The dual effect of adenovirus type 5 E1A 13S protein on NF-kappaB activation is antagonized by E1B 19K
The dual effect of adenovirus type 5 E1A 13S protein on NF-kappaB activation is antagonized by E1B 19K
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5 型腺病毒 E1A 13S 蛋白对 NF-kappaB 激活的双重作用被 E1B 19K 拮抗
DOI：
10.1128/mcb.16.8.4052
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发表时间：
1996
影响因子：
5.3
通讯作者：
P. Baeuerle
中科院分区：
文献类型：
--
作者：
M. Schmitz;Almut Indorf;Florian P. Limbourg;Heike Städtler;E. Traenckner;P. Baeuerle
The genomes of human adenoviruses encode several regulatory proteins, including the two differentially spliced gene products E1A and E1B. Here, we show that the 13S but not the 12S splice variant of E1A of adenovirus type 5 can activate the human transcription factor NF-kappaB in a bimodal fashion. One mode is the activation of NF-kappaB containing the p65 subunit from the cytoplasmic NF-kappaB-IkappaB complex. This activation required reactive oxygen intermediates and the phosphorylation of IkappaBalpha at serines 32 and 36, followed by IkappaBalpha degradation and the nuclear uptake of NF-kappaB. In addition, 13S E1A stimulated the transcriptional activity of the C-terminal 80 amino acids of p65 at a core promoter with either a TATA box or an initiator (INR) element. The C-terminal 80 amino acids of p65 were found to associate with E1A in vitro. The activation of NF-kappaB-dependent reporter gene transcription by E1A was potently suppressed upon coexpression of the E1B 19-kDa protein (19K). E1B 19K prevented both the activation of NF-kappaB and the E1A-mediated transcriptional enhancement of p65. These inhibitory effects were not found for the 55-kDa splice variant of the E1B protein. We suggest that the inductive effect of E1A 13S on the host factor NF-kappaB, whose activation is important for the transcription of various adenovirus genes, must be counteracted by the suppressive effect of E1B 19K so that the adenovirus-infected cell can escape the immune-stimulatory and apoptotic effects of NF-kappaB.
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DOI：
--
发表时间：
1995
期刊：
--
影响因子：
--
作者：
J. Brockman;D. Scherer;T. McKinsey;S. M. Hall;X. Qi;Wha-Young Lee;Anddean W. Ballard
通讯作者：
J. Brockman;D. Scherer;T. McKinsey;S. M. Hall;X. Qi;Wha-Young Lee;Anddean W. Ballard
影响因子：
5.2
作者：
B. Taródi;T. Subramanian;G. Chinnadurai
通讯作者：
B. Taródi;T. Subramanian;G. Chinnadurai
影响因子：
10.5
作者：
DEBBAS, M;WHITE, E
通讯作者：
WHITE, E
腺病毒诱导的 E4F 转录因子的 DNA 结合活性受磷酸化调节。
影响因子：
10.5
作者：
Raychaudhuri,P;Bagchi,S;Nevins,JR
通讯作者：
Nevins,JR
腺病毒 12S E1A 基因抑制 F9 畸胎癌细胞的分化。
DOI：
10.1073/pnas.87.24.9878
发表时间：
1990
影响因子：
11.1
作者：
Weigel,RJ;Devoto,SH;Nevins,JR
通讯作者：
Nevins,JR