Protein kinase Cθ gene expression is oppositely regulated by GCN5 and EBF1 in immature B cells.
Protein kinase Cθ gene expression is oppositely regulated by GCN5 and EBF1 in immature B cells.
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在未成熟 B 细胞中，蛋白激酶 Cθ 基因表达受到 GCN5 和 EBF1 相反的调节。
DOI：
10.1016/j.febslet.2014.03.025
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发表时间：
2014
期刊：
影响因子：
3.5
通讯作者：
Nakayama T
中科院分区：
文献类型：
--
作者：
Kikuchi H;Nakayama M;Kuribayashi F;Imajoh-Ohmi S;Nishitoh H;Takami Y;Nakayama T
在本研究中，我们发现GCN5和早期B细胞因子1 （EBF1）在未成熟B细胞中以相反的方式参与蛋白激酶Cθ (PKCθ)基因表达的调控。DT40中gcn5缺失导致PKCθ转录剧烈下调。而EBF1缺失导致PKCθ显著上调，EBF1的再表达显著抑制PKCθ的转录。染色质免疫沉淀分析显示，GCN5结合到鸡PKCθ基因的5 ' -侧翼区域并使组蛋白H3乙酰化，EBF1结合到假定的EBF1结合基序周围的基因的5 ' -侧翼区域。
In this study, we revealed that GCN5 and early B cell factor 1 (EBF1) participate in regulation of protein kinase Cθ (PKCθ) gene expression in an opposite manner in immature B cells. GCN5-deficiency in DT40 caused drastic down-regulation of transcription of PKCθ. In contrast, EBF1-deficiency brought about remarkable up-regulation of that of PKCθ, and re-expression of EBF1 dramatically suppressed transcription of PKCθ. Chromatin immunoprecipitation assay revealed that GCN5 binds to the 5′-flanking region of the chicken PKCθ gene and acetylates histone H3, and EBF1 binds to the 5′-flanking region of the gene surrounding putative EBF1 binding motifs.