Regulation of B cell differentiation by the ubiquitin-binding protein TAX1BP1.
Regulation of B cell differentiation by the ubiquitin-binding protein TAX1BP1.
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DOI：
10.1038/srep31266
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发表时间：
2016-08-12
影响因子：
4.6
通讯作者：
Yanagi S
中科院分区：
文献类型：
--
作者：
Matsushita N;Suzuki M;Ikebe E;Nagashima S;Inatome R;Asano K;Tanaka M;Matsushita M;Kondo E;Iha H;Yanagi S
税收蛋白1（税务1BP1）是一种泛素结合蛋白，限制了核因子-κB（NF-κB）激活，并促进了异常炎症的终止评估税务1bp1在B细胞中的功能，我们建立了税务1BP1缺陷DT40 B细胞，这些dt40 B细胞超反应至CD40诱导的细胞外信号调节激酶（ERK）激活信号传导，暴露于延长和夸张的ERK磷酸化并显示出增强的B淋巴细胞诱导的B淋巴细胞诱导的Blymphopyte-trompy诱导的BLymphopyte-promplocyte诱导的诱导成熟蛋白1（Blimp-1；转录因子诱导的浆细胞分化）表达ERK依赖性。组成和抗原特异性抗体的产生。
Tax1-binding protein 1 (TAX1BP1) is a ubiquitin-binding protein that restricts nuclear factor-κB (NF-κB) activation and facilitates the termination of aberrant inflammation. However, its roles in B-cell activation and differentiation are poorly understood. To evaluate the function of TAX1BP1 in B cells, we established TAX1BP1-deficient DT40 B cells that are hyper-responsive to CD40-induced extracellular signal-regulated kinase (ERK) activation signaling, exhibit prolonged and exaggerated ERK phosphorylation and show enhanced B lymphocyte-induced maturation protein 1 (Blimp-1; a transcription factor inducing plasma cell differentiation) expression that is ERK-dependent. Furthermore, TAX1BP1-deficient cells exhibit significantly decreased surface IgM expression and increased IgM secretion. Moreover, TAX1BP1-deficient mice display reduced germinal center formation and antigen-specific antibody production. These findings show that TAX1BP1 restricts ERK activation and Blimp-1 expression and regulates germinal center formation.