ArticleProceedings of the National Academy of Sciences of the United States of America2008
B-cell receptor activation inhibits AID expression through calmodulin inhibition of E-proteins.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 47 citations in OpenAlex.
- An attempt to explain what intrinsically disordered TCF4 does in its spare time when PTHS-related mutations prevent it from doing its job.Cell communication and signaling : CCS · 2025Review
- The molecular properties of the bHLH TCF4 protein as an intrinsically disordered hub transcription factor.Cell communication and signaling : CCS · 2025Article
- Integrated signaling and transcriptome analysis reveals Src family kinase individualities and novel pathways controlled by their constitutive activity.Frontiers in immunology · 2023Article
- USP10 regulates B cell response to SARS-CoV-2 or HIV-1 nanoparticle vaccines through deubiquitinating AID.Signal transduction and targeted therapy · 2022Article
- Helix-Loop-Helix Proteins in Adaptive Immune Development.Frontiers in immunology · 2022Review
- AID in Chronic Lymphocytic Leukemia: Induction and Action During Disease Progression.Frontiers in oncology · 2021Review
- MUC1 oncoprotein mitigates ER stress via CDA-mediated reprogramming of pyrimidine metabolism.Oncogene · 2020Article
- Myelin-specific multiple sclerosis antibodies cause complement-dependent oligodendrocyte loss and demyelination.Acta neuropathologica communications · 2017Article
- Molecular Mechanisms of Transcription Factor 4 in Pitt Hopkins Syndrome.Current genetic medicine reports · 2017Article
- Transcription factor 4 (TCF4) and schizophrenia: integrating the animal and the human perspective.Cellular and molecular life sciences : CMLS · 2014Review
- Activation-induced Cytidine Deaminase in B Cell Immunity and Cancers.Immune network · 2012Article
- Activation-induced cytidine deaminase (AID) linking immunity, chronic inflammation, and cancer.Cancer immunology, immunotherapy : CII · 2012Review
- A p53 axis regulates B cell receptor-triggered, innate immune system-driven B cell clonal expansion.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
- Functions and regulation of the APOBEC family of proteins.Seminars in cell & developmental biology · 2012Review
- HEB in the spotlight: Transcriptional regulation of T-cell specification, commitment, and developmental plasticity.Clinical & developmental immunology · 2012Review
- The B lineage transcription factor E2A regulates apoptosis in chronic lymphocytic leukemia (CLL) cells.International immunology · 2011Article
- Article
- AID and somatic hypermutation.Advances in immunology · 2010Review
- Induction of TLR4-target genes entails calcium/calmodulin-dependent regulation of chromatin remodeling.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
- Calcium regulation of myogenesis by differential calmodulin inhibition of basic helix-loop-helix transcription factors.Molecular biology of the cell · 2008Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Upon encountering antigens, B-lymphocytes can adapt to produce a highly specific and potent antibody response. Somatic hypermutation, which introduces point mutations in the variable regions of antibody genes, can increase the affinity for antigen, and antibody effector functions can be altered by class switch recombination (CSR), which changes the expressed constant region exons. Activation-induced cytidine deaminase (AID) is the mutagenic antibody diversification enzyme that is essential for both somatic hypermutation and CSR. The mutagenic AID enzyme has to be tightly controlled. Here, we show that engagement of the membrane-bound antibodies of the B-cell receptor (BCR), which signals that good antibody affinity has been reached, inhibits AID gene expression and that calcium (Ca(2+)) signaling is essential for this inhibition. Moreover, we show that overexpression of the Ca(2+) sensor protein calmodulin inhibits AID gene expression, and that the transcription factor E2A is required for regulation of the AID gene by the BCR. E2A mutated in the binding site for calmodulin, and thus showing calmodulin-resistant DNA binding, makes AID expression resistant to the inhibition through BCR activation. Thus, BCR activation inhibits AID gene expression through Ca(2+)/calmodulin inhibition of E2A.
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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.