<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Iizasa, Hisashi</style></author><author><style face="normal" font="default" size="100%">Wulff, Bjorn-Erik</style></author><author><style face="normal" font="default" size="100%">Alla, Nageswara R</style></author><author><style face="normal" font="default" size="100%">Maragkakis, Manolis</style></author><author><style face="normal" font="default" size="100%">Megraw, Molly</style></author><author><style face="normal" font="default" size="100%">Hatzigeorgiou, Artemis</style></author><author><style face="normal" font="default" size="100%">Iwakiri, Dai</style></author><author><style face="normal" font="default" size="100%">Takada, Kenzo</style></author><author><style face="normal" font="default" size="100%">Wiedmer, Andreas</style></author><author><style face="normal" font="default" size="100%">Showe, Louise</style></author><author><style face="normal" font="default" size="100%">Lieberman, Paul</style></author><author><style face="normal" font="default" size="100%">Nishikura, Kazuko</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Editing of Epstein-Barr virus-encoded BART6 microRNAs controls their dicer targeting and consequently affects viral latency.</style></title><secondary-title><style face="normal" font="default" size="100%">J Biol Chem</style></secondary-title><alt-title><style face="normal" font="default" size="100%">J. Biol. Chem.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Cell Line, Tumor</style></keyword><keyword><style  face="normal" font="default" size="100%">Epstein-Barr Virus Infections</style></keyword><keyword><style  face="normal" font="default" size="100%">Epstein-Barr Virus Nuclear Antigens</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene Silencing</style></keyword><keyword><style  face="normal" font="default" size="100%">Herpesvirus 4, Human</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Immediate-Early Proteins</style></keyword><keyword><style  face="normal" font="default" size="100%">MicroRNAs</style></keyword><keyword><style  face="normal" font="default" size="100%">Ribonuclease III</style></keyword><keyword><style  face="normal" font="default" size="100%">RNA Editing</style></keyword><keyword><style  face="normal" font="default" size="100%">RNA, Viral</style></keyword><keyword><style  face="normal" font="default" size="100%">Trans-Activators</style></keyword><keyword><style  face="normal" font="default" size="100%">Viral Proteins</style></keyword><keyword><style  face="normal" font="default" size="100%">Virus Latency</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2010</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2010 Oct 22</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">285</style></volume><pages><style face="normal" font="default" size="100%">33358-70</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Certain primary transcripts of miRNA (pri-microRNAs) undergo RNA editing that converts adenosine to inosine. The Epstein-Barr virus (EBV) genome encodes multiple microRNA genes of its own. Here we report that primary transcripts of ebv-miR-BART6 (pri-miR-BART6) are edited in latently EBV-infected cells. Editing of wild-type pri-miR-BART6 RNAs dramatically reduced loading of miR-BART6-5p RNAs onto the microRNA-induced silencing complex. Editing of a mutation-containing pri-miR-BART6 found in Daudi Burkitt lymphoma and nasopharyngeal carcinoma C666-1 cell lines suppressed processing of miR-BART6 RNAs. Most importantly, miR-BART6-5p RNAs silence Dicer through multiple target sites located in the 3&amp;#39;-UTR of Dicer mRNA. The significance of miR-BART6 was further investigated in cells in various stages of latency. We found that miR-BART6-5p RNAs suppress the EBNA2 viral oncogene required for transition from immunologically less responsive type I and type II latency to the more immunoreactive type III latency as well as Zta and Rta viral proteins essential for lytic replication, revealing the regulatory function of miR-BART6 in EBV infection and latency. Mutation and A-to-I editing appear to be adaptive mechanisms that antagonize miR-BART6 activities.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">43</style></issue></record></records></xml>