Shirasawa H, Jin M H, Shimizu K, Akutsu N, Shino Y, Simizu B
Department of Microbiology, School of Medicine, Chiba University, Japan.
Virology. 1994 Aug 15;203(1):36-42. doi: 10.1006/viro.1994.1452.
The E6 gene of human papillomavirus type 16 (HPV16) has the potential to encode full-length as well as truncated E6 proteins (E6I and E6II) by alternative splicings. Spliced ORF E6I is considered to facilitate the translation of the neighboring E7 ORF; however, the putative E6I protein is suspected to be functionless. In this study, the transcription-modulatory functions of full-length E6 and E6I proteins were examined using cDNAs from a cervical carcinoma cell line. E6I cDNA was able to trans-activate the autologous P97 promoter and the heterologous adenovirus E2 promoter. Full-length E6 was found to trans-activate the heterologous promoter, but repress transcription from the autologous P97 promoter. The transcription-modulatory functions of full-length E6 and E6*I proteins suggested that transcriptional regulation of HPVs associated with mucosal malignant lesions is complex.
人乳头瘤病毒16型（HPV16）的E6基因能够通过可变剪接编码全长E6蛋白以及截短的E6蛋白（E6I和E6II）。剪接的开放阅读框E6I被认为有助于邻近E7开放阅读框的翻译；然而，推测的E6I蛋白被怀疑没有功能。在本研究中，使用来自宫颈癌细胞系的cDNA检测了全长E6和E6I蛋白的转录调节功能。E6I cDNA能够反式激活自身的P97启动子和异源腺病毒E2启动子。发现全长E6能够反式激活异源启动子，但抑制自身P97启动子的转录。全长E6和E6*I蛋白的转录调节功能表明，与黏膜恶性病变相关的人乳头瘤病毒的转录调控是复杂的。
