Birchenall-Roberts M C, Yoo Y D, Bertolette D C, Lee K H, Turley J M, Bang O S, Ruscetti F W, Kim S J
Intramural Research Support Program, SAIC Frederick, National Cancer Institute-Frederick Cancer Research and Development Center, Frederick, Maryland 21702-1201, USA.
J Biol Chem. 1997 Apr 4;272(14):8905-11. doi: 10.1074/jbc.272.14.8905.
The E2F family of transcription factors regulates cell cycle progression, and deregulated expression of E2F-1 can lead to neoplastic transformation. In myeloid cells, introduction and expression of the Abelson leukemia virus causes growth factor independence. Here, the p120 v-Abl protein activates E2F-1-mediated transcription through a physical interaction with the E2F-1 transcription factor. BCR-Abl and c-Abl also stimulate E2F-1-mediated transcription. Our results suggest a new mechanism by which v-Abl leads to factor-independent myeloid cell proliferation: the activation of E2F-1-mediated transcription.
转录因子E2F家族调控细胞周期进程，E2F-1的表达失调可导致肿瘤转化。在髓系细胞中，引入并表达阿贝尔森白血病病毒可使细胞获得生长因子非依赖性。在此，p120 v-Abl蛋白通过与E2F-1转录因子的直接相互作用激活E2F-1介导的转录。BCR-Abl和c-Abl也能刺激E2F-1介导的转录。我们的结果提示了一种v-Abl导致髓系细胞因子非依赖性增殖的新机制：激活E2F-1介导的转录。
