B cell-specific and stimulation-responsive enhancers derepress Aicda by overcoming the effects of silencers View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2010-02

AUTHORS

Thinh Huy Tran, Mikiyo Nakata, Keiichiro Suzuki, Nasim A Begum, Reiko Shinkura, Sidonia Fagarasan, Tasuku Honjo, Hitoshi Nagaoka

ABSTRACT

Activation-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-kappaB. 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. More... »

PAGES

148-154

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/ni.1829

DOI

http://dx.doi.org/10.1038/ni.1829

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1007254106

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/19966806


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