miR-181b negatively regulates activation-induced cytidine deaminase in B cells.
miR-181b negatively regulates activation-induced cytidine deaminase in B cells.
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DOI：
10.1084/jem.20080579
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发表时间：
2008-09-29
期刊：
影响因子：
--
通讯作者：
Ramiro AR
中科院分区：
文献类型：
--
作者：
de Yébenes VG;Belver L;Pisano DG;González S;Villasante A;Croce C;He L;Ramiro AR
Activated B cells reshape their primary antibody repertoire after antigen encounter by two molecular mechanisms: somatic hypermutation (SHM) and class switch recombination (CSR). SHM and CSR are initiated by activation-induced cytidine deaminase (AID) through the deamination of cytosine residues on the immunoglobulin loci, which leads to the generation of DNA mutations or double-strand break intermediates. As a bystander effect, endogenous AID levels can also promote the generation of chromosome translocations, suggesting that the fine tuning of AID expression may be critical to restrict B cell lymphomagenesis. To determine whether microRNAs (miRNAs) play a role in the regulation of AID expression, we performed a functional screening of an miRNA library and identified miRNAs that regulate CSR. One such miRNA, miR-181b, impairs CSR when expressed in activated B cells, and results in the down-regulation of AID mRNA and protein levels. We found that the AID 3′ untranslated region contains multiple putative binding sequences for miR-181b and that these sequences can be directly targeted by miR-181b. Overall, our results provide evidence for a new regulatory mechanism that restricts AID activity and can therefore be relevant to prevent B cell malignant transformation.
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