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首页> 外文期刊>Molecular and Cellular Biology >Distinct Cellular Factors Regulate the c-myb Promoter through Its E2F Element
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Distinct Cellular Factors Regulate the c-myb Promoter through Its E2F Element

机译：不同的细胞因子通过其E2F元件调节c-myb启动子

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Most E2F-driven promoters are transiently activated around the G1/S transition. Although the promoter for the c-myb proto-oncogene harbors an E2F element, it is induced early in G1 following entry into the cell cycle. Furthermore, this promoter remains active throughout subsequent cell cycles. Since E2F sites function as repressor elements during G1 (due to the association of pRb with E2F factors), we investigated whether the E2F element in the c-myb promoter is regulated differently than E2F elements in promoters that are repressed during G1. By gel shift analysis, the E2F element from the c-myb promoter was found to form a unique complex, referred to as E2Fmyb-sp, which was not observed with E2F elements from several other promoters. Antibodies to DP-1, E2F1 to -5, p107, or pRb failed to either supershift or block E2Fmyb-sp complex formation. Methylation interference experiments indicate that the DNA contact residues for the E2Fmyb-sp complex are distinct from but overlapping with residues required for the binding of E2F proteins. In addition to the identification of E2Fmyb-sp, we have found that SP-1 binds to the c-myb E2F element. Functional studies revealed that E2Fmyb-sp and/or SP-1 are required to achieve full activation of the c-myb promoter in different cell types and to maintain elevated expression of the c-myb promoter during G1 in NIH 3T3 cells. These studies demonstrate that E2F elements can be regulated differently through the binding of unique sets of proteins.
机译：大多数E2F驱动的启动子在G 1 / S过渡附近被瞬时激活。尽管c- myb 原癌基因的启动子带有E2F元件，但是它在进入细胞周期后的G 1 中被早期诱导。此外，该启动子在整个随后的细胞周期中保持活性。由于E2F位点在G 1 期间起阻遏物的作用（由于pRb与E2F因子的关联），因此我们研究了c- myb 启动子中的E2F元件是否受到调控与在G 1 期间被抑制的启动子中的E2F元素不同。通过凝胶位移分析，发现来自c- myb 启动子的E2F元件形成了独特的复合物，称为E2Fmyb-sp，这是来自其他几个启动子的E2F元件未观察到的。针对DP-1，E2F1至-5，p107或pRb的抗体无法超移位或阻止E2Fmyb-sp复合物的形成。甲基化干扰实验表明，E2Fmyb-sp复合物的DNA接触残基与结合E2F蛋白所需的残基不同但重叠。除了鉴定E2Fmyb-sp外，我们还发现SP-1与c- myb E2F元件结合。功能研究表明，需要E2Fmyb-sp和/或SP-1才能在不同细胞类型中完全激活c- myb 启动子并维持c- myb < / em>启动子在NIH 3T3细胞的G 1 中。这些研究表明，通过结合独特的蛋白质组，可以不同地调节E2F元素。

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