Kaposi's sarcoma-associated herpesvirus (KSHV) Rta and cellular HMGB1 proteins synergistically transactivate the KSHVORF50 promoter

被引：25

作者：

Harrison, Sally M. ^{[1
]}

Whitehouse, Adrian ^{[1
,2
]}

机构：

[1] Univ Leeds, Fac Biol Sci, Inst Mol & Cellular Biol, Leeds LS2 9JT, W Yorkshire, England

[2] Univ Leeds, Astbury Ctr Struct Mol Biol, Leeds LS2 9JT, W Yorkshire, England

来源：

FEBS LETTERS | 2008年 / 582卷 / 20期

基金：

英国惠康基金;

关键词：

virus-host cell interaction; KSHV;

D O I：

10.1016/j.febslet.2008.07.055

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Kaposi's sarcoma-associated herpesvirus 'replication transcriptional activator' (Rta) plays a critical role in the switch from latency to lytic replication. Rta upregulates several lytic KSHV genes, including its own, through multiple mechanisms. We demonstrate that cellular HMGB1 binds and synergistically upregulates the ORF50 promoter in conjunction with Rta. No direct interaction between Rta and HMGB1 was observed, however a ternary complex is formed in the presence of Oct1. Furthermore, deletion of an Oct-1 binding site within the ORF50 promoter ablates the HMGB1-mediated synergistic response. These results suggest Rta autostimulation may be mediated by a transient complex involving Oct1 and HMGB1. (C) 2008 Federation of European Biochemical Societies. Published by Elsevier B. V. All rights reserved.

引用

页码：3080 / 3084

页数：5

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