ArticleThe Journal of experimental medicine2010
Regulation of activation-induced deaminase stability and antibody gene diversification by Hsp90.
Article in The Journal of experimental medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 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
55 citing papers in PubMed, 103 citations in OpenAlex.
- A Viral Protein Antagonist for Both AID and APOBEC3.Viruses · 2026Review
- Mechanism and regulation of secondary immunoglobulin diversification.Cell cycle (Georgetown, Tex.) · 2023Review
- POGZ promotes homology-directed DNA repair in an HP1-dependent manner.EMBO reports · 2022Article
- USP10 regulates B cell response to SARS-CoV-2 or HIV-1 nanoparticle vaccines through deubiquitinating AID.Signal transduction and targeted therapy · 2022Article
- Activation induced cytidine deaminase: An old friend with new faces.Frontiers in immunology · 2022Review
- Small Molecule Inhibitors of Activation-Induced Deaminase Decrease Class Switch Recombination in B Cells.ACS pharmacology & translational science · 2021Article
- Single Cell Label-Free Probing of Chromatin Dynamics During B Lymphocyte Maturation.Frontiers in cell and developmental biology · 2021Article
- AID in Chronic Lymphocytic Leukemia: Induction and Action During Disease Progression.Frontiers in oncology · 2021Review
- The Role of APOBECs in Viral Replication.Microorganisms · 2020Review
- Activation-induced cytidine deaminase: in sickness and in health.Journal of cancer research and clinical oncology · 2020Review
- Optimized high-fidelity 3DPCR to assess potential mitochondrial targeting by activation-induced cytidine deaminase.FEBS open bio · 2020Article
- AID modulates carcinogenesis network via DNA demethylation in bladder urothelial cell carcinoma.Cell death & disease · 2019Article
- Signaling control of antibody isotype switching.Advances in immunology · 2019Review
- Linking Endoplasmic Reticular Stress and Alternative Splicing.International journal of molecular sciences · 2018Review
- A licensing step links AID to transcription elongation for mutagenesis in B cells.Nature communications · 2018Article
- Transcription factor YY1 can control AID-mediated mutagenesis in mice.European journal of immunology · 2018Article
- Diversity in the Cow Ultralong CDR H3 Antibody Repertoire.Frontiers in immunology · 2018Review
- Epigenomic Modifications Mediating Antibody Maturation.Frontiers in immunology · 2018Review
- Heat shock proteins stimulate APOBEC-3-mediated cytidine deamination in the hepatitis B virus.The Journal of biological chemistry · 2017Article
- A Novel Regulator of Activation-Induced Cytidine Deaminase/APOBECs in Immunity and Cancer: Schrödinger's CATalytic Pocket.Frontiers in immunology · 2017Review
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 1 country.
Funding
Abstract
Activation-induced deaminase (AID) is the mutator enzyme that initiates somatic hypermutation and isotype switching of the antibody genes in B lymphocytes. Undesired byproducts of AID function are oncogenic mutations. AID expression levels seem to correlate with the extent of its physiological and pathological functions. In this study, we identify AID as a novel Hsp90 (heat shock protein 90 kD) client. We find that cytoplasmic AID is in a dynamic equilibrium regulated by Hsp90. Hsp90 stabilizes cytoplasmic AID, as specific Hsp90 inhibition leads to cytoplasmic polyubiquitination and proteasomal degradation of AID. Consequently, Hsp90 inhibition results in a proportional reduction in antibody gene diversification and off-target mutation. This evolutionarily conserved regulatory mechanism determines the functional steady-state levels of AID in normal B cells and B cell lymphoma lines. Thus, Hsp90 assists AID-mediated antibody diversification by stabilizing AID. Hsp90 inhibition provides the first pharmacological means to down-regulate AID expression and activity, which could be relevant for therapy of some lymphomas and leukemias.
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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.