<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="6.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Markljung, E</style></author><author><style face="normal" font="default" size="100%">Jiang, L</style></author><author><style face="normal" font="default" size="100%">Jaffe, JD</style></author><author><style face="normal" font="default" size="100%">Mikkelsen, TS</style></author><author><style face="normal" font="default" size="100%">Wallerman, O</style></author><author><style face="normal" font="default" size="100%">Larhammar, M</style></author><author><style face="normal" font="default" size="100%">Zhang, X</style></author><author><style face="normal" font="default" size="100%">Wang, L</style></author><author><style face="normal" font="default" size="100%">Saenz-Vash, V</style></author><author><style face="normal" font="default" size="100%">Gnirke, A</style></author><author><style face="normal" font="default" size="100%">Lindroth, AM</style></author><author><style face="normal" font="default" size="100%">Barrés, R</style></author><author><style face="normal" font="default" size="100%">Yan, J</style></author><author><style face="normal" font="default" size="100%">Strömberg, S</style></author><author><style face="normal" font="default" size="100%">De, S</style></author><author><style face="normal" font="default" size="100%">Pontén, F</style></author><author><style face="normal" font="default" size="100%">Lander,E S</style></author><author><style face="normal" font="default" size="100%">Carr, SA</style></author><author><style face="normal" font="default" size="100%">Zierath, JR</style></author><author><style face="normal" font="default" size="100%">Kullander, K</style></author><author><style face="normal" font="default" size="100%">Wadelius, C</style></author><author><style face="normal" font="default" size="100%">Lindblad-Toh,K</style></author><author><style face="normal" font="default" size="100%">Andersson, G</style></author><author><style face="normal" font="default" size="100%">Hjälm, G</style></author><author><style face="normal" font="default" size="100%">Andersson, L</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">ZBED6, a novel transcription factor derived from a domesticated DNA transposon regulates IGF2 expression and muscle growth.</style></title><secondary-title><style face="normal" font="default" size="100%">PLoS biology</style></secondary-title><short-title><style face="normal" font="default" size="100%">PLoS Biol</style></short-title></titles><dates><year><style  face="normal" font="default" size="100%">2009</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2009/12/01</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://dx.plos.org/10.1371/journal.pbio.1000256</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">7</style></volume><pages><style face="normal" font="default" size="100%">e1000256</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">A single nucleotide substitution in intron 3 of IGF2 in pigs abrogates a binding site for a repressor and leads to a 3-fold up-regulation of IGF2 in skeletal muscle. The mutation has major effects on muscle growth, size of the heart, and fat deposition. Here, we have identified the repressor and find that the protein, named ZBED6, is previously unknown, specific for placental mammals, and derived from an exapted DNA transposon. Silencing of Zbed6 in mouse C2C12 myoblasts affected Igf2 expression, cell proliferation, wound healing, and myotube formation. Chromatin immunoprecipitation (ChIP) sequencing using C2C12 cells identified about 2,500 ZBED6 binding sites in the genome, and the deduced consensus motif gave a perfect match with the established binding site in Igf2. Genes associated with ZBED6 binding sites showed a highly significant enrichment for certain Gene Ontology classifications, including development and transcriptional regulation. The phenotypic effects in mutant pigs and ZBED6-silenced C2C12 myoblasts, the extreme sequence conservation, its nucleolar localization, the broad tissue distribution, and the many target genes with essential biological functions suggest that ZBED6 is an important transcription factor in placental mammals, affecting development, cell proliferation, and growth.</style></abstract><issue><style face="normal" font="default" size="100%">12</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/20016685?dopt=Abstract</style></custom1><custom3><style face="normal" font="default" size="100%">20016685</style></custom3><custom4><style face="normal" font="default" size="100%">2009-12-01 12:00:00</style></custom4></record><record><source-app name="Biblio" version="6.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Li, Z</style></author><author><style face="normal" font="default" size="100%">Lu, J</style></author><author><style face="normal" font="default" size="100%">Sun, M</style></author><author><style face="normal" font="default" size="100%">Mi, S</style></author><author><style face="normal" font="default" size="100%">Zhang, H</style></author><author><style face="normal" font="default" size="100%">Luo, RT</style></author><author><style face="normal" font="default" size="100%">Chen, P</style></author><author><style face="normal" font="default" size="100%">Wang, Y</style></author><author><style face="normal" font="default" size="100%">Yan, M</style></author><author><style face="normal" font="default" size="100%">Qian, Z</style></author><author><style face="normal" font="default" size="100%">Neilly, MB</style></author><author><style face="normal" font="default" size="100%">Jin, J</style></author><author><style face="normal" font="default" size="100%">Zhang, Y</style></author><author><style face="normal" font="default" size="100%">Bohlander, SK</style></author><author><style face="normal" font="default" size="100%">Zhang, DE</style></author><author><style face="normal" font="default" size="100%">Larson, RA</style></author><author><style face="normal" font="default" size="100%">Le Beau, MM</style></author><author><style face="normal" font="default" size="100%">Thirman, MJ</style></author><author><style face="normal" font="default" size="100%">Golub,T R</style></author><author><style face="normal" font="default" size="100%">Rowley, JD</style></author><author><style face="normal" font="default" size="100%">Chen, J</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Distinct microRNA expression profiles in acute myeloid leukemia with common translocations.