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皮肤源性1型人乳头瘤病毒的E6蛋白抑制p53介导的反式激活作用，而5型、8型或47型则无此作用。

Inhibition of p53-mediated transactivation by E6 of type 1, but not type 5, 8, or 47, human papillomavirus of cutaneous origin.

作者信息

Kiyono T, Hiraiwa A, Ishii S, Takahashi T, Ishibashi M

机构信息

Laboratory of Viral Oncology, Aichi Cancer Center, Nagoya, Japan.

出版信息

J Virol. 1994 Jul;68(7):4656-61. doi: 10.1128/JVI.68.7.4656-4661.1994.

DOI:10.1128/JVI.68.7.4656-4661.1994
PMID:8207840
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC236394/
Abstract

Transient transfection experiments indicated (i) that E6 protein of non-cancer-associated cutaneous human papillomavirus type 1 (HPV-1) can inhibit p53-mediated transcriptional transactivation in both p53-deficient human cells (H358) and normal rat cells (3Y1), but those of cancer-associated cutaneous HPV-5, -8, and -47 cannot do so in either H358 or 3Y1 cells, and (ii) that E6 proteins of HPV-16 and -18 can inhibit the p53 function in H358 cells but not in 3Y1 cells.

摘要

瞬时转染实验表明

（i）非癌相关的皮肤人类乳头瘤病毒1型（HPV-1）的E6蛋白，在p53缺陷的人类细胞（H358）和正常大鼠细胞（3Y1）中均能抑制p53介导的转录反式激活，但癌相关的皮肤HPV-5、-8和-47的E6蛋白在H358或3Y1细胞中均无此作用；（ii）HPV-16和-18的E6蛋白能在H358细胞中抑制p53功能，但在3Y1细胞中则不能。

相似文献

1
Inhibition of p53-mediated transactivation by E6 of type 1, but not type 5, 8, or 47, human papillomavirus of cutaneous origin.皮肤源性1型人乳头瘤病毒的E6蛋白抑制p53介导的反式激活作用，而5型、8型或47型则无此作用。
J Virol. 1994 Jul;68(7):4656-61. doi: 10.1128/JVI.68.7.4656-4661.1994.
2
Mutational analysis of HPV-18 E6 identifies domains required for p53 degradation in vitro, abolition of p53 transactivation in vivo and immortalisation of primary BMK cells.人乳头瘤病毒18型E6基因的突变分析确定了体外p53降解、体内p53反式激活作用的消除以及原代BMK细胞永生化所需的结构域。
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Comparative study on E6 and E7 genes of some cutaneous and genital papillomaviruses of human origin for their ability to transform 3Y1 cells.对一些源自人类的皮肤和生殖器乳头瘤病毒的E6和E7基因转化3Y1细胞能力的比较研究。
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