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p53 and Sp1 cooperate to regulate the expression of epstein–barr viral Zta protein
Author(s) -
Chua HueyHuey,
Chiu HsinYi,
Lin SueJane,
Weng PeiLun,
Lin JiunHan,
Wu ShaoWen,
Tsai ShuChun,
Tsai ChingHwa
Publication year - 2012
Publication title -
journal of medical virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.782
H-Index - 121
eISSN - 1096-9071
pISSN - 0146-6615
DOI - 10.1002/jmv.23316
Subject(s) - lytic cycle , bzlf1 , biology , epstein–barr virus , transactivation , gene knockdown , virus latency , virology , microbiology and biotechnology , transcription factor , transcription (linguistics) , histone , virus , cell culture , dna , herpesviridae , genetics , viral replication , gene , viral disease , linguistics , philosophy
Epstein–Barr virus (EBV) belongs to the gammaherpesvirus family. To produce infectious progeny, EBV reactivates from latency into the lytic cycle by expressing the determinative lytic transactivator, Zta. In the presence of histone deacetylase inhibitor (HDACi), p53 is a prerequisite for the initiation of the EBV lytic cycle by facilitating the expression of Zta. In this study, a serial mutational analysis of Zta promoter (Zp) indicated an important role for the ZID element in responding to HDACi induction and p53 binds to this ZID element together with Sp1, a universal transcription factor. Abolition of the DNA‐binding ability of Sp1 reduces the inducibility of ZID by HDACi and also reduces the amount of p53 binding to ZID. Finally, it was shown that EBV in p53‐positive‐lymphoblastoid cell lines (LCLs) can enter into the lytic cycle spontaneously; however, knockdown of p53 in LCLs leads to retardation of EBV reactivation. J. Med. Virol. 84: 1279–1288, 2012. © 2012 Wiley Periodicals, Inc.