Leone G, Sears R, Huang E, Rempel R, Nuckolls F, Park C H, Giangrande P, Wu L, Saavedra H I, Field S J, Thompson M A, Yang H, Fujiwara Y, Greenberg M E, Orkin S, Smith C, Nevins J R
Division of Human Cancer Genetics, Department of Molecular Virology, Ohio State University Comprehensive Cancer Center, Columbus, OH 43210, USA.
Mol Cell. 2001 Jul;8(1):105-13. doi: 10.1016/s1097-2765(01)00275-1.
Previous work has shown that the Myc transcription factor induces transcription of the E2F1, E2F2, and E2F3 genes. Using primary mouse embryo fibroblasts deleted for individual E2F genes, we now show that Myc-induced S phase and apoptosis requires distinct E2F activities. The ability of Myc to induce S phase is impaired in the absence of either E2F2 or E2F3 but not E2F1 or E2F4. In contrast, the ability of Myc to induce apoptosis is markedly reduced in cells deleted for E2F1 but not E2F2 or E2F3. From this data, we propose that the induction of specific E2F activities is an essential component in the Myc pathways that control cell proliferation and cell fate decisions.
先前的研究表明,Myc转录因子可诱导E2F1、E2F2和E2F3基因的转录。利用缺失单个E2F基因的原代小鼠胚胎成纤维细胞,我们现在表明,Myc诱导的S期和凋亡需要不同的E2F活性。在缺乏E2F2或E2F3而非E2F1或E2F4时,Myc诱导S期的能力受损。相反,在缺失E2F1而非E2F2或E2F3的细胞中,Myc诱导凋亡的能力显著降低。根据这些数据,我们提出,特定E2F活性的诱导是Myc控制细胞增殖和细胞命运决定途径中的一个重要组成部分。