KyoT3, an isoform of murine FHL1, associates with the transcription factor RBP-J and represses the RBP-J-mediated transactivation
KyoT3, an isoform of murine FHL1, associates with the transcription factor RBP-J and represses the RBP-J-mediated transactivation
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KyoT3 是鼠 FHL1 的同种型，与转录因子 RBP-J 相关并抑制 RBP-J 介导的反式激活
DOI：
10.1016/j.bbagrm.2008.08.001
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发表时间：
2008-12-01
影响因子：
4.7
通讯作者：
Han, Hua
中科院分区：
文献类型：
--
作者：
Liang, Liang;Zhang, Hong-Wei;Han, Hua
以前，我们已经表明，KyoT 2，一个亚型的四个半LIM结构域蛋白1（FHL 1），调制Notch信号通过抑制RBP-J介导的反式激活。在这项研究中，我们研究了FHL 1，KyoT 3的另一种异forrin对RBP-J依赖性启动子的反式激活的影响。我们发现KyoT 3在多种组织中广泛表达。通过构建绿色荧光蛋白融合蛋白，我们发现KyoT 3优先定位于细胞核。KyoT 3与RBP-J相互作用，如通过免疫共沉淀测定所示。此外，我们通过报告分析证明KyoT 3抑制RBP-J依赖性启动子的反式激活，该启动子被Notch细胞内结构域和EB病毒核抗原2（EB病毒编码的癌蛋白）激活。这些结果表明Notch信号通路的多元素控制，这对于发育中的细胞分化至关重要。(C)2008 Elsevier B. V.保留所有权利。
Previously, we have shown that KyoT2, an isoform of the four and a half LIM domain protein 1 (FHL1), modulates Notch signaling via repressing RBP-J-mediated transactivation. In this study, we investigated the effect of another isoforrin of FHL1, KyoT3, on transactivation of a RBP-J-dependent promoter. We found that KyoT3 was expressed widely in a variety of tissues. By constructing EGFP fusion proteins, we showed that KyoT3 locates preferentially in nucleus. KyoT3 interacted with RBP-J, as shown by co-immunoprecipitation assays. Moreover, we demonstrated by a reporter assay that KyoT3 repressed transactivation of a RBP-J-dependent promoter, which was activated by both the Notch intracellular domain and Epstein-Barr virus nuclear antigen 2, an EB virus-encoded oncoprotein. These results suggest a multi-elemental control of the Notch signaling pathway, which is critical for cell differentiation in development. (C) 2008 Elsevier B.V. All rights reserved.