ReviewFrontiers in immunology2022
Activation induced cytidine deaminase: An old friend with new faces.
Review in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed.
- Copper homeostasis dysregulation promotes malignant transformation of renal tubular epithelial cells via the ROS/NF-κB/AID signaling axis.Translational andrology and urology · 2026Article
- Unraveling the lexicon of complex mutational phenomena in human cancers.Nature cancer · 2026Review
- Infectious bursal disease virus suppresses humoral immunity via blocking antibody affinity maturation in chickens.iScience · 2026Article
- Adverse Prognostic Significance of Activation-Induced Cytidine Deaminase in Diffuse Large B-Cell Lymphoma Patients Treated With R-CHOP.Cancer reports (Hoboken, N.J.) · 2026Article
- Gene expression in immune cells infected with Orientia tsutsugamushi and the antigenic variability of 56-kDa type-specific antigen.Scientific reports · 2026Article
- PTEN-mTORC2 signaling module controls antibody isotype selection and antiviral humoral immunity.Frontiers in immunology · 2026Article
- Increasing estrogen receptor alpha-positive follicular dendritic cells in enlarged germinal centers of IgG4-related sialadenitis.Journal of clinical and experimental hematopathology : JCEH · 2025Article
- Excessive activation?induced cytidine deaminase accumulated by proteasome inhibitors rescues abnormal class switch in activated B?cell?like diffuse large B?cell lymphoma.Experimental and therapeutic medicine · 2025Article
- Histone modifications and metabolic reprogramming in tumor-associated macrophages: a potential target of tumor immunotherapy.Frontiers in immunology · 2025Review
- Epigenetic activation of JAG1 by AID contributes to metastasis of hepatocellular carcinoma.The Journal of biological chemistry · 2025Article
- Activation-induced cytidine deaminase in tertiary lymphoid structures: dual roles and implications in cancer prognosis.Frontiers in oncology · 2025Review
- Tertiary lymphoid structures in diseases: immune mechanisms and therapeutic advances.Signal transduction and targeted therapy · 2024Review
- The Past and Future of Inflammation as a Target to Cancer Prevention.Cancer prevention research (Philadelphia, Pa.) · 2024Article
- Genomic Characteristics and Its Therapeutic Implications in Breast Cancer Patients with Detectable Molecular Residual Disease.Cancer research and treatment · 2024Article
- MCT1-governed pyruvate metabolism is essential for antibody class-switch recombination through H3K27 acetylation.Nature communications · 2024Article
- Article
- Interactions between the DNA Damage Response and the Telomere Complex in Carcinogenesis: A Hypothesis.Current issues in molecular biology · 2023Review
- Chronic inflammation and the hallmarks of aging.Molecular metabolism · 2023Review
- Potential Pathogenic Impact of Cow's Milk Consumption and Bovine Milk-Derived Exosomal MicroRNAs in Diffuse Large B-Cell Lymphoma.International journal of molecular sciences · 2023Review
- Generation and Next-Generation Sequencing-Based Characterization of a Large Human Combinatorial Antibody Library.International journal of molecular sciences · 2023Article
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Activation induced cytidine deaminase (AID) protein is a member of APOBEC family. AID converts cytidine to uracil, which is a key step for somatic hypermutation (SHM) and class switch recombination (CSR). AID also plays critical roles in B cell precursor stages, removing polyreactive B cells from immune repertoire. Since the main function of AID is inducing point mutations, dysregulation can lead to increased mutation load, translocations, disturbed genomic integrity, and lymphomagenesis. As such, expression of AID as well as its function is controlled strictly at various molecular steps. Other members of the APOBEC family also play crucial roles during carcinogenesis. Considering all these functions, AID represents a bridge, linking chronic inflammation to carcinogenesis and immune deficiencies to autoimmune manifestations.
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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.