<?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><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%">Kawahara, Yukio</style></author><author><style face="normal" font="default" size="100%">Megraw, Molly</style></author><author><style face="normal" font="default" size="100%">Kreider, Edward</style></author><author><style face="normal" font="default" size="100%">Iizasa, Hisashi</style></author><author><style face="normal" font="default" size="100%">Valente, Louis</style></author><author><style face="normal" font="default" size="100%">Hatzigeorgiou, Artemis G</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%">Frequency and fate of microRNA editing in human brain.</style></title><secondary-title><style face="normal" font="default" size="100%">Nucleic Acids Res</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Nucleic Acids Res.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Adenosine</style></keyword><keyword><style  face="normal" font="default" size="100%">Adenosine Deaminase</style></keyword><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Base Sequence</style></keyword><keyword><style  face="normal" font="default" size="100%">Brain</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Inosine</style></keyword><keyword><style  face="normal" font="default" size="100%">Mice</style></keyword><keyword><style  face="normal" font="default" size="100%">MicroRNAs</style></keyword><keyword><style  face="normal" font="default" size="100%">Molecular Sequence Data</style></keyword><keyword><style  face="normal" font="default" size="100%">RNA Editing</style></keyword><keyword><style  face="normal" font="default" size="100%">RNA Precursors</style></keyword><keyword><style  face="normal" font="default" size="100%">RNA Processing, Post-Transcriptional</style></keyword><keyword><style  face="normal" font="default" size="100%">RNA-Binding Proteins</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2008</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2008 Sep</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">36</style></volume><pages><style face="normal" font="default" size="100%">5270-80</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Primary transcripts of certain microRNA (miRNA) genes (pri-miRNAs) are subject to RNA editing that converts adenosine to inosine (A--&amp;gt;I RNA editing). However, the frequency of the pri-miRNA editing and the fate of edited pri-miRNAs remain largely to be determined. Examination of already known pri-miRNA editing sites indicated that adenosine residues of the UAG triplet sequence might be edited more frequently. In the present study, therefore, we conducted a large-scale survey of human pri-miRNAs containing the UAG triplet sequence. By direct sequencing of RT-PCR products corresponding to pri-miRNAs, we examined 209 pri-miRNAs and identified 43 UAG and also 43 non-UAG editing sites in 47 pri-miRNAs, which were highly edited in human brain. In vitro miRNA processing assay using recombinant Drosha-DGCR8 and Dicer-TRBP (the human immuno deficiency virus transactivating response RNA-binding protein) complexes revealed that a majority of pri-miRNA editing is likely to interfere with the miRNA processing steps. In addition, four new edited miRNAs with altered seed sequences were identified by targeted cloning and sequencing of the miRNAs that would be processed from edited pri-miRNAs. Our studies predict that approximately 16% of human pri-miRNAs are subject to A--&amp;gt;I editing and, thus, miRNA editing could have a large impact on the miRNA-mediated gene silencing.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">16</style></issue></record><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%">Zhang, Lin</style></author><author><style face="normal" font="default" size="100%">Volinia, Stefano</style></author><author><style face="normal" font="default" size="100%">Bonome, Tomas</style></author><author><style face="normal" font="default" size="100%">Calin, George Adrian</style></author><author><style face="normal" font="default" size="100%">Greshock, Joel</style></author><author><style face="normal" font="default" size="100%">Yang, Nuo</style></author><author><style face="normal" font="default" size="100%">Liu, Chang-Gong</style></author><author><style face="normal" font="default" size="100%">Giannakakis, Antonis</style></author><author><style face="normal" font="default" size="100%">Alexiou, Pangiotis</style></author><author><style face="normal" font="default" size="100%">Hasegawa, Kosei</style></author><author><style face="normal" font="default" size="100%">Johnstone, Cameron N</style></author><author><style face="normal" font="default" size="100%">Megraw, Molly S</style></author><author><style face="normal" font="default" size="100%">Adams, Sarah</style></author><author><style face="normal" font="default" size="100%">Lassus, Heini</style></author><author><style face="normal" font="default" size="100%">Huang, Jia</style></author><author><style face="normal" font="default" size="100%">Kaur, Sippy</style></author><author><style face="normal" font="default" size="100%">Liang, Shun</style></author><author><style face="normal" font="default" size="100%">Sethupathy, Praveen</style></author><author><style face="normal" font="default" size="100%">Leminen, Arto</style></author><author><style face="normal" font="default" size="100%">Simossis, Victor A</style></author><author><style face="normal" font="default" size="100%">Sandaltzopoulos, Raphael</style></author><author><style face="normal" font="default" size="100%">Naomoto, Yoshio</style></author><author><style face="normal" font="default" size="100%">Katsaros, Dionyssios</style></author><author><style face="normal" font="default" size="100%">Gimotty, Phyllis A</style></author><author><style face="normal" font="default" size="100%">DeMichele, Angela</style></author><author><style face="normal" font="default" size="100%">Huang, Qihong</style></author><author><style face="normal" font="default" size="100%">Bützow, Ralf</style></author><author><style face="normal" font="default" size="100%">Rustgi, Anil K</style></author><author><style face="normal" font="default" size="100%">Weber, Barbara L</style></author><author><style face="normal" font="default" size="100%">Birrer, Michael J</style></author><author><style face="normal" font="default" size="100%">Hatzigeorgiou, Artemis G</style></author><author><style face="normal" font="default" size="100%">Croce, Carlo M</style></author><author><style face="normal" font="default" size="100%">Coukos, George</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Genomic and epigenetic alterations deregulate microRNA expression in human epithelial ovarian cancer.</style></title><secondary-title><style face="normal" font="default" size="100%">Proc Natl Acad Sci U S A</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Proc. Natl. Acad. Sci. U.S.A.