Adeno-associated virus Rep78 restricts adenovirus E1B55K-mediated p53 nuclear exportation.

Adeno-associated virus Rep78 restricts adenovirus E1B55K-mediated p53 nuclear exportation.
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腺相关病毒 Rep78 限制腺病毒 E1B55K 介导的 p53 核输出。

DOI:
10.1093/abbs/gms097
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发表时间:
2013-02
期刊:
Acta Biochim Biophys Sin (Shanghai).
影响因子:
--
通讯作者:
陈金中
陈金中
中科院分区:
其他
文献类型:
--
作者:
陈金中

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在腺病毒5型DNA复制过程中需要p53的失活。E1B55K是一种腺病毒早期蛋白,据报道可与p53相互作用并抑制p53的转激活。先前的研究表明,腺相关病毒(AAV) 2型可以通过从腺病毒介导的降解中挽救p53来降低腺病毒的转化潜能,但细节尚不清楚。我们通过共免疫沉淀法检测了Rep78-p53的相互作用。共定位实验显示,Rep78抑制e1b55k介导的p53核输出。然而,由于E1B55K不能被Rep78从p53-E1B55K复合体中取代,Rep78对p53的稳定性没有明显的影响,也不能缓解p53的转录失活。我们的研究结果揭示了AAV-2 Rep78通过细胞核中p53的重定位抑制腺病毒5的可能机制,这可能有助于揭示AAV-2对其辅助病毒腺病毒的调控机制。
Inactivation of p53 is needed during adenovirus type 5 DNA replication. E1B55K, an adenovirus early protein, has been reported to interact with p53 and inhibit p53 transactivation. Previous studies have shown that adeno-associated virus (AAV) type 2 could reduce the transforming potential of adenovirus by rescuing p53 from adenovirus-mediated degradation, but the details are not clear yet. We detected the Rep78-p53 interaction by co-immunoprecipitation assay. The co-localization assay revealed that Rep78 inhibits E1B55K-mediated p53 nuclear exportation. However, Rep78 did not detectably influence p53 stability and could not relieve the transcriptional inactivation of p53, as E1B55K could not be replaced from the p53-E1B55K complex by Rep78. Our results reveal a new possible mechanism that AAV-2 Rep78 inhibits adenovirus 5 by relocalizing p53 in the nucleus, which may shed some light on the regulatory mechanism of AAV-2 on its helper virus, adenovirus.
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