Activation-induced cytidine deaminase auto-activates and triggers aberrant gene expression
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- 作者：Tomoyasu Isobe ; Soken-Nakazawa J. Song ; Prabha Tiwari ; Hiroki Ito ; Yuki Yamaguchi ; Kazuyuki Yoshizaki
- 关键词：ChIP ; chromatin immunoprecipitation ; COBRA ; combined bisulfite restriction analysis ; Gadd45 ; growth arrest and DNA damage inducible protein 45 ; H-Ras ; Harvey rat sarcoma viral oncogene homolog ; HSV-TK ; herpes simplex virus-thymidine kinase ; NF-¦ÊB ; nuclea
- 刊名：FEBS Letters
- 出版年：2013
- 出版时间：19 August, 2013
- 年：2013
- 卷：587
- 期：16
- 页码：2487-2492
- 全文大小：718 K
文摘
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.