miR-181b negatively regulates activation-induced cytidine deaminase in B cells

摘要: Activated B cells reshape their primary antibody repertoire after antigen encounter by two molecular mechanisms: somatic hypermutation (SHM) and class switch recombination (CSR). SHM CSR are initiated activation-induced cytidine deaminase (AID) through the deamination of cytosine residues on immunoglobulin loci, which leads to generation DNA mutations or double-strand break intermediates. As a bystander effect, endogenous AID levels can also promote chromosome translocations, suggesting that fine tuning expression may be critical restrict cell lymphomagenesis. To determine whether microRNAs (miRNAs) play role in regulation expression, we performed functional screening an miRNA library identified miRNAs regulate CSR. One such miRNA, miR-181b, impairs when expressed activated cells, results down-regulation mRNA protein levels. We found 3′ untranslated region contains multiple putative binding sequences for miR-181b these directly targeted miR-181b. Overall, our provide evidence new regulatory mechanism restricts activity therefore relevant prevent malignant transformation.