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首页> 外文期刊>Nature >Forced degradation of Fas inhibits apoptosis in adenovirus-infected cells.
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Forced degradation of Fas inhibits apoptosis in adenovirus-infected cells.

机译：Fas的强迫降解抑制了腺病毒感染细胞的凋亡。

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摘要

DNA viruses have evolved elaborate mechanisms to overcome host antiviral defences. In adenovirus-infected cells, programmed cell death (apoptosis) induced by the cytokine tumour necrosis factor (TNF) is inhibited by several adenovirus-encoded proteins. Occupation of the cell-surface receptor Fas, a member of the TNF-receptor superfamily that is expressed on most cell types, triggers apoptosis of that cell. Here we show that the adenovirus RID (for receptor internalization and degradation) protein complex, which is an inhibitor of TNF-induced apoptosis, mediates internalization of cell-surface Fas and its destruction inside lysosomes within the cell. Fas has not previously been shown to be internalized and then degraded. RID also mediates internalization of the receptor for epidermal growth factor, but it does not affect the transferrin receptor or class I antigens of the major histocompatibility complex. Removal of Fas from the surface of adenovirus-infected cells expressing RID may allow infected cells to resist Fas-mediated cell death and thus promote their survival.
机译：DNA病毒已经发展出完善的机制来克服宿主的抗病毒防御。在腺病毒感染的细胞中，由细胞因子肿瘤坏死因子（TNF）诱导的程序性细胞死亡（凋亡）被几种腺病毒编码的蛋白抑制。细胞表面受体Fas（在大多数细胞类型中表达的TNF受体超家族的成员）的存在会触发该细胞的凋亡。在这里，我们显示了腺病毒RID（用于受体内在化和降解）蛋白复合物，它是TNF诱导的细胞凋亡的抑制剂，介导细胞表面Fas的内在化及其在细胞内溶酶体内的破坏。 Fas以前没有被证明会被内在化然后降解。 RID还介导表皮生长因子受体的内在化，但它不影响主要组织相容性复合物的运铁蛋白受体或I类抗原。从表达RID的腺病毒感染细胞表面去除Fas可能使感染细胞抵抗Fas介导的细胞死亡，从而促进其存活。

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