ゲノムに抗体の記憶を刻むAID蛋白質遺伝子(Aicda)の発現制御機構-何故非Bリンパ球にAIDが発現し、癌化が起こり得るのか-を解明しました. 京都大学プレスリリース. 2009-12-07. http://www.kyoto-u.ac.jp/ja/news_data/h/h1/news6/2009/091207_1.htmActivation-induced cytidine deaminase (AID) is essential for the generation of antibody memory but also targets oncogenes, among other genes. We investigated the transcriptional regulation of Aicda (which encodes AID) in class switch–inducible CH12F3-2 cells and found that Aicda regulation involved derepression by several layers of positive regulatory elements in addition to the 5′ promoter region. The 5′ upstream region contained functional motifs for the response to signaling by cytokines, the ligand for the costimulatory molecule CD40 or stimuli that activated the transcription factor NF-κB. The first intron contained functional binding elements for the ubiquitous silencers c-Myb and E2f and for the B cell–specific activator Pax5 and E-box-binding proteins. Our results show that Aicda is regulated by the balance between B cell–specific and stimulation-responsive elements and ubiquitous silencers.