ArticleMolecular immunology2008
Expression of AID transgene is regulated in activated B cells but not in resting B cells and kidney.
Article in Molecular immunology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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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Who cites it
11 citing papers in PubMed, 26 citations in OpenAlex.
- Know your enemy or find your friend?-Induction of IgA at mucosal surfaces.Immunological reviews · 2021Review
- Deletion of Murine Gammaherpesvirus GeneJournal of virology · 2020Article
- Interplay between UNG and AID governs intratumoral heterogeneity in mature B cell lymphoma.PLoS genetics · 2020Article
- Infectious stimuli promote malignant B-cell acute lymphoblastic leukemia in the absence of AID.Nature communications · 2019Article
- The regulation of gut mucosal IgA B-cell responses: recent developments.Mucosal immunology · 2017Review
- 53BP1 Contributes toJournal of immunology (Baltimore, Md. : 1950) · 2017Article
- The RNA editing enzyme APOBEC1 induces somatic mutations and a compatible mutational signature is present in esophageal adenocarcinomas.Genome biology · 2014Article
- 53BP1 alters the landscape of DNA rearrangements and suppresses AID-induced B cell lymphoma.Molecular cell · 2013Article
- Review
- AID produces DNA double-strand breaks in non-Ig genes and mature B cell lymphomas with reciprocal chromosome translocations.Molecular cell · 2009Article
- The AID/APOBEC family of nucleic acid mutators.Genome biology · 2008Review
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
Activation-induced DNA cytidine deaminase (AID) is required for somatic hypermutation (SHM) and efficient class switch recombination (CSR) of immunoglobulin (Ig) genes. We created AID-transgenic mice that express AID ubiquitously under the control of a beta-actin promoter. When crossed with AID-/- mice, the AID-transgenic,AID-/- mice carried out SHM and CSR, showing that the AID transgenes were functional. However, the frequencies of SHM in V- and switch-regions, and CSR were reduced compared to those in a wild type AID background. Several criteria suggested that the inefficiency of SHM was due to reduced AID activity, rather than lack of recruiting error-prone DNA repair. High levels of AID mRNA were produced in resting B cells and kidney, cells that do not express AID in wild type mice. Compared with these cells, activated B cells expressed about an order of magnitude less AID mRNA suggesting that there may be a post-transcriptional mechanism that regulates AID mRNA levels in professional AID producers but not other cells. The AID protein expressed in resting B cells and kidney was phosphorylated at serine-38. Despite this modification, known to enhance AID activity, resting B cells did not undergo SHM. Apparently, the large amounts of AID in resting B cells are not targeted to Ig genes in vivo, in contrast to findings in vitro.
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