Galaktionov K, Chen X, Beach D
Howard Hughes Medical Institute, Cold Spring Harbor Laboratory, New York 11724, USA.
Nature. 1996 Aug 8;382(6591):511-7. doi: 10.1038/382511a0.
The product of the proto-oncogene c-myc, in partnership with Max, forms a transcription factor that can promote either oncogenic transformation or apoptosis. The Myc/Max heterodimer binds to elements in the cdc25A gene and activates transcription. Like myc, cdc25A, itself a proto-oncogene, can induce apoptosis in cells depleted of growth factor, and Myc-induced apoptosis also requires cdc25A. These findings indicate that cdc25A is a physiologically relevant transcriptional target of c-myc.
原癌基因c-myc的产物与Max协同作用，形成一种转录因子，该转录因子既能促进致癌转化，也能引发细胞凋亡。Myc/Max异源二聚体与cdc25A基因中的元件结合并激活转录。与myc一样，cdc25A本身也是一种原癌基因，在缺乏生长因子的细胞中可诱导细胞凋亡，且Myc诱导的细胞凋亡也需要cdc25A。这些发现表明，cdc25A是c-myc在生理上相关的转录靶点。
