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FEBS Lett. 2013 Aug 19;587(16):2487-92. doi: 10.1016/j.febslet.2013.06.028. Epub 2013 Jun 29.

Activation-induced cytidine deaminase auto-activates and triggers aberrant gene expression.

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Immuno-Medical Science, Division of Applied Chemistry, Graduate School of Engineering, Osaka University, 2-1 Yamadaoka, Suita, Osaka 565-0871, Japan.


DNA methylation is a well-characterized epigenetic landmark involved in transcriptional regulation; however, mechanisms underlying its regulation remain poorly characterized. Recent studies demonstrate that activation-induced cytidine deaminase (AID) is involved in active DNA demethylation. AID is aberrantly expressed in inflammation-associated cancers and generates point mutations; however, cellular disorders attributed to its demethylation function are largely unexplored. Here we demonstrate that ectopic AID expression perturbs tumor-related gene expression. AID (with Gadd45) activated a methylated paired box gene 5 (Pax5) reporter construct, and induced expression and association of endogenous Pax5 with the AID promoter, suggesting that aberrant AID expression triggers an auto-activation circuit to consolidate self-expression.


5-aza-2′-deoxycytidine; 5-aza-dC; AID; COBRA; ChIP; Demethylation; Gadd45; H-Ras; HSV-TK; Harvey rat sarcoma viral oncogene homolog; NF-κB; PGCs; Pax5; RT-PCR; SV40; TNFα; TSS; chromatin immunoprecipitation; combined bisulfite restriction analysis; growth arrest and DNA damage inducible protein 45; herpes simplex virus-thymidine kinase; nuclear factor-κB; paired box gene 5; primordial germ cells; qRT-PCR; quantitative RT-PCR; reverse transcription-polymerase chain reaction; simian vacuolating virus 40; transcription start site; tumor necrosis factor α

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