ReviewPhilosophical transactions of the Royal Society of London. Series B, Biological sciences2001
Somatic hypermutation of immunoglobulin and non-immunoglobulin genes.
Review in Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
18 citing papers in PubMed.
- AID function in somatic hypermutation and class switch recombination.Acta biochimica et biophysica Sinica · 2022Review
- Signaling control of antibody isotype switching.Advances in immunology · 2019Review
- AID targeting: old mysteries and new challenges.Trends in immunology · 2015Review
- Disruption of Transcriptional Coactivator Sub1 Leads to Genome-Wide Re-distribution of Clustered Mutations Induced by APOBEC in Active Yeast Genes.PLoS genetics · 2015Article
- AID-initiated DNA lesions are differentially processed in distinct B cell populations.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- Generation and repair of AID-initiated DNA lesions in B lymphocytes.Frontiers of medicine · 2014Review
- Transcription-associated mutagenesis.Annual review of genetics · 2014Review
- The role of activation-induced deaminase in antibody diversification and genomic instability.Immunologic research · 2013Review
- Attracting AID to targets of somatic hypermutation.The Journal of experimental medicine · 2010Article
- Post-translational regulation of activation-induced cytidine deaminase.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2009Review
- Detection of chromatin-associated single-stranded DNA in regions targeted for somatic hypermutation.The Journal of experimental medicine · 2007Article
- The transcription elongation complex directs activation-induced cytidine deaminase-mediated DNA deamination.Molecular and cellular biology · 2006Article
- The very 5' end and the constant region of Ig genes are spared from somatic mutation because AID does not access these regions.The Journal of experimental medicine · 2005Article
- AID-dependent generation of resected double-strand DNA breaks and recruitment of Rad52/Rad51 in somatic hypermutation.Immunity · 2003Article
- Genetic variants of NHEJ DNA ligase IV can affect the risk of developing multiple myeloma, a tumour characterised by aberrant class switch recombination.Journal of medical genetics · 2002Article
- Negative autoregulation of BCL-6 is bypassed by genetic alterations in diffuse large B cell lymphomas.Proceedings of the National Academy of Sciences of the United States of America · 2002Article
- The configuration of the immunoglobulin genes in B cell chronic lymphocytic leukemia.Leukemia · 2002Review
- Somatic immunoglobulin hypermutation.Current opinion in immunology · 2002Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
Somatic hypermutation (SHM) of immunoglobulin (Ig) genes is a highly specific mechanism restricted to B lymphocytes during only a few cell generations. Data presented here suggest that transcription of the target genes is required, but not sufficient for SHM. Presumably, cis-acting elements, such as those present in the Ig enhancers, are required to target a mutator factor (MuF) to Ig and human BCL-6 genes. It is postulated that the MuF travels with the transcribing RNA polymerase and is deposited on the target gene when the polymerase pauses. Point mutations, and rare deletions and insertions, are created by the combined actions of MuF and certain DNA polymerases. A subset of the mutations is corrected during SHM by DNA mismatch repair.
Indexed as
Identifiers
What OpenQuestion holds
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.