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Kaposi's sarcoma‐associated herpesvirus (KSHV) Rta and cellular HMGB1 proteins synergistically transactivate the KSHV ORF50 promoter
Author(s) -
Harrison Sally M.,
Whitehouse Adrian
Publication year - 2008
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2008.07.055
Subject(s) - lytic cycle , kaposi's sarcoma associated herpesvirus , cancer research , activator (genetics) , chemistry , transcriptional activity , promoter , virology , microbiology and biotechnology , gene , biology , transcription factor , virus , gene expression , herpesviridae , biochemistry , viral disease
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.