What is included with this book?
Contributors | p. ix |
Preface | p. xiii |
Discovery of Activation-Induced Cytidine Deaminase, the Engraver of Antibody Memory | |
Abstract | p. 1 |
Introduction | p. 2 |
Identification of AID as a Key Molecule in CSR and SHM | p. 4 |
AID Is the Only B-Cell-Specific Factor Required for Both CSR and SHM | p. 87 |
Functional Domains of AID | p. 11 |
AID Is Involved in a DNA Cleavage Step | p. 14 |
Major Hypotheses for the Action of AID | p. 16 |
Critical Examination of the DNA Deamination Model | p. 19 |
Evidence for a Novel Function of UNG in CSR | p. 24 |
Conclusion | p. 28 |
References | p. 29 |
DNA Deamination in Immunity: AID in the Context of Its APOBEC Relatives | |
Abstract | p. 37 |
Introduction | p. 38 |
AID: The DNA Deaminase Trigger for Antibody Diversification | p. 38 |
The Zn-Dependent Deaminase Superfamily | p. 39 |
Timeline of AID/APOBEC Evolution | p. 48 |
APOBEC1: An RNA-Editing Enzyme That Can Also Act on DNA | p. 49 |
APOBEC2: A Muscle-Specific Family Member of Unknown Function/Activity | p. 50 |
APOBEC4: A Distant or Ancestral Member of the AID/APOBEC Family | p. 51 |
APOBEC3s: DNA Deaminases Active in Viral Restriction | p. 52 |
Conclusion | p. 63 |
References | p. 63 |
The Role of Activation-Induced Deaminase in Antibody Diversification and Chromosome Translocations | |
Abstract | p. 75 |
Introduction | p. 76 |
Events Preceding the DNA Lesion | p. 77 |
The DNA Lesion | p. 78 |
DNA Damage Detection and Resolution During CSR | p. 85 |
AID and Lymphomagenic Lesions | p. 93 |
Conclusions and Perspectives | p. 96 |
References | p. 96 |
Targeting of AID-Mediated Sequence Diversification by cis-Acting Determinants | |
Abstract | p. 109 |
Introduction | p. 109 |
The Link Between Transcription and AID-Mediated Sequence Diversification | p. 111 |
Other cis-Acting Determinants Involved in the Targeting of AID | p. 116 |
Future Outlook | p. 120 |
References | p. 120 |
AID-Initiated Purposeful Mutations in Immunoglobulin Genes | |
Abstract | p. 127 |
Introduction | p. 128 |
Biochemical Basis of C Deamination by APOBEC Enzymes | p. 132 |
How and Why Might AID-Specific Mutations Be Targeted? | p. 141 |
Selection of AID-Induced Mutations During Ab Maturation | p. 143 |
References | p. 149 |
Evolution of the Immunoglobulin Heavy Chain Class Switch Recombination Mechanism | |
Abstract | p. 157 |
Overview of Genetic Alterations in B Lymphocytes | p. 158 |
Activation-Induced Cytidine Deaminase | p. 162 |
Role of Germ Line Transcription and Switch Regions in CSR | p. 169 |
Posttranscriptional Regulation of AID | p. 180 |
Mechanisms Involved in Synapsis of AID Initiated DSBs in Widely Separated S Regions | p. 184 |
General DNA Repair Systems in the Joining Phase of CSR | p. 189 |
Evolution of CSR | p. 197 |
References | p. 198 |
Beyond SHM and CSR: AID and Related Cytidine Deaminases in the Host Response to Viral Infection | |
Abstract | p. 215 |
Introduction | p. 215 |
Evolution of the AID/APOBEC Cytidine Deaminase Family | p. 216 |
APOBEC3: A Subfamily of Antiviral Cytidine Deaminases | p. 217 |
AID in the Host Response to Viral Infection | p. 229 |
Concluding Remarks | p. 235 |
References | p. 237 |
Role of AID in Tumorigenesis | |
Abstract | p. 245 |
Introduction | p. 246 |
AID Transgenic Mouse Models | p. 247 |
Role of AID in Chromosomal Translocation and Subsequent Lymphomagenesis | p. 249 |
AID Expression in Human B-Cell Malignancies | p. 252 |
Mechanism of AID Expression in Normal and Malignant B Cells | p. 259 |
AID Expression in Normal and Malignant Nonlymphoid Cells | p. 263 |
Concluding Remarks | p. 265 |
References | p. 265 |
Pathophysiology of B-Cell Intrinsic Immunoglobulin Class Switch Recombination Deficiencies | |
Abstract | p. 275 |
Introduction | p. 276 |
Ig-CSR Deficiency Type 1 Caused by Activation-Induced Cytidine Deaminase Deficiency | p. 279 |
Ig-CSR Deficiency Type 2 Caused by UNG Deficiency | p. 289 |
Molecularly Undefined Ig-CSR Deficiency with Normal SHM | p. 292 |
Concluding Remarks | p. 296 |
References | p. 298 |
Index | p. 307 |
Contents of Recent Volumes | p. 317 |
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