<?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%">Sparks, E. E.</style></author><author><style face="normal" font="default" size="100%">Drapek, C.</style></author><author><style face="normal" font="default" size="100%">Gaudinier, A.</style></author><author><style face="normal" font="default" size="100%">Li, S.</style></author><author><style face="normal" font="default" size="100%">Ansariola, M.</style></author><author><style face="normal" font="default" size="100%">Shen, N.</style></author><author><style face="normal" font="default" size="100%">Hennacy, J. H.</style></author><author><style face="normal" font="default" size="100%">Zhang, J.</style></author><author><style face="normal" font="default" size="100%">Turco, G.</style></author><author><style face="normal" font="default" size="100%">Petricka, J. J.</style></author><author><style face="normal" font="default" size="100%">Foret, J.</style></author><author><style face="normal" font="default" size="100%">Hartemink, A. J.</style></author><author><style face="normal" font="default" size="100%">Gordan, R.</style></author><author><style face="normal" font="default" size="100%">Megraw, M.</style></author><author><style face="normal" font="default" size="100%">Brady, S. M.</style></author><author><style face="normal" font="default" size="100%">Benfey, P. N.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Establishment of Expression in the SHORTROOT-SCARECROW Transcriptional Cascade through Opposing Activities of Both Activators and Repressors</style></title><secondary-title><style face="normal" font="default" size="100%">Dev Cell</style></secondary-title><short-title><style face="normal" font="default" size="100%">Developmental cell</style></short-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Arabidopsis Proteins/ genetics/ metabolism</style></keyword><keyword><style  face="normal" font="default" size="100%">Arabidopsis/ genetics/growth &amp; development/ metabolism</style></keyword><keyword><style  face="normal" font="default" size="100%">Computer Simulation</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene Expression Regulation, Plant</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene Regulatory Networks</style></keyword><keyword><style  face="normal" font="default" size="100%">Genes, Plant</style></keyword><keyword><style  face="normal" font="default" size="100%">Genes, Reporter</style></keyword><keyword><style  face="normal" font="default" size="100%">Genes, Synthetic</style></keyword><keyword><style  face="normal" font="default" size="100%">Models, Genetic</style></keyword><keyword><style  face="normal" font="default" size="100%">Plant Roots/cytology/metabolism</style></keyword><keyword><style  face="normal" font="default" size="100%">Plants, Genetically Modified</style></keyword><keyword><style  face="normal" font="default" size="100%">Promoter Regions, Genetic</style></keyword><keyword><style  face="normal" font="default" size="100%">Repressor Proteins/genetics/metabolism</style></keyword><keyword><style  face="normal" font="default" size="100%">Trans-Activators/genetics/metabolism</style></keyword><keyword><style  face="normal" font="default" size="100%">Transcription Factors/ genetics/ metabolism</style></keyword><keyword><style  face="normal" font="default" size="100%">Two-Hybrid System Techniques</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2016</style></year><pub-dates><date><style  face="normal" font="default" size="100%">12/2016</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">https://doi.org/10.1016/j.devcel.2016.09.031</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">39</style></volume><pages><style face="normal" font="default" size="100%">585-596</style></pages><isbn><style face="normal" font="default" size="100%">1878-1551 (Electronic)1534-5807 (Linking)</style></isbn><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Tissue-specific gene expression is often thought to arise from spatially restricted transcriptional cascades. However, it is unclear how expression is established at the top of these cascades in the absence of pre-existing specificity. We generated a transcriptional network to explore how transcription factor expression is established in the Arabidopsis thaliana root ground tissue. Regulators of the SHORTROOT-SCARECROW transcriptional cascade were validated in planta. At the top of this cascade, we identified both activators and repressors of SHORTROOT. The aggregate spatial expression of these regulators is not sufficient to predict transcriptional specificity. Instead, modeling, transcriptional reporters, and synthetic promoters support a mechanism whereby expression at the top of the SHORTROOT-SCARECROW cascade is established through opposing activities of activators and repressors.&lt;/p&gt;</style></abstract></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%">Ivanchenko, Maria G</style></author><author><style face="normal" font="default" size="100%">Zhu, Jinsheng</style></author><author><style face="normal" font="default" size="100%">Wang, Bangjun</style></author><author><style face="normal" font="default" size="100%">Medvecká, Eva</style></author><author><style face="normal" font="default" size="100%">Du, Yunlong</style></author><author><style face="normal" font="default" size="100%">Azzarello, Elisa</style></author><author><style face="normal" font="default" size="100%">Mancuso, Stefano</style></author><author><style face="normal" font="default" size="100%">Megraw, Molly</style></author><author><style face="normal" font="default" size="100%">Filichkin, Sergei</style></author><author><style face="normal" font="default" size="100%">Dubrovsky, Joseph G</style></author><author><style face="normal" font="default" size="100%">Friml, Jiří</style></author><author><style face="normal" font="default" size="100%">Geisler, Markus</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">The cyclophilin A DIAGEOTROPICA gene affects auxin transport in both root and shoot to control lateral root formation.