O'Hagan R C, Schreiber-Agus N, Chen K, David G, Engelman J A, Schwab R, Alland L, Thomson C, Ronning D R, Sacchettini J C, Meltzer P, DePinho R A
Department of Adult Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts, USA.
Nat Genet. 2000 Feb;24(2):113-9. doi: 10.1038/72761.
Myc and Mad family proteins regulate multiple biological processes through their capacity to influence gene expression directly. Here we show that the basic regions of Myc and Mad proteins are not functionally equivalent in oncogenesis, have separable E-box-binding activities and engage both common and distinct gene targets. Our data support the view that the opposing biological actions of Myc and Mxi1 extend beyond reciprocal regulation of common gene targets. Identification of differentially regulated gene targets provides a framework for understanding the mechanism through which the Myc superfamily governs the growth, proliferation and survival of normal and neoplastic cells.
Myc和Mad家族蛋白通过其直接影响基因表达的能力来调节多种生物学过程。我们在此表明,Myc和Mad蛋白的碱性区域在肿瘤发生中功能并不等同,具有可分离的E盒结合活性,并涉及共同和不同的基因靶点。我们的数据支持这样一种观点,即Myc和Mxi1相反的生物学作用不仅限于对共同基因靶点的相互调节。鉴定差异调节的基因靶点为理解Myc超家族控制正常和肿瘤细胞生长、增殖及存活的机制提供了一个框架。