[Protein p53 inhibits the activity of the enhancer of the immediate-early genes of murine cytomegalovirus].

D Lembo, A Angeretti, R Cavallo, M Gariglio, G Gribaudo, S Landolfo
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Abstract

The protein encoded by the tumor suppressor gene p53 can complex and functionally interact with cytomegalovirus proteins produced during the immediate-early phase of infection. The functions of these complex are unclear but there is some evidence to suggest that binding of p53 to these viral proteins may inactivate p53 functions. Recent reports have shown that p53 is involved in regulation of transcription. In this study we have considered the possibility that p53 may regulate transcription of cytomegalovirus immediate early genes which play a crucial role for virus replication. Here we report that experiments in which NIH 3T3 cells were cotransfected with a p53 expression plasmid together with a reporter gene linked to the mouse cytomegalovirus immediate-early enhancer/promoter revealed that wild type p53 could efficiently reduce the transcriptional activity of this viral regulatory sequence. By contrast expression of a mutated p53 correlated with a much smaller reduction of transcription. Deletion mutants analysis of the enhancer revealed that repression of transcription by p53 requires a minimal promoter containing an SP1 consensus sequence and a TATA box.

[蛋白p53抑制小鼠巨细胞病毒立即早期基因增强子的活性]。
由肿瘤抑制基因p53编码的蛋白可以与感染早期产生的巨细胞病毒蛋白复合并在功能上相互作用。这些复合物的功能尚不清楚,但有证据表明p53与这些病毒蛋白结合可能使p53功能失活。最近的报道表明p53参与转录调控。在这项研究中,我们考虑了p53可能调节巨细胞病毒即时早期基因转录的可能性,这些基因在病毒复制中起着至关重要的作用。在NIH 3T3细胞中,我们用p53表达质粒和与小鼠巨细胞病毒即时早期增强子/启动子相关的报告基因共转染的实验显示,野生型p53可以有效降低该病毒调控序列的转录活性。相比之下,突变p53的表达与转录减少的幅度要小得多。对增强子的缺失突变体分析显示,p53的转录抑制需要一个包含SP1共识序列和TATA盒的最小启动子。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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