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首页> 外文期刊>Cell cycle >Deciphering AP-1 function in tumorigenesis: fra-ternizing on target promoters.
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Deciphering AP-1 function in tumorigenesis: fra-ternizing on target promoters.

机译：破译AP-1在肿瘤发生中的功能：对目标启动子进行构图。

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Multi-gene families of transcription factors pose a formidable challenge to molecular and functional analysis. Dissecting distinct functions for individual family members requires a combination of approaches in different cellular and animal models. The AP-1 transcription factor complex serves as a paradigm for understanding the dynamics of transcriptional regulation. Knockout, knockdown and transgenic strategies, inducible alleles, mutational analysis, chemical genetics, etc.; researchers have applied all the tricks of the trade to understand how AP-1 works. AP-1 refers to a mixture of dimers formed between members of the Jun, Fos and ATF families. The complexity of the AP-1 biological functions reflects the wide combinatorial diversity of its components. AP-1 has been linked to cancer and neoplastic transformation ever since the first jun and fos genes were cloned as cellular homologues of viral oncogenes twenty years ago. Because of the oncogenic or tumor suppressive activity exhibited by distinct Jun and Fos nuclear proteins depending on the cell context and the genetic background of the tumor, the AP-1 complex has been called a "double-edged sword" in tumorigenesis. The cumulating results over the last decade are finally leading to the identification of specific functions for individual AP-1 components and their contribution to neoplastic disease. Here, we focus on the Fra-1 protein in tumorigenesis, which offers an illustrative example of this helter-skelter voyage.
机译：转录因子的多基因家族对分子和功能分析提出了巨大的挑战。剖析单个家庭成员的不同功能需要在不同的细胞和动物模型中结合多种方法。 AP-1转录因子复合物可作为理解转录调控动力学的范例。敲除，敲除和转基因策略，诱导型等位基因，突变分析，化学遗传学等;研究人员运用了所有的技巧来了解AP-1的工作原理。 AP-1是指Jun，Fos和ATF家族成员之间形成的二聚体混合物。 AP-1生物功能的复杂性反映了其组件的广泛组合多样性。自从20年前第一个jun和fos基因被克隆为病毒癌基因的细胞同源物以来，AP-1就已经与癌症和肿瘤转化联系在一起。由于取决于肿瘤的细胞背景和遗传背景，不同的Jun和Fos核蛋白表现出的致癌或抑癌活性，因此AP-1复合物在肿瘤发生中被称为“双刃剑”。过去十年的累积结果最终导致了对单个AP-1组分及其对肿瘤性疾病的贡献的特定功能的鉴定。在这里，我们专注于肿瘤发生中的Fra-1蛋白，这提供了这种潜航的例证。

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