The adenovirus e3 promoter is sensitive to activation signals in human T cells.

The adenovirus e3 promoter is sensitive to activation signals in human T cells.
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腺病毒 e3 启动子对人类 T 细胞中的激活信号敏感。

DOI:
10.1128/jvi.77.2.1112-1119.2003
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发表时间:
2003
影响因子:
5.4
通讯作者:
Gooding,LindaR
Gooding,LindaR
中科院分区:
医学2区
文献类型:
--
作者:
Mahr,JeffreyA;Boss,JeremyM;Gooding,LindaR

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The group C adenoviruses typically cause acute respiratory disease in young children. In addition, a persistent phase of infection has been observed in which virus may be shed for years without producing overt pathology. Our laboratory recently reported that group C adenovirus DNA can be found in tonsil and adenoid T lymphocytes from the majority of pediatric donors (C. T. Garnett, D. Erdman, W. Xu, and L. R. Gooding, J. Virol. 76:10608-10616, 2002). This finding suggests that immune evasion strategies of human adenoviruses may be directed, in part, toward protection of persistently or latently infected T lymphocytes. Many of the adenoviral gene products implicated in prevention of immune destruction of virus-infected cells are encoded within the E3 transcription unit. In this study, the E3 promoter was evaluated for sensitivity to T-cell activation signals by using a promoter reporter plasmid. Indeed, this promoter is extremely sensitive to T-cell activation, with phorbol myristate acetate (PMA) plus ionomycin increasing E3-directed transcription 100-fold. By comparison, in the same cells E1A expression leads to a 5.5-fold increase in transcription from the E3 promoter. In contrast to induction by E1A, activation by PMA plus ionomycin requires the two E3 NF-κB binding sites. Interestingly, expression of E1A inhibits induction of the E3 promoter in response to T-cell activation while increasing E3 promoter activity in unactivated cells. Collectively, these data suggest that the E3 promoter may have evolved the capacity to respond to T-cell activation in the absence of E1A expression and may act to upregulate antiapoptotic gene expression in order to promote survival of persistently infected T lymphocytes.
肿瘤坏死因子 α 通过激活 NF-κB 诱导腺病毒早期 3 启动子。
DOI: --
发表时间: 1996
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发表时间: 1996
影响因子: 5.3
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