Zhang H S, Postigo A A, Dean D C
Department of Medicine, Washington University School of Medicine, St. Louis, Missouri 63110, USA.
Cell. 1999 Apr 2;97(1):53-61. doi: 10.1016/s0092-8674(00)80714-x.
Rb inhibits progression from G1 to S phase of the cell cycle. It associates with a number of cellular proteins; however, the nature of these interactions and their relative significance in cell cycle regulation are still unclear. We present evidence that Rb must normally interact with the E2F family of transcription factors to arrest cells in G1, and that this arrest results from active transcriptional repression by the Rb-E2F complex, not from inactivation of E2F. Thus, a major role of E2F in cell cycle regulation is assembly of this repressor complex. We demonstrate that active repression by Rb-E2F mediates the G1 arrest triggered by TGFbeta, p16INK4a, and contact inhibition.
视网膜母细胞瘤（Rb）抑制细胞周期从G1期向S期的进展。它与多种细胞蛋白相关联；然而，这些相互作用的性质及其在细胞周期调控中的相对重要性仍不清楚。我们提供的证据表明，Rb通常必须与E2F转录因子家族相互作用，才能将细胞阻滞在G1期，并且这种阻滞是由Rb-E2F复合物的活性转录抑制导致的，而非E2F的失活。因此，E2F在细胞周期调控中的一个主要作用是组装这种阻遏复合物。我们证明，Rb-E2F的活性抑制介导了由转化生长因子β（TGFβ）、p16INK4a和接触抑制引发的G1期阻滞。
