Regulated localization of an AID complex with E2A, PAX5 and IRF4 at the Igh locus

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• 作者：Jannek Hauser ; Christine Grundströ ; m ; Ramesh Kumar ; Thomas Grundströ ; m ; ^{Thomas.Grundstrom@umu.se}
• 关键词：CSR ; class switch recombination ; SH ; Somatic hypermutation ; AID ; activation-induced cytidine deaminase ; PLA ; proximity ligation assay ; BCR ; B-cell receptor ; CaM ; calmodulin
• 刊名：Molecular Immunology
• 出版年：2016
• 出版时间：December 2016
• 年：2016
• 卷：80
• 期：Complete
• 页码：78-90
• 全文大小：3392 K
• 卷排序：80

文摘

Defective calmodulin inhibition of E2A reduces CSR to IgE by BCR, IL4 plus CD40L. AID is in a complex with E2A, PAX5 and IRF4 on key sequences of the Igh locus. The CSR complex is redistributed on the Igh locus through calmodulin binding to E2A. AID binds directly to the bHLH domain of E2A and to the PD domain of PAX5.