ArticleProceedings of the National Academy of Sciences of the United States of America2003
Somatic hypermutation of the B cell receptor genes B29 (Igbeta, CD79b) and mb1 (Igalpha, CD79a).
Article in Proceedings of the National Academy of Sciences of the United States of America, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed, 140 citations in OpenAlex.
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- Molecular classification and therapeutics in diffuse large B-cell lymphoma.Frontiers in molecular biosciences · 2023Review
- A new nomogram model for prognosis of hepatocellular carcinoma based on novel gene signature that regulates cross-talk between immune and tumor cells.BMC cancer · 2022Article
- Structure-Based Design of First-Generation Small Molecule Inhibitors Targeting the Catalytic Pockets of AID, APOBEC3A, and APOBEC3B.ACS pharmacology & translational science · 2021Article
- Identification of the atypically modified autoantigen Ars2 as the target of B-cell receptors from activated B-cell-type diffuse large B-cell lymphoma.Haematologica · 2021Article
- Review
- Genetic alterations and their clinical implications in DLBCL.Nature reviews. Clinical oncology · 2019Review
- De novo gene mutations in normal human memory B cells.Leukemia · 2019Article
- Signaling control of antibody isotype switching.Advances in immunology · 2019Review
- A broad atlas of somatic hypermutation allows prediction of activation-induced deaminase targets.The Journal of experimental medicine · 2018Article
- Review
- Metabolic Reprogramming of Non-Hodgkin's B-Cell Lymphomas and Potential Therapeutic Strategies.Frontiers in oncology · 2018Review
- Activation-induced cytidine deaminase targets SUV4-20-mediated histone H4K20 trimethylation to class-switch recombination sites.Scientific reports · 2017Article
- Differential regulation of mTOR signaling determines sensitivity to AKT inhibition in diffuse large B cell lymphoma.Oncotarget · 2016Article
- AID targeting: old mysteries and new challenges.Trends in immunology · 2015Review
- RNA Exosome Regulates AID DNA Mutator Activity in the B Cell Genome.Advances in immunology · 2015Review
- AID/APOBEC deaminases and cancer.Oncoscience · 2015Review
- The majority of human memory B cells recognizing RhD and tetanus resides in IgM+ B cells.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- Generation and repair of AID-initiated DNA lesions in B lymphocytes.Frontiers of medicine · 2014Review
- Epigenetic function of activation-induced cytidine deaminase and its link to lymphomagenesis.Frontiers in immunology · 2014Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Somatic hypermutation (SHM), coupled to selection by antigen, generates high-affinity antibodies during germinal center (GC) B cell maturation. SHM is known to affect Bcl6, four additional oncogenes in diffuse large B cell lymphoma, and the CD95Fas gene and is regarded as a major mechanism of B cell tumorigenesis. We find that mutations in the genes encoding the B cell receptor (BCR) accessory proteins B29 (Igbeta, CD79b) and mb1 (Igalpha, CD79a) occur as often as Ig genes in a broad spectrum of GC- and post-GC-derived malignant B cell lines, as well as in normal peripheral B cells. These B29 and mb1 mutations are typical SHM consisting largely of single nucleotide substitutions targeted to hotspots. The B29 and mb1 mutations appear at frequencies similar to those of other non-Ig genes but lower than Ig genes. The distribution of mb1 mutations followed the characteristic pattern found in Ig and most non-Ig genes. In contrast, B29 mutations displayed a bimodal distribution resembling the CD95Fas gene, in which promoter distal mutations conferred resistance to apoptosis. Distal B29 mutations in the cytoplasmic domain may contribute to B cell survival by limiting BCR signaling. B29 and mb1 are mutated in a much broader spectrum of GC-derived B cells than any other known somatically hypermutated non-Ig gene. This may be caused by the common cis-acting regulatory sequences that control the requisite coexpression of the B29, mb1, and Ig chains in the BCR.
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