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">DNA, Neoplasm</style></keyword><keyword><style  face="normal" font="default" size="100%">Down-Regulation</style></keyword><keyword><style  face="normal" font="default" size="100%">Epigenesis, Genetic</style></keyword><keyword><style  face="normal" font="default" size="100%">Epithelial Cells</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene Expression Profiling</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene Expression Regulation, Neoplastic</style></keyword><keyword><style  face="normal" font="default" size="100%">Genome, Human</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">MicroRNAs</style></keyword><keyword><style  face="normal" font="default" size="100%">Neoplasm Staging</style></keyword><keyword><style  face="normal" font="default" size="100%">Ovarian Neoplasms</style></keyword><keyword><style  face="normal" font="default" size="100%">Ribonuclease III</style></keyword><keyword><style  face="normal" font="default" size="100%">RNA, Messenger</style></keyword><keyword><style  face="normal" font="default" size="100%">Survival Analysis</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2008</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2008 May 13</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">105</style></volume><pages><style face="normal" font="default" size="100%">7004-9</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;MicroRNAs (miRNAs) are an abundant class of small noncoding RNAs that function as negative gene regulators. miRNA deregulation is involved in the initiation and progression of human cancer; however, the underlying mechanism and its contributions to genome-wide transcriptional changes in cancer are still largely unknown. We studied miRNA deregulation in human epithelial ovarian cancer by integrative genomic approach, including miRNA microarray (n = 106), array-based comparative genomic hybridization (n = 109), cDNA microarray (n = 76), and tissue array (n = 504). miRNA expression is markedly down-regulated in malignant transformation and tumor progression. Genomic copy number loss and epigenetic silencing, respectively, may account for the down-regulation of approximately 15% and at least approximately 36% of miRNAs in advanced ovarian tumors and miRNA down-regulation contributes to a genome-wide transcriptional deregulation. Last, eight miRNAs located in the chromosome 14 miRNA cluster (Dlk1-Gtl2 domain) were identified as potential tumor suppressor genes. Therefore, our results suggest that miRNAs may offer new biomarkers and therapeutic targets in epithelial ovarian cancer.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">19</style></issue></record><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%">Zhang, Lin</style></author><author><style face="normal" font="default" size="100%">Huang, Jia</style></author><author><style face="normal" font="default" size="100%">Yang, Nuo</style></author><author><style face="normal" font="default" size="100%">Greshock, Joel</style></author><author><style face="normal" font="default" size="100%">Megraw, Molly S</style></author><author><style face="normal" font="default" size="100%">Giannakakis, Antonis</style></author><author><style face="normal" font="default" size="100%">Liang, Shun</style></author><author><style face="normal" font="default" size="100%">Naylor, Tara L</style></author><author><style face="normal" font="default" size="100%">Barchetti, Andrea</style></author><author><style face="normal" font="default" size="100%">Ward, Michelle R</style></author><author><style face="normal" font="default" size="100%">Yao, George</style></author><author><style face="normal" font="default" size="100%">Medina, Angelica</style></author><author><style face="normal" font="default" size="100%">O'brien-Jenkins, Ann</style></author><author><style face="normal" font="default" size="100%">Katsaros, Dionyssios</style></author><author><style face="normal" font="default" size="100%">Hatzigeorgiou, Artemis</style></author><author><style face="normal" font="default" size="100%">Gimotty, Phyllis A</style></author><author><style face="normal" font="default" size="100%">Weber, Barbara L</style></author><author><style face="normal" font="default" size="100%">Coukos, George</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">microRNAs exhibit high frequency genomic alterations in human cancer.</style></title><secondary-title><style face="normal" font="default" size="100%">Proc Natl Acad Sci U S A</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Proc. Natl. Acad. Sci. U.S.A.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Breast Neoplasms</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene Dosage</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene Expression Profiling</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">MicroRNAs</style></keyword><keyword><style  face="normal" font="default" size="100%">Neoplasms</style></keyword><keyword><style  face="normal" font="default" size="100%">Nucleic Acid Hybridization</style></keyword><keyword><style  face="normal" font="default" size="100%">Oligonucleotide Array Sequence Analysis</style></keyword><keyword><style  face="normal" font="default" size="100%">Ovarian Neoplasms</style></keyword><keyword><style  face="normal" font="default" size="100%">Statistics as Topic</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2006</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2006 Jun 13</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">103</style></volume><pages><style face="normal" font="default" size="100%">9136-41</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;MicroRNAs (miRNAs) are endogenous noncoding RNAs, which negatively regulate gene expression. To determine genomewide miRNA DNA copy number abnormalities in cancer, 283 known human miRNA genes were analyzed by high-resolution array-based comparative genomic hybridization in 227 human ovarian cancer, breast cancer, and melanoma specimens. A high proportion of genomic loci containing miRNA genes exhibited DNA copy number alterations in ovarian cancer (37.1%), breast cancer (72.8%), and melanoma (85.9%), where copy number alterations observed in &amp;gt;15% tumors were considered significant for each miRNA gene. We identified 41 miRNA genes with gene copy number changes that were shared among the three cancer types (26 with gains and 15 with losses) as well as miRNA genes with copy number changes that were unique to each tumor type. Importantly, we show that miRNA copy changes correlate with miRNA expression. Finally, we identified high frequency copy number abnormalities of Dicer1, Argonaute2, and other miRNA-associated genes in breast and ovarian cancer as well as melanoma. These findings support the notion that copy number alterations of miRNAs and their regulatory genes are highly prevalent in cancer and may account partly for the frequent miRNA gene deregulation reported in several tumor types.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">24</style></issue></record></records></xml>