy.

Mendeley readers

The data shown below were compiled from readership statistics for 20 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
United Kingdom 1 5%
Unknown 19 95%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 4 20%
Student > Bachelor 3 15%
Other 2 10%
Lecturer > Senior Lecturer 1 5%
Student > Doctoral Student 1 5%
Other 2 10%
Unknown 7 35%
Readers by discipline Count As %
Medicine and Dentistry 3 15%
Agricultural and Biological Sciences 3 15%
Biochemistry, Genetics and Molecular Biology 2 10%
Immunology and Microbiology 2 10%
Mathematics 1 5%
Other 2 10%
Unknown 7 35%