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  • 1
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    Unknown
    Nature Publishing Group (NPG)
    Publication Date: 2010-02-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Slack, Frank J -- England -- Nature. 2010 Feb 4;463(7281):616. doi: 10.1038/463616a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20130638" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caenorhabditis elegans/cytology/genetics ; Caenorhabditis elegans Proteins/genetics ; Cell Dedifferentiation/genetics ; *Cell Proliferation ; Embryonic Stem Cells/*cytology/*metabolism ; Humans ; Induced Pluripotent Stem Cells/cytology/metabolism ; MicroRNAs/*genetics/*metabolism ; Repressor Proteins/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 2
    Publication Date: 2010-08-10
    Description: MicroRNAs (miRNAs) belong to a recently discovered class of small RNA molecules that regulate gene expression at the post-transcriptional level. miRNAs have crucial functions in the development and establishment of cell identity, and aberrant metabolism or expression of miRNAs has been linked to human diseases, including cancer. Components of the miRNA machinery and miRNAs themselves are involved in many cellular processes that are altered in cancer, such as differentiation, proliferation and apoptosis. Some miRNAs, referred to as oncomiRs, show differential expression levels in cancer and are able to affect cellular transformation, carcinogenesis and metastasis, acting either as oncogenes or tumour suppressors. The phenomenon of 'oncogene addiction' reveals that despite the multistep nature of tumorigenesis, targeting of certain single oncogenes can have therapeutic value, and the possibility of oncomiR addiction has been proposed but never demonstrated. MicroRNA-21 (miR-21) is a unique miRNA in that it is overexpressed in most tumour types analysed so far. Despite great interest in miR-21, most of the data implicating it in cancer have been obtained through miRNA profiling and limited in vitro functional assays. To explore the role of miR-21 in cancer in vivo, we used Cre and Tet-off technologies to generate mice conditionally expressing miR-21. Here we show that overexpression of miR-21 leads to a pre-B malignant lymphoid-like phenotype, demonstrating that mir-21 is a genuine oncogene. When miR-21 was inactivated, the tumours regressed completely in a few days, partly as a result of apoptosis. These results demonstrate that tumours can become addicted to oncomiRs and support efforts to treat human cancers through pharmacological inactivation of miRNAs such as miR-21.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Medina, Pedro P -- Nolde, Mona -- Slack, Frank J -- England -- Nature. 2010 Sep 2;467(7311):86-90. doi: 10.1038/nature09284. Epub 2010 Aug 8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular, Cellular and Developmental Biology, Yale University, PO Box 208103, New Haven, Connecticut 06520, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20693987" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Lymphoma, B-Cell/*metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; MicroRNAs/genetics/*metabolism ; Precursor Cells, B-Lymphoid/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 3
    Publication Date: 2014-11-20
    Description: MicroRNAs are short non-coding RNAs expressed in different tissue and cell types that suppress the expression of target genes. As such, microRNAs are critical cogs in numerous biological processes, and dysregulated microRNA expression is correlated with many human diseases. Certain microRNAs, called oncomiRs, play a causal role in the onset and maintenance of cancer when overexpressed. Tumours that depend on these microRNAs are said to display oncomiR addiction. Some of the most effective anticancer therapies target oncogenes such as EGFR and HER2; similarly, inhibition of oncomiRs using antisense oligomers (that is, antimiRs) is an evolving therapeutic strategy. However, the in vivo efficacy of current antimiR technologies is hindered by physiological and cellular barriers to delivery into targeted cells. Here we introduce a novel antimiR delivery platform that targets the acidic