</style></title><secondary-title><style face="normal" font="default" size="100%">Development</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Development</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Arabidopsis</style></keyword><keyword><style  face="normal" font="default" size="100%">Biological Transport</style></keyword><keyword><style  face="normal" font="default" size="100%">Cyclophilin A</style></keyword><keyword><style  face="normal" font="default" size="100%">Indoleacetic Acids</style></keyword><keyword><style  face="normal" font="default" size="100%">Lycopersicon esculentum</style></keyword><keyword><style  face="normal" font="default" size="100%">Plant Proteins</style></keyword><keyword><style  face="normal" font="default" size="100%">Plant Roots</style></keyword><keyword><style  face="normal" font="default" size="100%">Plant Shoots</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2015</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2015 Feb 15</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">142</style></volume><pages><style face="normal" font="default" size="100%">712-21</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Cyclophilin A is a conserved peptidyl-prolyl cis-trans isomerase (PPIase) best known as the cellular receptor of the immunosuppressant cyclosporine A. Despite significant effort, evidence of developmental functions of cyclophilin A in non-plant systems has remained obscure. Mutations in a tomato (Solanum lycopersicum) cyclophilin A ortholog, DIAGEOTROPICA (DGT), have been shown to abolish the organogenesis of lateral roots; however, a mechanistic explanation of the phenotype is lacking. Here, we show that the dgt mutant lacks auxin maxima relevant to priming and specification of lateral root founder cells. DGT is expressed in shoot and root, and localizes to both the nucleus and cytoplasm during lateral root organogenesis. Mutation of ENTIRE/IAA9, a member of the auxin-responsive Aux/IAA protein family of transcriptional repressors, partially restores the inability of dgt to initiate lateral root primordia but not the primordia outgrowth. By comparison, grafting of a wild-type scion restores the process of lateral root formation, consistent with participation of a mobile signal. Antibodies do not detect movement of the DGT protein into the dgt rootstock; however, experiments with radiolabeled auxin and an auxin-specific microelectrode demonstrate abnormal auxin fluxes. Functional studies of DGT in heterologous yeast and tobacco-leaf auxin-transport systems demonstrate that DGT negatively regulates PIN-FORMED (PIN) auxin efflux transporters by affecting their plasma membrane localization. Studies in tomato support complex effects of the dgt mutation on PIN expression level, expression domain and plasma membrane localization. Our data demonstrate that DGT regulates auxin transport in lateral root formation.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">4</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%">Brady, Siobhan M</style></author><author><style face="normal" font="default" size="100%">Zhang, Lifang</style></author><author><style face="normal" font="default" size="100%">Megraw, Molly</style></author><author><style face="normal" font="default" size="100%">Martinez, Natalia J</style></author><author><style face="normal" font="default" size="100%">Jiang, Eric</style></author><author><style face="normal" font="default" size="100%">Yi, Charles S</style></author><author><style face="normal" font="default" size="100%">Liu, Weilin</style></author><author><style face="normal" font="default" size="100%">Zeng, Anna</style></author><author><style face="normal" font="default" size="100%">Taylor-Teeples, Mallorie</style></author><author><style face="normal" font="default" size="100%">Kim, Dahae</style></author><author><style face="normal" font="default" size="100%">Ahnert, Sebastian</style></author><author><style face="normal" font="default" size="100%">Ohler, Uwe</style></author><author><style face="normal" font="default" size="100%">Ware, Doreen</style></author><author><style face="normal" font="default" size="100%">Walhout, Albertha J M</style></author><author><style face="normal" font="default" size="100%">Benfey, Philip N</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">A stele-enriched gene regulatory network in the Arabidopsis root.</style></title><secondary-title><style face="normal" font="default" size="100%">Mol Syst Biol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Mol. Syst. Biol.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Arabidopsis</style></keyword><keyword><style  face="normal" font="default" size="100%">Arabidopsis Proteins</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene Expression Profiling</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene Regulatory Networks</style></keyword><keyword><style  face="normal" font="default" size="100%">MicroRNAs</style></keyword><keyword><style  face="normal" font="default" size="100%">Plant Roots</style></keyword><keyword><style  face="normal" font="default" size="100%">Reproducibility of Results</style></keyword><keyword><style  face="normal" font="default" size="100%">Systems Biology</style></keyword><keyword><style  face="normal" font="default" size="100%">Transcription Factors</style></keyword><keyword><style  face="normal" font="default" size="100%">Two-Hybrid System Techniques</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2011</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2011 Jan 18</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">7</style></volume><pages><style face="normal" font="default" size="100%">459</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Tightly controlled gene expression is a hallmark of multicellular development and is accomplished by transcription factors (TFs) and microRNAs (miRNAs). Although many studies have focused on identifying downstream targets of these molecules, less is known about the factors that regulate their differential expression. We used data from high spatial resolution gene expression experiments and yeast one-hybrid (Y1H) and two-hybrid (Y2H) assays to delineate a subset of interactions occurring within a gene regulatory network (GRN) that determines tissue-specific TF and miRNA expression in plants. We find that upstream TFs are expressed in more diverse cell types than their targets and that promoters that are bound by a relatively large number of TFs correspond to key developmental regulators. The regulatory consequence of many TFs for their target was experimentally determined using genetic analysis. Remarkably, molecular phenotypes were identified for 65% of the TFs, but morphological phenotypes were associated with only 16%. This indicates that the GRN is robust, and that gene expression changes may be canalized or buffered.&lt;/p&gt;</style></abstract></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>