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E-raamat: Dna Deamination And The Immune System: Aid In Health And Disease

Edited by (National Inst Of Health, Usa), Edited by (Rockefeller Univ, Usa), Edited by (National Inst Of Health, Usa)
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This book covers the current understanding of the role of activation-induced cytidine deaminase (AID) in the generation of antibody response to antigenic challenge. Since the discovery of AID, and the genetic demonstration of its role in somatic hypermutation and class-switch recombination of antibody genes, much has been learned about the biochemistry of this enzyme. However, some key questions remain hotly contested, such as: how does this enzyme get to the antibody locus leaving the rest of the genome intact, and why are DNA repair pathways which normally repair deamination events co-opted into actually fixing mutations into the genome? These questions, among others, will be addressed in this monograph from various perspectives. Being leading experts in their respective fields, the contributors of this highly valued title summarize current research in the field of AID and put forth hypotheses in order to provide a platform for future experiments.
Preface v
List of Tables
xi
List of Figures
xiii
1 Introduction
1(11)
1.1 Discovery of AID
2(1)
1.2 Current Model of AID Function
3(1)
1.3 Open Questions
4(2)
1.4 A Unifying Model for AID Function
6(2)
1.5 Acknowledgements
8(1)
1.6 References
8(4)
2 Switch Regions, Chromatin Accessibility and AID Targeting
12(19)
2.1 Introduction
13(2)
2.2 Transcriptional Elements Determine Long-Range Regulation of CSR
15(2)
2.3 Cis-Regulatory Elements as Recruiters for AID
17(1)
2.4 Transcription and Accessibility to AID Attack
17(3)
2.5 S Region Sequence Determines Chromatin Accessibility
20(1)
2.6 AID-Induced Mutation Distribution and Transcription
21(1)
2.7 Processing of GLTs and the Introduction of AID-Induced Mutations
22(1)
2.8 Future Directions
23(1)
2.9 Acknowledgements
24(1)
2.10 References
24(7)
3 Cis-Regulatory Elements that Target AID to Immunoglobulin Loci
31(31)
3.1 Introduction
32(1)
3.2 Targeting by Ig Promoters - Are High Levels of Transcription All There is to It?
33(5)
3.2.1 Genome-wide SHM
34(1)
3.2.2 Targeting of SHM by promoters
35(3)
3.3 SHM Targeting Elements in Ig Light Chain Loci
38(5)
3.3.1 The murine Ig light chain loci
38(2)
3.3.2 The chicken IgL locus
40(3)
3.4 Targeting Elements in the Murine IgH Locus
43(9)
3.4.1 Targeting of CSR
43(5)
3.4.2 Is enhancement of CSR only secondary to enhancement of germline transcription?
48(1)
3.4.3 Targeting of SHM to the murine IgH loci
49(2)
3.4.4 Targeting elements for CSR and SHM- A comparison
51(1)
3.5 Outlook
52(3)
3.6 Acknowledgements
55(1)
3.7 References
55(7)
4 Partners in Diversity: The Search for AID Co-Factors
62(21)
4.1 Introduction and Overview
63(3)
4.2 Compartmentalization of AID
66(1)
4.3 The C-Terminal Domain of AID
67(4)
4.3.1 Tethering of DNA damage sensors/transducers
67(2)
4.3.2 MDM2
69(2)
4.4 Targeting AID in the Context of Cotranscriptional Pre-mRNA Splicing byCTNNBLl
71(1)
4.5 Replication Protein A (RPA)
72(1)
4.6 Protein Kinase A (PKA) and Regulation of AID Activity by Phosphorylation
72(3)
4.7 Recruitment of PKA to Switch Region Sequences
75(2)
4.8 Concluding Remarks
77(1)
4.9 Acknowledgements
78(1)
4.10 References
78(5)
5 Resolution of AID Lesions in Class Switch Recombination
83(14)
5.1 Introduction
83(1)
5.2 Conversion of AID Lesions to Double-Strand DNA Breaks
84(5)
5.2.1 Uracils in switch region DNA
84(1)
