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人乳头瘤病毒16型E6蛋白的天然变体在改变角质形成细胞分化和诱导p53降解的能力方面存在差异。

Natural variants of the human papillomavirus type 16 E6 protein differ in their abilities to alter keratinocyte differentiation and to induce p53 degradation.

作者信息

Stöppler M C, Ching K, Stöppler H, Clancy K, Schlegel R, Icenogle J

机构信息

Department of Pathology, Georgetown University School of Medicine, Washington, DC 20007, USA.

出版信息

J Virol. 1996 Oct;70(10):6987-93. doi: 10.1128/JVI.70.10.6987-6993.1996.

Abstract

Three naturally occurring variant human papillomavirus type 16 (HPV-16) E6 proteins, which contained amino acid substitutions predominantly near the N terminus, exhibited significant differences in their abilities to abrogate keratinocyte differentiation in response to serum and calcium and to induce the degradation of p53 in vitro. One variant surpassed the reference E6 protein in its ability to abrogate keratinocyte differentiation responses, whereas another showed a reduction in this activity. Interestingly, the biological activities of the HPV-16 E6 proteins and their abilities to induce p53 degradation in vitro were directly correlated. These results demonstrate that naturally occurring variants of HPV-16 differ in biological and biochemical properties which might result in differences in pathogenicity.

摘要

三种天然存在的16型人乳头瘤病毒(HPV - 16)E6蛋白,其氨基酸取代主要集中在N端附近,在体外消除角质形成细胞对血清和钙的分化反应以及诱导p53降解的能力上表现出显著差异。一种变体在消除角质形成细胞分化反应的能力上超过了参考E6蛋白,而另一种则表现出该活性降低。有趣的是,HPV - 16 E6蛋白的生物学活性与其在体外诱导p53降解的能力直接相关。这些结果表明,HPV - 16的天然变体在生物学和生化特性上存在差异,这可能导致致病性的差异。

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本文引用的文献

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Human papillomavirus 16 E6 expression disrupts the p53-mediated cellular response to DNA damage.
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