Papillomavirus E6 proteins

被引:249
作者
Howie, Heather L. [1 ]
Katzenellenbogen, Rachel A. [1 ,2 ]
Galloway, Denise A. [1 ]
机构
[1] Fred Hutchinson Canc Res Ctr, Div Human Biol, Seattle, WA 98109 USA
[2] Univ Washington, Dept Pediat, Seattle, WA 98195 USA
关键词
HPV; E6; oncogene; p53; Apoptosis; hTERT; TELOMERASE REVERSE-TRANSCRIPTASE; MAMMARY EPITHELIAL-CELLS; ANCHORAGE-INDEPENDENT GROWTH; PRIMARY HUMAN KERATINOCYTES; POLY(A) BINDING-PROTEINS; CATALYTIC SUBUNIT HTERT; UBIQUITIN LIGASE E6-AP; P53; DNA-BINDING; TYPE-16; E6; HPV E6;
D O I
10.1016/j.virol.2008.11.017
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
The papillomaviruses are small DNA viruses that encode approximately eight genes, and require the host cell DNA replication machinery for their viral DNA replication. Thus papillomaviruses have evolved strategies to induce host cell DNA synthesis balanced with strategies to protect the cell from unscheduled replication. While the papillomavirus E1 and E2 genes are directly involved in viral replication by binding to and unwinding the origin of replication, the E6 and E7 proteins have auxillary functions that promote proliferation. As a consequence of disrupting the normal checkpoints that regulate cell cycle entry and progression, the E6 and E7 proteins play a key role in the oncogenic properties of human papillomaviruses with a high risk of causing anogenital cancers (HR HPVs). As a consequence, E6 and E7 of HR HPVs are invariably expressed in cervical cancers. This article will focus on the E6 protein and its numerous activities including inactivating p53, blocking apoptosis, activating telomerase, disrupting cell adhesion, polarity and epithelial differentiation, altering transcription and reducing immune recognition. (C) 2008 Elsevier Inc. All rights reserved.
引用
收藏
页码:324 / 334
页数:11
相关论文
共 156 条
[1]   TELOMERE LENGTH PREDICTS REPLICATIVE CAPACITY OF HUMAN FIBROBLASTS [J].
ALLSOPP, RC ;
VAZIRI, H ;
PATTERSON, C ;
GOLDSTEIN, S ;
YOUNGLAI, EV ;
FUTCHER, AB ;
GREIDER, CW ;
HARLEY, CB .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1992, 89 (21) :10114-10118
[2]   Hypoxic regulation of telomerase gene expression by transcriptional and post-transcriptional mechanisms [J].
Anderson, CJ ;
Hoare, SF ;
Ashcroft, M ;
Bilsland, AE ;
Keith, WN .
ONCOGENE, 2006, 25 (01) :61-69
[3]   Regulation of p53 stability [J].
Ashcroft, M ;
Vousden, KH .
ONCOGENE, 1999, 18 (53) :7637-7643
[4]   PAPILLOMAVIRUS POLYPEPTIDE-E6 AND POLYPEPTIDE-E7 ARE ZINC-BINDING PROTEINS [J].
BARBOSA, MS ;
LOWY, DR ;
SCHILLER, JT .
JOURNAL OF VIROLOGY, 1989, 63 (03) :1404-1407
[5]   Acetylation of p53 activates transcription through recruitment of coactivators/histone acetyltransferases [J].
Barlev, NA ;
Liu, L ;
Chehab, NH ;
Mansfield, K ;
Harris, KG ;
Halazonetis, TD ;
Berger, SL .
MOLECULAR CELL, 2001, 8 (06) :1243-1254
[6]   Solution structure determination and mutational analysis of the papillomavirus E6 interacting peptide of E6AP [J].
Be, XB ;
Hong, YH ;
Wei, J ;
Androphy, EJ ;
Chen, JJ ;
Baleja, JD .
BIOCHEMISTRY, 2001, 40 (05) :1293-1299
[7]   The E6 oncoproteins from human betapapillomaviruses differentially activate telomerase through an E6AP-dependent mechanism and prolong the lifespan of primary keratinocytes [J].
Bedard, Kristin M. ;
Underbrink, Michael P. ;
Howie, Heather L. ;
Galloway, Denise A. .
JOURNAL OF VIROLOGY, 2008, 82 (08) :3894-3902
[8]   Epithelial polarity and proliferation control:: links from the Drosophila neoplastic tumor suppressors [J].
Bilder, D .
GENES & DEVELOPMENT, 2004, 18 (16) :1909-1925
[9]   Effects of human papillomavirus type 16 oncoproteins on survivin gene expression [J].
Borbély, AA ;
Murvai, M ;
Kónya, J ;
Beck, Z ;
Gergely, L ;
Li, FZ ;
Veress, G .
JOURNAL OF GENERAL VIROLOGY, 2006, 87 :287-294
[10]   Functional interaction of a novel cellular protein with the papillomavirus E2 transactivation domain [J].
Breiding, DE ;
Sverdrup, F ;
Grossel, MJ ;
Moscufo, N ;
Boonchai, W ;
Androphy, EJ .
MOLECULAR AND CELLULAR BIOLOGY, 1997, 17 (12) :7208-7219