Wang Z M, Yang H, Livingston D M
Dana-Farber Cancer Institute and Harvard Medical School, 44 Binney Street, Boston, MA 02115, USA.
Proc Natl Acad Sci U S A. 1998 Dec 22;95(26):15583-6. doi: 10.1073/pnas.95.26.15583.
Much evidence strongly suggests a positive role for one or more E2F species in the control of exit from G0/G1. Results described here provide direct evidence that endogenous E2F-1, as predicted, contributes to progression from G0 to S. By contrast, cycling cells lacking an intact E2F-1 gene demonstrated normal cell cycle distribution. Therefore, E2F-1 exerts a unique function leading to timely G0 exit of resting cultured primary cells, while at the same time being unnecessary for normal G1 to S phase progression of cycling cells.
大量证据有力地表明，一种或多种E2F蛋白在控制细胞从G0/G1期退出过程中发挥着积极作用。本文所述结果提供了直接证据，正如所预测的那样，内源性E2F-1有助于细胞从G0期进入S期。相比之下，缺乏完整E2F-1基因的循环细胞表现出正常的细胞周期分布。因此，E2F-1发挥着独特的功能，促使静止的培养原代细胞及时退出G0期，而对于循环细胞从正常G1期进入S期的进程则并非必需。
