Relief of p53-mediated transcriptional repression by the adenovirus E1B 19-kDa protein or the cellular Bcl-2 protein.
Relief of p53-mediated transcriptional repression by the adenovirus E1B 19-kDa protein or the cellular Bcl-2 protein.
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DOI：
10.1073/pnas.91.19.8940
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发表时间：
1994-09
影响因子：
11.1
通讯作者：
Yuqiao Shen;Thomas Shenk
中科院分区：
文献类型：
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作者：
Yuqiao Shen;Thomas Shenk
P53抑癌基因产物是一种转录调节蛋白。它激活含有P53 DNA结合位点的启动子的转录，但抑制许多缺乏其结合位点的启动子。野生型P53的高水平表达可以诱导某些细胞类型的凋亡，这种活性可以被腺病毒E1B19-kDa癌蛋白或细胞内的Bcl2癌蛋白阻断。在这里，我们报告了P53介导的缺乏P53结合位点的启动子的抑制被E1B19-kDa蛋白或Bcl2癌蛋白取消。相反，在任何一种蛋白质存在的情况下，P53的转录激活仍然发生。两种能够阻止P53介导的细胞凋亡的癌蛋白也能阻止P53的转录抑制，这一事实增加了P53可能至少部分地通过抑制转录来诱导细胞凋亡的可能性。
The p53 tumor suppressor gene product is a transcriptional regulatory protein. It activates transcription from promoters that contain a p53 DNA binding site but represses many promoters that lack its binding site. High-level expression of wild-type p53 can induce apoptosis in certain cell types, and this activity can be blocked by the adenovirus E1B 19-kDa oncoprotein or by the cellular Bcl-2 oncoprotein. Here we report that p53-mediated repression of promoters that lack a p53 binding site is abrogated by the E1B 19-kDa protein or Bcl-2 oncoprotein. In contrast, transcriptional activation by p53 still occurs in the presence of either protein. The fact that two oncoproteins capable of preventing p53-mediated apoptosis also block transcriptional repression by p53 raises the possibility that p53 might induce apoptosis, at least in part, by repressing transcription.