Roy A L, Carruthers C, Gutjahr T, Roeder R G
Laboratory of Biochemistry and Molecular Biology, Rockefeller University, New York, New York 10021.
Nature. 1993 Sep 23;365(6444):359-61. doi: 10.1038/365359a0.
The nuclear proto-oncoprotein Myc has been implicated in the control of cell proliferation and differentiation. Myc participates in transcription and belongs to the basic-helix-loop-helix (bHLH) family of regulatory proteins. Here we show that Myc interacts with TFII-I, a transcription initiation factor that activates core promoters through an initiator element (Inr). As previously observed for the bHLH activator USF, Myc was found to interact cooperatively with TFII-I at both Inr and upstream E-box promoter elements. However, in this case Myc interactions with TFII-I at the Inr lead to an inhibition of transcription initiation. This inhibition is selective for a TFII-I-dependent (as opposed to TFIIA-dependent) initiation pathway and correlates with the prevention of complex formation between the TATA-binding protein TBP (TFIID tau), TFII-I and the promoter. TBP probably interacts with Myc, but only slowly. These observations indicate that Myc has the potential to interact physically and functionally with components of the general transcription machinery.
核原癌蛋白Myc与细胞增殖和分化的调控有关。Myc参与转录，属于调控蛋白的碱性螺旋-环-螺旋（bHLH）家族。我们在此表明，Myc与TFII-I相互作用，TFII-I是一种通过起始子元件（Inr）激活核心启动子的转录起始因子。正如之前观察到的bHLH激活因子USF一样，发现Myc在Inr和上游E-box启动子元件处均与TFII-I协同相互作用。然而，在这种情况下，Myc在Inr处与TFII-I的相互作用导致转录起始受到抑制。这种抑制对TFII-I依赖型（而非TFIIA依赖型）起始途径具有选择性，并且与防止TATA结合蛋白TBP（TFIID tau）、TFII-I和启动子之间形成复合物相关。TBP可能与Myc相互作用，但速度较慢。这些观察结果表明，Myc具有与通用转录机制的组分在物理和功能上相互作用的潜力。
