ADENOVIRUS INHIBITION OF CELLULAR PROTEIN-SYNTHESIS INVOLVES INACTIVATION OF CAP-BINDING PROTEIN

ADENOVIRUS INHIBITION OF CELLULAR PROTEIN-SYNTHESIS INVOLVES INACTIVATION OF CAP-BINDING PROTEIN
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DOI:
10.1016/0092-8674(91)90161-q
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发表时间:
1991-04-19
期刊:
影响因子:
64.5
通讯作者:
SCHNEIDER, RJ
SCHNEIDER, RJ
中科院分区:
生物学1区
文献类型:
--
作者:
HUANG, J;SCHNEIDER, RJ

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腺病毒(Ad)感染导致在病毒感染周期的后期启动的细胞蛋白质合成受到显著抑制。我们发现,在细胞周期进程中用于抑制细胞蛋白质合成的机制被Ad用来抑制宿主并增强晚期病毒mRNA的翻译。区分细胞和晚期的Ad mRNAs和抑制宿主蛋白的合成涉及病毒介导的帽结合蛋白(CBP)的低磷酸化和随后CBP复合体的失活,CBP复合体是帽依赖的mRNA翻译所需的大型酶复合体。晚期AdmRNAs与脊髓灰质炎病毒一样,具有独立于正常帽子识别过程进行翻译的独特能力,不需要CBP复合体的活性。这两种病毒对细胞翻译的抑制非常相似,不同的是CBP复合体被脊髓灰质炎病毒蛋白降解,而它被Ad功能灭活。
Adenovirus (Ad) infection results in a marked inhibition of cellular protein synthesis that initiates during the late phase of the viral infectious cycle. We show that the mechanism used for suppression of cellular protein synthesis during cell cycle progression is exploited by Ad to repress host and enhance late viral mRNA translation. Discrimination between cellular and late Ad mRNAs and inhibition of host protein synthesis are shown to involve viral-mediated underphosphorylation of cap-binding protein (CBP) and subsequent inactivation of CBP complex, a large enzymatic complex required for cap-dependent mRNA translation. Late Ad mRNAs, like those of poliovirus, possess the unique ability to translate independent of a normal cap recognition process and do not require the activity of CBP complex. Inhibition of cellular translation by these two viruses is quite similar, except that whereas CBP complex is proteolytically degraded by poliovirus, it is functionally inactivated by Ad.