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p300和ATF-2是DRF复合物的组成成分,该复合物在F9细胞中调节视黄酸和E1A介导的c-jun基因转录。

p300 and ATF-2 are components of the DRF complex, which regulates retinoic acid- and E1A-mediated transcription of the c-jun gene in F9 cells.

作者信息

Kawasaki H, Song J, Eckner R, Ugai H, Chiu R, Taira K, Shi Y, Jones N, Yokoyama K K

机构信息

Tsukuba Life Science Center, The Institute of Physical and Chemical Research (RIKEN), Tsukuba 305, Japan.

出版信息

Genes Dev. 1998 Jan 15;12(2):233-45. doi: 10.1101/gad.12.2.233.

Abstract

Transcriptional activation of the c-jun gene is a critical event in the differentiation of F9 cells. In our previous studies we characterized an element [differentiation response element (DRE)] in the c-jun promoter that is both necessary and sufficient to confer the capacity for differentiation-dependent up-regulation. This element binds the differentiation regulatory factor (DRF) complex, of which one component is the adenovirus E1A-associated protein p300. We have now identified activation transcription factor-2 (ATF-2) as a DNA-binding subunit of the DRF complex. p300 and ATF-2 interact with each other in vivo and in vitro. The bromodomain and the C/H2 domain of p300 mediate the binding to ATF-2, which in turn requires a proline-rich region between amino acids 112 and 350 for its interaction with p300. The phosphorylation of the serine residue at position 121 of ATF-2 appears to be induced by protein kinase C alpha (PKC alpha) after treatment of cells with retinoic acid (RA) or induction with E1A. In cotransfection assays, wild-type ATF-2 enhanced the transcription of an E2/tk-luciferase construct, in conjunction with p300-E2. However, a mutant form of ATF-2 with a mutation at position 121 (pCMVATF-2(Ser121-Ala)) did not. These results suggest that ATF-2 and p300 cooperate in the control of transcription by forming a protein complex that is responsive to differentiation-inducing signals, such as RA or E1A, and moreover, that the phosphorylation of ATF-2 by PKC alpha is probably a signaling event in the pathway that leads to the transactivation of the c-jun gene in F9 cells.

摘要

c-jun基因的转录激活是F9细胞分化过程中的关键事件。在我们之前的研究中,我们鉴定了c-jun启动子中的一个元件[分化反应元件(DRE)],它对于赋予分化依赖性上调能力而言既是必需的也是充分的。该元件结合分化调节因子(DRF)复合物,其中一个组分是腺病毒E1A相关蛋白p300。我们现已确定激活转录因子-2(ATF-2)是DRF复合物的一个DNA结合亚基。p300和ATF-2在体内和体外相互作用。p300的溴结构域和C/H2结构域介导其与ATF-2的结合,而ATF-2反过来需要其112至350位氨基酸之间富含脯氨酸的区域才能与p300相互作用。在用视黄酸(RA)处理细胞或用E1A诱导后,ATF-2第121位丝氨酸残基的磷酸化似乎是由蛋白激酶Cα(PKCα)诱导的。在共转染实验中,野生型ATF-2与p300-E2共同增强了E2/tk-荧光素酶构建体的转录。然而,第121位发生突变的ATF-2突变体形式(pCMVATF-2(Ser121-Ala))则没有。这些结果表明,ATF-2和p300通过形成对分化诱导信号(如RA或E1A)有反应的蛋白质复合物来协同控制转录,此外,PKCα对ATF-2的磷酸化可能是F9细胞中导致c-jun基因反式激活的信号通路中的一个信号事件。

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