Journal
CELLULAR AND MOLECULAR LIFE SCIENCES
Volume 64, Issue 5, Pages 555-565Publisher
SPRINGER BASEL AG
DOI: 10.1007/s00018-007-6434-2
Keywords
activation-induced deaminase; immunoglobulin; somatic hypermutation; class switch recombination; gene conversion
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Funding
- NIGMS NIH HHS [GM41712, R01 GM039799, R01 GM041712, GM39799] Funding Source: Medline
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R01GM039799, R01GM041712] Funding Source: NIH RePORTER
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Expressed immunoglobulin (Ig) genes undergo alterations in sequence and genomic structure in order to optimize antibody function. A single B cellspecific factor, activation-induced deaminase (AID), initiates these changes by deamination of cytosine to uracil. Uracil in DNA is encountered commonly, and conserved pathways are responsible for its faithful repair. However, at the Ig loci of B cells, AID-initiated damage is processed to produce three distinct outcomes: somatic hypermutation, class switch recombination and gene conversion. This review focuses on the role of AID in Ig gene diversification, emphasizing how AID functions within the mechanism of the Ig gene diversification pathway; and highlights open questions for future research, particularly the most provocative current question: what makes a gene a target for AID-initiated mutagenesis?
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