Regulation of p53 levels by the E1B 55-kilodalton protein and E4orf6 in adenovirus-infected cells
Regulation of p53 levels by the E1B 55-kilodalton protein and E4orf6 in adenovirus-infected cells
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腺病毒感染细胞中 E1B 55 kilodalton 蛋白和 E4orf6 对 p53 水平的调节
DOI：
10.1128/jvi.71.5.3788-3798.1997
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发表时间：
1997
影响因子：
5.4
通讯作者：
P. Branton
中科院分区：
文献类型：
--
作者：
E. Querido;R. Marcellus;A. Lai;Rachel Charbonneau;J. G. Teodoro;G. Ketner;P. Branton
The adenovirus type 5 243R E1A protein induces p53-dependent apoptosis in the absence of the 19- and 55-kDa E1B polypeptides. This effect appears to result from an accumulation of p53 protein and is unrelated to expression of E1B products. We now report that in the presence of the E1B 55-kDa polypeptide, the 289R E1A protein does not induce such p53 accumulation and, in fact, is able to block that induced by E1A 243R. This inhibition also requires the 289R-dependent transactivation of E4orf6 expression. E4orf6 is known to form complexes with the E1B 55-kDa protein and to function both in the transport and stabilization of viral mRNA and in shutoff of host cell protein synthesis. We demonstrated that the block in p53 accumulation is not due to the generalized shutoff of host cell metabolism. Rather, it appears to result from a mechanism targeted specifically to p53, most likely involving a decrease in the stability of p53 protein. The E1B 55-kDa protein is known to interact with both E4orf6 and p53, and as demonstrated recently by others, we showed that E4orf6 also binds directly to p53. Thus, multiple interactions between all three proteins may regulate p53 stability, resulting in the maintenance of low levels of p53 following virus infection.
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影响因子：
10.5
作者：
DEBBAS, M;WHITE, E
通讯作者：
WHITE, E
通过抑制连接子插入诱变对腺病毒 2 早期 1B 55K 多肽中的功能域进行剖析。
影响因子：
3.7
作者：
Yew,PR;Kao,CC;Berk,AJ
通讯作者：
Berk,AJ
DOI：
10.1073/pnas.93.21.11295
发表时间：
1996-10-15
影响因子：
11.1
作者：
Moore, M;Horikoshi, N;Shenk, T
通讯作者：
Shenk, T
影响因子：
8
作者：
J. G. Teodoro;Gordon C. Shore;P. Branton
通讯作者：
J. G. Teodoro;Gordon C. Shore;P. Branton
影响因子：
10.5
作者：
LOWE, SW;RULEY, HE
通讯作者：
RULEY, HE