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Identification of novel targets of MYC whose transcription requires the essential MbII domain.

机译：鉴定其转录需要必需的MbII结构域的MYC新靶标。

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The MYC oncoprotein is among the most potent regulators of cell cycle progression and malignant transformation in human cells. Current models suggest that much of MYC's role in these processes is related to its ability to regulate the transcription of downstream target genes that encode the ultimate effector proteins. In addition to its carboxy-terminal DNA binding and dimerization domains, an enigmatic motif in the amino terminus termed MbII is required for all of MYC's biological activities. In spite of historical observations demonstrating the absolute requirement for MbII in these biological functions, clues implicating this domain in target gene transcription have only recently appeared. Based on this emerging link between MbII and transcriptional activation, we hypothesized that the identification of individual MYC targets whose transactivation requires MbII would help define the essential downstream effectors of MYC in transformation and cell cycle progression. In hopes of directly identifying new MbII-dependent MYC target genes, an expression profiling screen was conducted. This screen resulted in our identification of ten novel downstream targets of MYC. As a proof of principle, we recently demonstrated using RNAi-mediated depletion that one of these targets, the metastasis regulator MTA1, is absolutely required for MYC mediated transformation. Here we report the identity of these previously uncharacterized MYC targets and discuss their potential roles in MYC function. In addition, we attempt to reconcile the historical and contemporary evidence linking MbII to transcriptional activation.
机译：MYC癌蛋白是人类细胞中细胞周期进程和恶性转化最有效的调节剂之一。当前模型表明，MYC在这些过程中的许多作用与其调节编码最终效应蛋白的下游靶基因转录的能力有关。除其羧基末端DNA结合和二聚结构域外，MYC的所有生物活性均需要在氨基末端称为MbII的神秘基序。尽管有历史观察表明在这些生物学功能中对MbII的绝对需要，但在最近才出现了暗示该域参与靶基因转录的线索。基于MbII和转录激活之间的这种新兴联系，我们假设鉴定其反式激活需要MbII的单个MYC靶标将有助于定义MYC在转化和细胞周期进程中的重要下游效应子。为了直接鉴定依赖于MbII的新MYC靶基因，进行了表达谱筛选。此屏幕导致我们鉴定了MYC的十个新型下游靶标。作为原理的证明，我们最近使用RNAi介导的消耗证明了MYC介导的转化绝对需要这些靶标之一，转移调节剂MTA1。在这里，我们报告这些以前未表征的MYC目标的身份，并讨论它们在MYC功能中的潜在作用。此外，我们试图调和将MbII与转录激活联系起来的历史和当代证据。

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