Journal
GENES & DEVELOPMENT
Volume 27, Issue 1, Pages 1-17Publisher
COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
DOI: 10.1101/gad.200014.112
Keywords
activation-induced deaminase; DNA repair; transcription; somatic mutations
Categories
Funding
- NIH [1DP2OD008651-01]
- National Institute of Allergy and Infectious Diseases (NIAID) [1R01AI099195-01A1]
- Columbia University
- Irma Hirschl Foundation
- Columbia University, Pathology Educational Fund
- NIAID [F31AI098411-01A1]
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI099195, F31AI098411] Funding Source: NIH RePORTER
- OFFICE OF THE DIRECTOR, NATIONAL INSTITUTES OF HEALTH [DP2OD008651] Funding Source: NIH RePORTER
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The mechanisms by which B cells somatically engineer their genomes to generate the vast diversity of antibodies required to challenge the nearly infinite number of antigens that immune systems encounter are of tremendous clinical and academic interest. The DNA cytidine deaminase activation-induced deaminase (AID) catalyzes two of these mechanisms: class switch recombination (CSR) and somatic hypermutation (SHM). Recent discoveries indicate a significant promiscuous targeting of this B-cell mutator enzyme genome-wide. Here we discuss the various regulatory elements that control AID activity and prevent AID from inducing genomic instability and thereby initiating oncogenesis.
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