DNA Deamination and the Immune System: Aid in Health and Disease

Author(s): Sebastian Fugmann, Marilyn Diaz, Nina Papavasiliou

Date: Format: pdf Language: English ISBN/ASIN: 1848165927
Pages: OCR: Quality: ISBN13:
Uploader: Upload Date: 3/9/2019 1:06:01 PM

1. Introduction. 1.1. Discovery of AID. 1.2. Current style of AID serve as. 1.3. Open questions. 1.4. A unifying style for AID serve as. 1.5. Acknowledgements. 1.6. References 2. Switch areas, chromatin accessibility and AID focused on. 2.1. Introduction. 2.2. Transcriptional components resolve long-range legislation of CSR. 2.3. Cis-regulatory components as recruiters for AID. 2.4. Transcription and accessibility to AID assault. 2.5. S area collection determines chromatin accessibility. 2.6. AID-induced mutation distribution and transcription. 2.7. Processing of GLTs and the advent of AID-induced mutations. 2.8. Future instructions. 2.9. Acknowledgements. 2.10. References 3. Cis-regulatory components that concentrate on AID to immunoglobulin loci. 3.1. Introduction. 3.2. Targeting through Ig promoters – Are prime ranges of transcription all there may be to it? 3.3. SHM focused on components in Ig mild chain loci. 3.4. Targeting components within the murine IgH locus. 3.5. Outlook. 3.6. Acknowledgements. 3.7. References 4. Partners in variety : The seek for AID co-factors. 4.1. Introduction and evaluate. 4.2. Compartmentalization of AID. 4.3. The C-terminal area of AID. 4.4. Targeting AID within the context of cotranscriptional pre-mRNA splicing through CTNNBL1. 4.5. Replication Protein A (RPA). 4.6. Protein kinase A (PKA) and legislation of AID task through phosphorylation. 4.7. Recruitment of PKA to change area sequences. 4.8. Concluding remarks. 4.9. Acknowledgements. 4.10. References 5. Resolution of AID lesions in school transfer recombination. 5.1. Introduction. 5.2. Conversion of AID lesions to double-strand DNA breaks. 5.3. Repair of double-strand DNA breaks in school transfer recombination. 5.4. Concluding feedback and long term questions. 5.5. References 6. Error-prone and error-free answer of AID lesions in SHM. 6.1. Introduction. 6.2. Direct replication around the Uracil : G/C transitions. 6.3. UNG2-dependent SHM throughout AP websites : G/C transversions and transitions. 6.4. MutS[symbol]-dependent SHM at MMR gaps : A/T mutations. 6.5. UNG-dependent A/T mutations. 6.6. Half of all G/C transversions require MutS[symbol] and UNG2. 6.7. Translesion synthesis DNA polymerases. 6.8. Regulating TLS through ubiquitylation of PCNA. 6.9. SHM : Mutagenesis at template A/T calls for PCNA-Ub. 6.10. PCNA-Ub-independent G/C transversions right through SHM. 6.11. MutS[symbol] and UNG2 don’t compete right through SHM : Cell cycle and error-free restore. 6.12. Aberrant focused on of AID and error-free restore of AID-induced uracils. 6.13. Acknowledgements. 6.14. References 7. Regulatory mechanisms of AID serve as. 7.1. Introduction. 7.2. Transcriptional legislation of AID gene expression. 7.3. Posttranscriptional legislation of mRNA ranges. 7.4. Posttranslational keep an eye on of AID. 7.5. Integration of AID legislation : The remarkable questions. 7.6. Acknowledgements. 7.7. References 8. AID in immunodeficiency and most cancers. 8.1. AID and immunodeficiencies. 8.2. AID and most cancers. 8.3. Acknowledgements. 8.4. References 9. AID in growing older and in autoimmune illness. 9.1. AID and growing older. 9.2. Aging decreases humoral immune responses. 9.3. AID in autoimmunity. 9.4. Conclusion. 9.5. Acknowledgements. 9.6. References
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