Truss M, Beato M
Institut für Molekularbiologie und Tumorforschung, Philipps-Universität Marburg, Germany.
Endocr Rev. 1993 Aug;14(4):459-79. doi: 10.1210/edrv-14-4-459.
Gene regulation by steroid hormones is mediated by binding of the hormone ligand to the corresponding receptor that triggers a complex set of interactions of the hormone receptors with each other, with DNA in chromatin, and with a variety of other proteins. In this review we attempt to summarize what is known about these interactions using as the main example the regulation of mouse mammary tumor virus transcription by glucocorticoids and progestins. We describe in some detail the interaction of monomers and homodimers of the steroid receptors with their recognition sequences, and the molecular mechanism used to discriminate between the responsive elements for glucocorticoids/progestins and estrogens. We then review the interactions between homologous and heterologous hormone receptors on complex hormone regulatory regions, before devoting some attention to the synergistic and inhibitory interactions of hormone receptors with other transcription factors. Finally we briefly summarize some of the possible mechanisms that modulate the molecular interactions of hormone receptors. In addition to ligand binding, these include receptor phosphorylation, changes in DNA topology, and the organization of DNA in nucleosomes. From this overview we draw the tentative conclusion that the specificity of the hormonal response in different cells results from a combination of developmental restrictions both in the accessibility of genomic sequence and in the repertoire of regulatory proteins present in each particular cell. In addition, the array of regulatory sequences in DNA and chromatin determines the precise nature of macromolecular interactions of the receptors that are modulated by their degree of phosphorylation.
类固醇激素的基因调控是通过激素配体与相应受体的结合来介导的,这种结合会引发激素受体之间、与染色质中的DNA以及与多种其他蛋白质之间一系列复杂的相互作用。在本综述中,我们试图以糖皮质激素和孕激素对小鼠乳腺肿瘤病毒转录的调控为例,总结目前已知的这些相互作用。我们详细描述了类固醇受体的单体和同二聚体与其识别序列的相互作用,以及用于区分糖皮质激素/孕激素和雌激素反应元件的分子机制。然后,我们回顾了复杂激素调控区域上同源和异源激素受体之间的相互作用,之后关注了激素受体与其他转录因子的协同和抑制相互作用。最后,我们简要总结了一些可能调节激素受体分子相互作用的机制。除了配体结合外,这些机制还包括受体磷酸化、DNA拓扑结构的变化以及核小体中DNA的组织形式。从这一概述中,我们初步得出结论,不同细胞中激素反应的特异性源于基因组序列可及性和每个特定细胞中存在的调节蛋白库的发育限制的组合。此外,DNA和染色质中的调控序列阵列决定了受体大分子相互作用的精确性质,这些相互作用会因其磷酸化程度而受到调节。