中文摘要：

p53 的 Inactivation 在侵入人体气管粘膜的病菌类型 5 DNA 复制期间被需要。E1B55K，侵入人体气管粘膜的病菌早蛋白质，被报导了与 p53 交往并且禁止 p53 transactivation。以前的研究证明了联系 adeno 的病毒(AAV ) 类型 2 能从调停侵入人体气管粘膜的病菌的降级由 rescuing p53 减少侵入人体气管粘膜的病菌的转变潜力，但是细节还不是清楚的。我们由 co-immunoprecipitation 试金检测了 Rep78p53 相互作用。合作本地化试金表明 Rep78 禁止调停 E1B55K 的 p53 原子出口。然而， Rep78 detectably 没影响 p53 稳定性并且不能减轻 p53 的 transcriptional inactivation，当 E1B55K 不能被 Rep78 从 p53E1B55K 建筑群代替。我们的结果揭示 AAV-2 Rep78 禁止的新可能的机制由重新本地化的侵入人体气管粘膜的病菌 5 在原子核的 p53，可以在它的助手病毒上阐明 AAV-2 的规章的机制，侵入人体气管粘膜的病菌。

英文摘要：

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 ElB55K-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.