ReviewSeminars in immunology2012
Combinatorial mechanisms regulating AID-dependent DNA deamination: interacting proteins and post-translational modifications.
Review in Seminars in immunology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 29 citations in OpenAlex.
- Immunoglobulin class-switch recombination: Mechanism, regulation, and related diseases.MedComm · 2024Review
- Generation and Next-Generation Sequencing-Based Characterization of a Large Human Combinatorial Antibody Library.International journal of molecular sciences · 2023Article
- TRAF3 Acts as a Checkpoint of B Cell Receptor Signaling to Control Antibody Class Switch Recombination and Anergy.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- Endonuclease and redox activities of human apurinic/apyrimidinic endonuclease 1 have distinctive and essential functions in IgA class switch recombination.The Journal of biological chemistry · 2019Article
- Single Cell Imaging of Nuclear Architecture Changes.Frontiers in cell and developmental biology · 2019Article
- Signaling control of antibody isotype switching.Advances in immunology · 2019Review
- Transcription factor YY1 can control AID-mediated mutagenesis in mice.European journal of immunology · 2018Article
- PARP activation promotes nuclear AID accumulation in lymphoma cells.Oncotarget · 2016Article
- AID targeting: old mysteries and new challenges.Trends in immunology · 2015Review
- HSP90 inhibitors decrease AID levels and activity in mice and in human cells.European journal of immunology · 2015Article
- Consecutive interactions with HSP90 and eEF1A underlie a functional maturation and storage pathway of AID in the cytoplasm.The Journal of experimental medicine · 2015Article
- Epigenetic Codes Programing Class Switch Recombination.Frontiers in immunology · 2015Review
- AID-induced remodeling of immunoglobulin genes and B cell fate.Oncotarget · 2014Review
- Regulation of immunoglobulin class-switch recombination: choreography of noncoding transcription, targeted DNA deamination, and long-range DNA repair.Advances in immunology · 2014Review
- Mouse endometrial stromal cells and progesterone inhibit the activation and regulate the differentiation and antibody secretion of mouse B cells.International journal of clinical and experimental pathology · 2014Article
- A DNA break- and phosphorylation-dependent positive feedback loop promotes immunoglobulin class-switch recombination.Nature immunology · 2013Article
- Polyclonal hyper-IgE mouse model reveals mechanistic insights into antibody class switch recombination.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- The AID-induced DNA damage response in chromatin.Molecular cell · 2013Review
- Regulation of AID, the B-cell genome mutator.Genes & development · 2013Review
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Protective humoral immune responses result from immunoglobulin (Ig) diversification reactions that proceed through programmed DNA double-strand breaks and mutations in developing or mature B cells. While primary Ig diversity is dependent on V(D)J recombination and the RAG proteins, secondary diversification is achieved through class switch recombination (CSR) and somatic hypermutation (SHM), which require AID (activation induced deaminase). Because aberrant AID activity can result in mutations in non-Ig loci and DNA translocations between the Ig locus and non-Ig genes, the activity of AID must be stringently regulated. AID mRNA expression is regulated transcriptionally by cytokine stimulation and post-transcriptionally by miRNAs. AID activity is regulated by post-translational modifications, subcellular localization, and interaction with other proteins. All of these molecular mechanisms have evolved to specifically induce AID-dependent mutations and DNA double-strand breaks at the Ig loci to promote maximal Ig gene diversification while limiting the access of this mutator to non-Ig regions.
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What OpenQuestion holds
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.