ReviewJournal of clinical immunology2003
Immunoglobulin somatic hypermutation: double-strand DNA breaks, AID and error-prone DNA repair.
Review in Journal of clinical immunology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 44 citations in OpenAlex.
- Article
- Article
- Shared bias in H chain V-J pairing in naive and memory B cells.Frontiers in immunology · 2023Article
- Review
- A Protein Antagonist of Activation-Induced Cytidine Deaminase Encoded by a Complex Mouse Retrovirus.mBio · 2019Article
- Article
- Decreased mutation frequencies among immunoglobulin G variable region genes during viremic HIV-1 infection.PloS one · 2014Article
- Gene Conversion-Like Events in the Diversification of Human Rearranged IGHV3-23*01 Gene Sequences.Frontiers in immunology · 2012Article
- Article
- Endonuclease G plays a role in immunoglobulin class switch DNA recombination by introducing double-strand breaks in switch regions.Molecular immunology · 2011Article
- Estrogen receptors bind to and activate the HOXC4/HoxC4 promoter to potentiate HoxC4-mediated activation-induced cytosine deaminase induction, immunoglobulin class switch DNA recombination, and somatic hypermutation.The Journal of biological chemistry · 2010Article
- HoxC4 binds to the promoter of the cytidine deaminase AID gene to induce AID expression, class-switch DNA recombination and somatic hypermutation.Nature immunology · 2009Article
- Article
- AID- and Ung-dependent generation of staggered double-strand DNA breaks in immunoglobulin class switch DNA recombination: a post-cleavage role for AID.Molecular immunology · 2008Article
- Non-conservative homologous recombination in human B lymphocytes is promoted by activation-induced cytidine deaminase and transcription.Nucleic acids research · 2008Article
- Article
- A novel human B cell subpopulation representing the initial germinal center population to express AID.Blood · 2007Article
- DNA repair in antibody somatic hypermutation.Trends in immunology · 2006Review
- A role for the MutL mismatch repair Mlh3 protein in immunoglobulin class switch DNA recombination and somatic hypermutation.Journal of immunology (Baltimore, Md. : 1950) · 2006Article
- Biased dA/dT somatic hypermutation as regulated by the heavy chain intronic iEmu enhancer and 3'Ealpha enhancers in human lymphoblastoid B cells.Molecular immunology · 2006Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Somatic hypermutation (SHM) is critical for antibody affinity maturation and the generation of memory B cells. Somatic mutations consist mainly of single nucleotide changes with rare insertions and deletions. Such changes would be introduced during error-prone repair of lesions involving single-strand DNA breaks (SSBs) or, more likely, double-strand DNA breaks (DSBs), as DSBs occur exclusively in genes that have the potentials to undergo SHM. In the human, such genes include Ig V, BCL6, and c-MYC. In these germline genes, DSBs are blunt. In rearranged Ig V, BCL6, and translocated c-MYC genes, blunt DSBs are processed to yield resected DNA ends. This process is dependent on the expression of activation-induced cytidine deaminase (AID), which is selectively expressed upon CD40-signaling in hypermutating B cells. CD40-induced and AID-dependent free 5'- and 3'-staggered DNA ends critically channel the repair of DSBs through the homologous recombination (HR) repair pathway. During HR, the modulation of critical translesion DNA polymerases, as signaled by cross-linking of the B cell receptor (BCR) for antigen, leads to the insertions of mismatches, i.e., mutations. The nature of DSBs, the possible roles of AID in the modification of DSBs and that of the translesion DNA polymerases zeta and iota in the subsequent repair process that lead to the insertions of mutations are discussed here within the context of an integrated model of SHM.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.