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this study reports the clinical and AID genetic features of six Iranian hyper IgM syndrome patients
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induction of AID expression would result in chromosomal translocations in the process of differentiation from B cell derived induced pluripotent stem cells.
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The distribution of AID and A3s in the epithelial cells as well as germinal centres.
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patients with AS expressed significantly higher levels of sv2 than HC. TNFi treatment restored the gene expression of the AID variants (FL, sv1, and sv2) in patients with AS. Therefore pre-existing TNFalpha-induced AID expression in B cells may play a role in the pathogenesis of AS.
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we reported high AID, low miR-181b and high miR-155 expression in de novo adult B-ALL patients. Univariate high AID or low miR-181b expression was an unfavorable prognostic factor. High AID with low miR-181b or with low miR-155 expression is better in predicting unfavorable OS than univariate factor. High AID with low miR-181b and low miR-155 expression confers worst prognosis.
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AID expression was increased in chronic lymphocytic leukemia patients with del17p or del11q who have poor prognosis.
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Results indicate activation-induced cytidine deaminase (AICDA) as a driver of epigenetic heterogeneity in B-cell lymphomas with potential significance for other tumors with aberrant expression of cytidine deaminases.
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The binding and catalytic behavior of purified AID was tested on DNA/RNA hybrid substrates bearing either random sequences or GC-rich sequences simulating Ig S regions. AID exhibited a higher affinity for binding DNA/RNA hybrid substrates made of S region sequences, than any other DNA substrates. In the absence of any other cellular processes or factors, AID itself favors binding and mutating S-region DNA/RNA hybrids.
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Expression of human AID or increased oxidative stress induces DNA breaks within human chromosomal translocation fragile zones.
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Data implicate intrinsic preference of AID for structured substrates and uncover the importance of G4 recognition and oligomerization of AID in class switch recombination.
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the His130Pro mutation allows the enzyme to retain its mutagenic activity and would prevent the interaction of AID with specific cofactors required for class switch recombination but not for somatic hypermutation. Thus, there would be no contradiction between maintaining the catalytic and mutagenic activity of AID and the presence of function defects at the genomic level.
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The authors found that the viral epsilon RNA and C-terminus of AID are required for AID-mediated hepatitis B virus RNA reduction.
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silencing of AID in human bone marrow cells skews differentiation toward myelomonocytic lineage. However, in contrast to Tet2 loss, Aid loss does not contribute to enhanced HSC self-renewal or cooperate with Flt3-ITD to induce myeloid transformation. Genome-wide transcription and differential methylation analysis uncover the critical role of Aid as a key epigenetic regulator
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AID protein is expressed in a large proportion of Philadelphia chromosome-positive B-cell acute lymphoblastic leukemia cases at levels detectable by immunohistochemistry.
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These data, showing the direct targeting and induction of functional AID by EBNA3C, suggest a novel role for EBV in the etiology of B cell cancers, including endemic Burkitt lymphoma
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These findings indicated that TNF-alpha-induced AID expression is involved with class switch recombination in cancer.
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Finnish founder allele causing HIGM2 identified.
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Structural analysis of AID protein required in immunoglobulin diversification has been reported.
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this study reports a case of growth hormone deficiency with an autosomal recessive Hyper-immunoglobulin M syndrome by phenotype and genotype, with a novel mutation in AICDA that has not been reported formerly
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We also report that AID activity results in epigenetic, genetic and genomic damage in fallopian tube epithelial cells
