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DDX1 Promotes Proliferation of the JC Virus through Transactivation of Its Promoter
Author(s) -
Sunden Yuji,
Semba Shingo,
Suzuki Tadaki,
Okada Yuki,
Orba Yasuko,
Nagashima Kazuo,
Umemura Takashi,
Sawa Hirofumi
Publication year - 2007
Publication title -
microbiology and immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.664
H-Index - 70
eISSN - 1348-0421
pISSN - 0385-5600
DOI - 10.1111/j.1348-0421.2007.tb03907.x
Subject(s) - biology , transactivation , rna helicase a , gene knockdown , small interfering rna , transcription factor , viral replication , transcription (linguistics) , jc virus , microbiology and biotechnology , virology , dead box , cell culture , rna binding protein , rna , helicase , virus , transfection , gene , genetics , linguistics , philosophy , progressive multifocal leukoencephalopathy
Recently, we demonstrated that the DEAD box protein 1 (DDX1), an RNA helicase, and the cleavage stimulation factor (CstF) form a complex that binds to the JC virus transcriptional control region (JCV‐TCR). Here, we examined the function of DDX1, which is expressed at much higher levels in the JCV‐susceptible cell line IMR‐32 than in non‐susceptible cell lines. DDX1 had no effect on the replication efficiency of JCV, but over expression of DDX1 significantly increased transactivation of the JCV promoter. Furthermore, DDX1 enhanced the expression of JCV proteins in JCV infected cells, and knockdown of DDX1 using small interfering (si) RNA suppressed the expression of JCV proteins. Our results clearly demonstrate that DDX1 regulates proliferation of JCV in vitro through transcriptional activation.