5.2.2 Base excision repair in class switch recombination
85(1)
5.2.3 Mismatch repair in class switch recombination
86(1)
5.2.4 Generation of DNA double-strand breaks in switch regions
86(3)
5.3 Repair of Double-Strand DNA Breaks in Class Switch Recombination
89(4)
5.3.1 Ku and the initial phase of NHEJ
89(1)
5.3.2 Nucleases for NHEJ
90(1)
5.3.3 Polymerases for NHEJ
90(1)
5.3.4 Ligases for NHEJ
91(1)
5.3.5 Terminal microhomology usage in NHEJ
91(1)
5.3.6 Alternative NHEJ
91(2)
5.4 Concluding Comments and Future Questions
93(1)
5.5 References
93(4)
6 Error-Prone and Error-Free Resolution of AID Lesions in SHM
97(30)
6.1 Introduction
98(1)
6.2 Direct Replication Across the Uracil: G/C Transitions
98(3)
6.3 UNG2-Dependent SHM Across AP Sites: G/C Transversions and Transitions
101(1)
6.4 MulSα-Dependent SHM at MMR Gaps: A/T Mutations
102(2)
6.5 UNG-Dependent A/T Mutations
104(1)
6.6 Half of all G/C Transversions Require MutSα and UNG2
104(1)
6.7 Translesion Synthesis DNA Polymerases
105(5)
6.7.1 Polη generates most A/T mutations
106(1)
6.7.2 Polκ can partially compensate for Polη deficiency
107(1)
6.7.3 TLS polymerase Rev I generates G to C transversions
107(1)
6.7.4 Polι, a story to be finished
108(1)
6.7.5 Polζ, an extender polymerase that might be replaceable
109(1)
6.7.6 Polθ is dispensable during SHM
109(1)
6.7.7 Other TLS polymerases: Polλ and Polμ
110(1)
6.8 Regulating TLS by Ubiquitylation of PCNA
110(2)
6.9 SHM: Mutagenesis at Template A/T Requires PCNA-Ub
112(1)
6.10 PCNA-Ub-Independent G/C Transversions During SHM
113(1)
6.11 MutSα and UNG2 do not Compete During SHM: Cell Cycle and Error-Free Repair
114(2)
6.12 Aberrant Targeting of AID and Error-Free Repair of AID-Induced Uracils
116(3)
6.13 Acknowledgements
119(1)
6.14 References
119(8)
7 Regulatory Mechanisms of AID Function
127(25)
7.1 Introduction
128(1)
7.2 Transcriptional Regulation of AID Gene Expression
128(9)
7.2.1 Expression of AID in and outside B cells
128(2)
7.2.2 Signal transduction pathways leading to Aicda induction
130(1)
7.2.3 Transcription factors inducing AID
131(4)
7.2.4 AID haploinsufficiency
135(2)
7.3 Posttranscriptional Regulation of mRNA Levels
137(4)
7.3.1 Regulation of AID expression by microRNAs
137(2)
7.3.2 AID alternative splicing
139(2)
7.4 Posttranslational Control of AID
141(3)
7.4.1 AID subcellular localization and stability
141(3)
7.5 Integration of AID Regulation: The Outstanding Questions
144(1)
7.6 Acknowledgements
145(1)
7.7 References
146(6)
8 AID in Immunodeficiecy and Cancer
152(35)
8.1 AID and Immunodeficiencies
153(6)
8.1.1 Autosomal recessive CSR-D caused by bi-allelic Aicda mutations
153(5)
8.1.2 Autosomal dominant CSR-D caused by mono-allelic Aicda mutations
158(1)
8.2 AID and Cancer
159(16)
8.2.1 AID is a mutagen
160(1)
8.2.2 AID is a carcinogen
161(1)
8.2.3 Cancer markers and AID
162(1)
8.2.4 AID regulation and cancer correlation
163(12)
8.3 Acknowledgements
175(1)
8.4 References
175(12)
9 AID in Aging and in Autoimmune Disease
187(28)
9.1 AID and Aging
188(1)
9.2 Aging Decreases Humoral Immune Responses
189(9)
9.2.1 Molecular mechanisms for reduced CSR in aging
192(6)
9.3 AID in Autoimmunity
198(8)
9.3.1 Potential novel mouse models designed to distinguish the role of SHM, CSR and the naive repertoire in autoimmunity
200(2)
9.3.2 AID-deficient autoimmune-prone mice
202(2)
9.3.3 AID overexpression effects and autoimmunity in mice
204(1)
9.3.4 AID deficiency and autoimmunity in humans
205(1)
9.4 Conclusion
206(1)
9.5 Acknowledgements
207(1)
9.6 References
207(8)
Index 215
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