Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
10767058 | Biochemical and Biophysical Research Communications | 2007 | 6 Pages |
Abstract
Activation-induced cytidine deaminase (AID) is an inducible gene that plays a critical role in Ig class switch recombination and somatic hypermutation in B cells. We explored the mechanisms by which IL-4 induces AID expression in mouse B cells. IL-4 increased AID expression and over-expression of Stat6 further augmented IL-4-induced promoter activity. The involvement of Stat6 in the promoter activity was confirmed using ChIP assays and site-directed mutagenesis. Treatment with H89, a PKA inhibitor, markedly decreased IL-4-induced AID expression, and over-expression of CREB enhanced it. These results indicate that Stat6 and PKA/CREB are involved in IL-4-induced AID expression. The relevance of these signal transducing molecules was verified using the TGFβ1-induced IgA isotype switching model. Our results indicate that IL-4, through Stat6 and PKA/CREB, induces AID expression leading to Ig isotype switching event.
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Authors
Ran Ju Kim, Hyun-A Kim, Jae-Bong Park, Seok-Rae Park, Seong-Hyun Jeon, Goo-Young Seo, Dong-Wan Seo, Su Ryeon Seo, Gie-Taek Chun, Nam-Soo Kim, Se-Won Yie, Woo-Hyeon Byeon, Pyeung-Hyeun Kim,