ArticleEuropean journal of immunology2008
Identification of murine B cell lines that undergo somatic hypermutation focused to A:T and G:C residues.
Article in European journal of immunology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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.
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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.
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Who cites it
6 citing papers in PubMed, 16 citations in OpenAlex.
- Knockdown of USF1 and USF2 drives prolonged changes in the gene expression response of M12-5B3 cells to DNA damage.PloS one · 2025Article
- Review
- DNA Methylation, Deamination, and Translesion Synthesis Combine to Generate Footprint Mutations in Cancer Driver Genes in B-Cell Derived Lymphomas and Other Cancers.Frontiers in genetics · 2021Article
- Effects of prostaglandin E2 on p53 mRNA transcription and p53 mutagenesis during T-cell-independent human B-cell clonal expansion.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2014Article
- Article
- Low-fidelity DNA synthesis by human DNA polymerase theta.Nucleic acids research · 2008Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 5 institutions in 2 countries.
Funding
Abstract
Activation-induced deaminase (AID) is the master regulator of class switch recombination (CSR) and somatic hypermutation (SHM), but the mechanisms regulating AID function are obscure. The differential pattern of switch plasmid activity in three IgM(+)/AID(+) and two IgG(+)/AID(+) B cell lines prompted an analysis of global gene expression to discover the origin of these cells. Gene profiling suggested that the IgG(+)/AID(+) B cell lines derived from germinal center B cells. Analysis of SHM potential demonstrates that the IgVkappa domains are inducibly diversified at high rate during in vitro culture. The mutation spectra focused to A:T base pairs, revealing a component of the hypermutation program that occurs preferentially during phase 2 of SHM. The A:T error spectra were analyzed and were not characteristic of polymerase eta activity. A differential pattern of three consensus motifs used for A:T base substitutions was observed in WT and Poleta-, Msh2- and Msh6-deficient B cells. Strikingly, mutations in our B cell lines recapitulated the mutable motif profile for Poleta and Msh2 deficiency, respectively, and suggest that an additional pathway for the generation of A:T mutations in SHM is conserved in mouse and human.
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Registered trials
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