tumour microenvironment, evades systemic clearance by the liver, and facilitates cell entry via a non-endocytic pathway. We find that the attachment of peptide nucleic acid antimiRs to a peptide with a low pH-induced transmembrane structure (pHLIP) produces a novel construct that could target the tumour microenvironment, transport antimiRs across plasma membranes under acidic conditions such as those found in solid tumours (pH approximately 6), and effectively inhibit the miR-155 oncomiR in a mouse model of lymphoma. This study introduces a new model for using antimiRs as anti-cancer drugs, which can have broad impacts on the field of targeted drug delivery.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4367962/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4367962/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cheng, Christopher J -- Bahal, Raman -- Babar, Imran A -- Pincus, Zachary -- Barrera, Francisco -- Liu, Connie -- Svoronos, Alexander -- Braddock, Demetrios T -- Glazer, Peter M -- Engelman, Donald M -- Saltzman, W Mark -- Slack, Frank J -- 2T32HL007974/HL/NHLBI NIH HHS/ -- F32 CA174247/CA/NCI NIH HHS/ -- F32CA174247/CA/NCI NIH HHS/ -- P30 CA016359/CA/NCI NIH HHS/ -- R00 AG042487/AG/NIA NIH HHS/ -- R01 CA131301/CA/NCI NIH HHS/ -- R01 CA148996/CA/NCI NIH HHS/ -- R01 CA149128/CA/NCI NIH HHS/ -- R01 EB000487/EB/NIBIB NIH HHS/ -- R01 ES005775/ES/NIEHS NIH HHS/ -- R01 GM073857/GM/NIGMS NIH HHS/ -- R01 HL085416/HL/NHLBI NIH HHS/ -- R01CA131301/CA/NCI NIH HHS/ -- R01CA148996/CA/NCI NIH HHS/ -- R01EB000487/EB/NIBIB NIH HHS/ -- R01ES005775/ES/NIEHS NIH HHS/ -- R01GM073857/GM/NIGMS NIH HHS/ -- R01HL085416/HL/NHLBI NIH HHS/ -- T32 GM007205/GM/NIGMS NIH HHS/ -- T32 HL007974/HL/NHLBI NIH HHS/ -- UL1 TR000142/TR/NCATS NIH HHS/ -- England -- Nature. 2015 Feb 5;518(7537):107-10. doi: 10.1038/nature13905. Epub 2014 Nov 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Department of Molecular, Cellular and Developmental Biology, Yale University, New Haven, Connecticut 06511, USA [2] Department of Biomedical Engineering, Yale University, New Haven, Connecticut 06511, USA [3] Department of Molecular Biophysics and Biochemistry, Yale University, New Haven, Connecticut 06511, USA. ; Department of Therapeutic Radiology, Yale University, New Haven, Connecticut 06511, USA. ; Department of Molecular, Cellular and Developmental Biology, Yale University, New Haven, Connecticut 06511, USA. ; Department of Molecular Biophysics and Biochemistry, Yale University, New Haven, Connecticut 06511, USA. ; Department of Pathology, Yale University, New Haven, Connecticut 06511, USA. ; Department of Biomedical Engineering, Yale University, New Haven, Connecticut 06511, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25409146" target="_blank"〉PubMed〈/a〉
    Keywords: Acids ; Animals ; Cell Membrane/metabolism ; Cell Membrane Permeability ; Disease Models, Animal ; *Drug Delivery Systems ; Female ; *Gene Expression Regulation, Neoplastic ; *Gene Silencing ; Hydrogen-Ion Concentration ; Lymphoma/*genetics/pathology/*therapy ; Male ; Mice ; MicroRNAs/*antagonists & inhibitors/genetics ; Molecular Targeted Therapy ; Nanoparticles/administration & dosage/chemistry ; Oncogenes/genetics ; Peptide Nucleic Acids/administration & dosage/chemistry/therapeutic use ; *Tumor Microenvironment/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 4
    Publication Date: 2010-12-24
    Description: We systematically generated large-scale data sets to improve genome annotation for the nematode Caenorhabditis elegans, a key model organism. These data sets include transcriptome profiling across a developmental time course, genome-wide identification of transcription factor-binding sites, and maps of chromatin organization. From this, we created more complete and accurate gene models, including alternative splice forms and candidate noncoding RNAs. We constructed hierarchical networks of transcription factor-binding and microRNA interactions and discovered chromosomal locations bound by an unusually large number of transcription factors. Different patterns of chromatin composition and histone modification were revealed between chromosome arms and centers, with similarly prominent differences between autosomes and the X chromosome. Integrating data types, we built statistical models relating chromatin, transcription factor binding, and gene expression. Overall, our analyses ascribed putative functions to most of the conserved genome.