</style></title><secondary-title><style face="normal" font="default" size="100%">Proceedings of the National Academy of Sciences of the United States of America</style></secondary-title><short-title><style face="normal" font="default" size="100%">Proc Natl Acad Sci U S A</style></short-title></titles><dates><year><style  face="normal" font="default" size="100%">2008</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2008/10/07</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.pnas.org/cgi/pmidlookup?view=long&pmid=18832181</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">105</style></volume><pages><style face="normal" font="default" size="100%">15535-40</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">MicroRNAs (miRNAs) are postulated to be important regulators in cancers. Here, we report a genome-wide miRNA expression analysis in 52 acute myeloid leukemia (AML) samples with common translocations, including t(8;21)/AML1(RUNX1)-ETO(RUNX1T1), inv(16)/CBFB-MYH11, t(15;17)/PML-RARA, and MLL rearrangements. Distinct miRNA expression patterns were observed for t(15;17), MLL rearrangements, and core-binding factor (CBF) AMLs including both t(8;21) and inv(16) samples. Expression signatures of a minimum of two (i.e., miR-126/126*), three (i.e., miR-224, miR-368, and miR-382), and seven (miR-17-5p and miR-20a, plus the aforementioned five) miRNAs could accurately discriminate CBF, t(15;17), and MLL-rearrangement AMLs, respectively, from each other. We further showed that the elevated expression of miR-126/126* in CBF AMLs was associated with promoter demethylation but not with amplification or mutation of the genomic locus. Our gain- and loss-of-function experiments showed that miR-126/126* inhibited apoptosis and increased the viability of AML cells and enhanced the colony-forming ability of mouse normal bone marrow progenitor cells alone and particularly, in cooperation with AML1-ETO, likely through targeting Polo-like kinase 2 (PLK2), a tumor suppressor. Our results demonstrate that specific alterations in miRNA expression distinguish AMLs with common translocations and imply that the deregulation of specific miRNAs may play a role in the development of leukemia with these associated genetic rearrangements.</style></abstract><issue><style face="normal" font="default" size="100%">40</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/18832181?dopt=Abstract</style></custom1><custom3><style face="normal" font="default" size="100%">18832181</style></custom3><custom4><style face="normal" font="default" size="100%">2008-10-07 12:00:00</style></custom4></record><record><source-app name="Biblio" version="6.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Huang,Guosheng</style></author><author><style face="normal" font="default" size="100%">Eisenberg,Rosana</style></author><author><style face="normal" font="default" size="100%">Yan,Min</style></author><author><style face="normal" font="default" size="100%">Monti,Stefano</style></author><author><style face="normal" font="default" size="100%">Lawrence,Earl</style></author><author><style face="normal" font="default" size="100%">Fu,Pingfu</style></author><author><style face="normal" font="default" size="100%">Walbroehl,Jaclyn</style></author><author><style face="normal" font="default" size="100%">L</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">15-Hydroxyprostaglandin dehydrogenase is a target of hepatocyte nuclear factor 3beta and a tumor suppressor in lung cancer</style></title><secondary-title><style face="normal" font="default" size="100%">Cancer Research</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Adenocarcinoma</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%">Binding Sites</style></keyword><keyword><style  face="normal" font="default" size="100%">Cancer</style></keyword><keyword><style  face="normal" font="default" size="100%">Down-Regulation</style></keyword><keyword><style  face="normal" font="default" size="100%">Enzymologic</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</style></keyword><keyword><style  face="normal" font="default" size="100%">Genes</style></keyword><keyword><style  face="normal" font="default" size="100%">Hepatocyte Nuclear Factor 3-beta</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Hydroxyp</style></keyword><keyword><style  face="normal" font="default" size="100%">Neoplastic</style></keyword><keyword><style  face="normal" font="default" size="100%">Tumor Suppressor</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%">2008/07/01/</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/18593902</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">68</style></volume><pages><style face="normal" font="default" size="100%">5040 - 8</style></pages><isbn><style face="normal" font="default" size="100%">1538-7445</style></isbn><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">The forkhead transcription factor hepatocyte nuclear factor 3beta (HNF3beta) is essential in foregut development and the regulation of lung-specific genes. HNF3beta expression leads to growth arrest and apoptosis in lung cancer cells and HNF3beta is a candidate tumor suppressor in lung cancer. In a transcriptional profiling study using a conditional cell line system, we now identify 15-PGDH as one of the major genes induced by HNF3beta expression. 15-PGDH is a critical metabolic enzyme of proliferative prostaglandins, an antagonist to cyclooxygenase-2 and a tumor suppressor in colon cancer. We confirmed the regulation of 15-PGDH expression by HNF3beta in a number of systems and showed direct binding of HNF3beta to 15-PGDH promoter elements. Western blotting of lung cancer cell lines and immunohistochemical examination of human lung cancer tissues found loss of 15-PGDH expression in approximately 65% of lung cancers. Further studies using in vitro cell-based assays and in vivo xenograft tumorigenesis assays showed a lack of in vitro but significant in vivo tumor suppressor activity of 15-PGDH via an antiangiogenic mechanism analogous to its role in colon cancer. In summary, we identify 15-PGDH as a direct downstream effector of HNF3beta and show that 15-PGDH acts as a tumor suppressor in lung cancer.</style></abstract><issue><style face="normal" font="default" size="100%">13</style></issue></record></records></xml>
