Literature DB >> 17380054

DDX1 promotes proliferation of the JC virus through transactivation of its promoter.

Yuji Sunden1, Shingo Semba, Tadaki Suzuki, Yuki Okada, Yasuko Orba, Kazuo Nagashima, Takashi Umemura, Hirofumi Sawa.   

Abstract

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 overexpression 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.

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Year:  2007        PMID: 17380054     DOI: 10.1111/j.1348-0421.2007.tb03907.x

Source DB:  PubMed          Journal:  Microbiol Immunol        ISSN: 0385-5600            Impact factor:   1.955


  13 in total

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Review 10.  DExD/H-box RNA helicases as mediators of anti-viral innate immunity and essential host factors for viral replication.

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