ArticleNature immunology2009
Specific recruitment of protein kinase A to the immunoglobulin locus regulates class-switch recombination.
Article in Nature immunology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 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.
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
73 citing papers in PubMed, 114 citations in OpenAlex.
- DNA secondary structures in BCL2 and MYC elicit activation-induced cytidine deaminase binding and activity.Nucleic acids research · 2026Article
- A Germinal Center Checkpoint of AIRE in B Cells Limits Antibody Diversification.bioRxiv : the preprint server for biology · 2024Article
- Mechanism and regulation of secondary immunoglobulin diversification.Cell cycle (Georgetown, Tex.) · 2023Review
- APE2 Promotes AID-Dependent Somatic Hypermutation in Primary B Cell Cultures That Is Suppressed by APE1.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Functions and consequences of AID/APOBEC-mediated DNA and RNA deamination.Nature reviews. Genetics · 2022Review
- Activation induced cytidine deaminase: An old friend with new faces.Frontiers in immunology · 2022Review
- SAMHD1-mediated dNTP degradation is required for efficient DNA repair during antibody class switch recombination.The EMBO journal · 2020Article
- AID Phosphorylation Regulates Mismatch Repair-Dependent Class Switch Recombination and Affinity Maturation.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- NME proteins regulate class switch recombination.FEBS letters · 2019Article
- AICDA drives epigenetic heterogeneity and accelerates germinal center-derived lymphomagenesis.Nature communications · 2018Article
- Targeting mutagenesis in B cells: Phosphorylation goes beyond AID association.Molecular & cellular oncology · 2018Article
- Generating and repairing genetically programmed DNA breaks during immunoglobulin class switch recombination.F1000Research · 2018Review
- Phosphorylation promotes activation-induced cytidine deaminase activity at the Myc oncogene.The Journal of experimental medicine · 2017Article
- Enzyme cycling contributes to efficient induction of genome mutagenesis by the cytidine deaminase APOBEC3B.Nucleic acids research · 2017Article
- Cutting Edge: The Transcription Factor Sox2 Regulates AID Expression in Class-Switched B Cells.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- The aryl hydrocarbon receptor controls cell-fate decisions in B cells.The Journal of experimental medicine · 2017Article
- Immuno-engineered organoids for regulating the kinetics of B-cell development and antibody production.Nature protocols · 2017Article
- AID expression increased by TNF-α is associated with class switch recombination of Igα gene in cancers.Cellular & molecular immunology · 2016Article
- PARP activation promotes nuclear AID accumulation in lymphoma cells.Oncotarget · 2016Article
- Mutations, kataegis and translocations in B cells: understanding AID promiscuous activity.Nature reviews. Immunology · 2016Review
13 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Immunoglobulin class-switch recombination (CSR) requires activation-induced cytidine deaminase (AID). Deamination of DNA by AID in transcribed switch (S) regions leads to double-stranded breaks in DNA that serve as obligatory CSR intermediates. Here we demonstrate that the catalytic and regulatory subunits of protein kinase A (PKA) were specifically recruited to S regions to promote the localized phosphorylation of AID, which led to binding of replication protein A and subsequent propagation of the CSR cascade. Accordingly, inactivation of PKA resulted in considerable disruption of CSR because of decreased AID phosphorylation and recruitment of replication protein A to S regions. We propose that PKA nucleates the formation of active AID complexes specifically on S regions to generate the high density of DNA lesions required for CSR.
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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.