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3142569/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3142569/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gerstein, Mark B -- Lu, Zhi John -- Van Nostrand, Eric L -- Cheng, Chao -- Arshinoff, Bradley I -- Liu, Tao -- Yip, Kevin Y -- Robilotto, Rebecca -- Rechtsteiner, Andreas -- Ikegami, Kohta -- Alves, Pedro -- Chateigner, Aurelien -- Perry, Marc -- Morris, Mitzi -- Auerbach, Raymond K -- Feng, Xin -- Leng, Jing -- Vielle, Anne -- Niu, Wei -- Rhrissorrakrai, Kahn -- Agarwal, Ashish -- Alexander, Roger P -- Barber, Galt -- Brdlik, Cathleen M -- Brennan, Jennifer -- Brouillet, Jeremy Jean -- Carr, Adrian -- Cheung, Ming-Sin -- Clawson, Hiram -- Contrino, Sergio -- Dannenberg, Luke O -- Dernburg, Abby F -- Desai, Arshad -- Dick, Lindsay -- Dose, Andrea C -- Du, Jiang -- Egelhofer, Thea -- Ercan, Sevinc -- Euskirchen, Ghia -- Ewing, Brent -- Feingold, Elise A -- Gassmann, Reto -- Good, Peter J -- Green, Phil -- Gullier, Francois -- Gutwein, Michelle -- Guyer, Mark S -- Habegger, Lukas -- Han, Ting -- Henikoff, Jorja G -- Henz, Stefan R -- Hinrichs, Angie -- Holster, Heather -- Hyman, Tony -- Iniguez, A Leo -- Janette, Judith -- Jensen, Morten -- Kato, Masaomi -- Kent, W James -- Kephart, Ellen -- Khivansara, Vishal -- Khurana, Ekta -- Kim, John K -- Kolasinska-Zwierz, Paulina -- Lai, Eric C -- Latorre, Isabel -- Leahey, Amber -- Lewis, Suzanna -- Lloyd, Paul -- Lochovsky, Lucas -- Lowdon, Rebecca F -- Lubling, Yaniv -- Lyne, Rachel -- MacCoss, Michael -- Mackowiak, Sebastian D -- Mangone, Marco -- McKay, Sheldon -- Mecenas, Desirea -- Merrihew, Gennifer -- Miller, David M 3rd -- Muroyama, Andrew -- Murray, John I -- Ooi, Siew-Loon -- Pham, Hoang -- Phippen, Taryn -- Preston, Elicia A -- Rajewsky, Nikolaus -- Ratsch, Gunnar -- Rosenbaum, Heidi -- Rozowsky, Joel -- Rutherford, Kim -- Ruzanov, Peter -- Sarov, Mihail -- Sasidharan, Rajkumar -- Sboner, Andrea -- Scheid, Paul -- Segal, Eran -- Shin, Hyunjin -- Shou, Chong -- Slack, Frank J -- Slightam, Cindie -- Smith, Richard -- Spencer, William C -- Stinson, E O -- Taing, Scott -- Takasaki, Teruaki -- Vafeados, Dionne -- Voronina, Ksenia -- Wang, Guilin -- Washington, Nicole L -- Whittle, Christina M -- Wu, Beijing -- Yan, Koon-Kiu -- Zeller, Georg -- Zha, Zheng -- Zhong, Mei -- Zhou, Xingliang -- modENCODE Consortium -- Ahringer, Julie -- Strome, Susan -- Gunsalus, Kristin C -- Micklem, Gos -- Liu, X Shirley -- Reinke, Valerie -- Kim, Stuart K -- Hillier, LaDeana W -- Henikoff, Steven -- Piano, Fabio -- Snyder, Michael -- Stein, Lincoln -- Lieb, Jason D -- Waterston, Robert H -- 054523/Wellcome Trust/United Kingdom -- R01 GM088565/GM/NIGMS NIH HHS/ -- R01 GM088565-03/GM/NIGMS NIH HHS/ -- R01GM088565/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2010 Dec 24;330(6012):1775-87. doi: 10.1126/science.1196914. Epub 2010 Dec 22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program in Computational Biology and Bioinformatics, Yale University, Bass 432, 266 Whitney Avenue, New Haven, CT 06520, USA. modencode.worm.pi@gersteinlab.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21177976" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caenorhabditis elegans/*genetics/growth & development/metabolism ; Caenorhabditis elegans Proteins/genetics/metabolism ; Chromatin/genetics/metabolism/ultrastructure ; *Chromosomes/genetics/metabolism/ultrastructure ; Computational Biology/methods ; Conserved Sequence ; Evolution, Molecular ; *Gene Expression Profiling ; *Gene Expression Regulation ; Gene Regulatory Networks ; Genes, Helminth ; *Genome, Helminth ; Genomics/methods ; Histones/metabolism ; Models, Genetic ; *Molecular Sequence Annotation ; RNA, Helminth/genetics/metabolism ; RNA, Untranslated/genetics/metabolism ; Regulatory Sequences, Nucleic Acid ; Transcription Factors/genetics/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-12-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Anastasiadou, Eleni -- