| AID Targeting in Antibody Diversity. | |
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MedLine Citation:
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PMID: 21762814 Owner: NLM Status: In-Data-Review |
Abstract/OtherAbstract:
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Antibody maturation requires class switch recombination (CSR) and somatic hypermutation (SHM), both of which are initiated by activation-induced cytidine deaminase (AID). AID deaminates cytosine residues resulting in mismatches that are differentially processed to produce double-strand breaks in Ig switch (S) regions that lead to CSR, or to point mutations in variable (V) exons resulting in SHM. Although AID was first thought to be Ig-specific, recent work indicates that it also targets a diverse group of non-Ig loci, including genes such as Bcl6 and c-myc, whose modification by AID results in lymphoma-associated mutations and translocations. Here, we review the recent literature on AID targeting and the role for transcriptional stalling in recruitment of this enzyme to Ig and non-Ig loci. We propose a model for AID recruitment based on transcriptional stalling, which reconciles several of the key features of SHM, CSR, and lymphoma-associated translocation. |
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Authors:
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Rushad Pavri; Michel C Nussenzweig |
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Publication Detail:
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Type: Journal Article |
Journal Detail:
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Title: Advances in immunology Volume: 110 ISSN: 1557-8445 ISO Abbreviation: Adv. Immunol. Publication Date: 2011 |
Date Detail:
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Created Date: 2011-07-18 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 0370425 Medline TA: Adv Immunol Country: United States |
Other Details:
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Languages: eng Pagination: 1-26 Citation Subset: IM |
Copyright Information:
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Copyright © 2011 Elsevier Inc. All rights reserved. |
Affiliation:
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Laboratory of Molecular Immunology, The Rockefeller University, New York, USA. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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