Sabbatini P, Lin J, Levine A J, White E
Center for Advanced Biotechnology and Medicine, Rutgers University, Piscataway, New Jersey 08854, USA.
Genes Dev. 1995 Sep 1;9(17):2184-92. doi: 10.1101/gad.9.17.2184.
Baby rat kidney (BRK) cell lines transformed by E1A and a temperature-sensitive p53 [tsp53(val135)] undergo rapid apoptosis when p53 assumes the wild-type conformation at the permissive temperature. Wild-type p53 function is therefore required for induction of apoptosis in response to growth deregulation by E1A. BRK cells transformed by E1A and a transcriptionally defective temperature-sensitive p53 [tsp53(22-23val135)] are dramatically impaired for the ability to mediate E1A-induced apoptosis at the permissive temperature. The tsp53(22-23val135), however, still retains some ability to suppress cell growth. Thus, the activity of p53 as a transcription factor is directly correlated with the ability of E1A to induce apoptosis. In addition, there may exist at least two different mechanisms by which p53 can suppress cell-cycle progression, only one of which is dependent on p53-mediated transcription.
由E1A和温度敏感型p53[tsp53(val135)]转化的幼鼠肾（BRK）细胞系，当p53在允许温度下呈现野生型构象时会迅速发生凋亡。因此，野生型p53功能是响应E1A引起的生长失调而诱导凋亡所必需的。由E1A和转录缺陷型温度敏感型p53[tsp53(22 - 23val135)]转化的BRK细胞，在允许温度下介导E1A诱导凋亡的能力受到显著损害。然而，tsp53(22 - 23val135)仍保留一些抑制细胞生长的能力。因此，p53作为转录因子的活性与E1A诱导凋亡的能力直接相关。此外，可能至少存在两种不同的机制，p53可通过这些机制抑制细胞周期进程，其中只有一种机制依赖于p53介导的转录。
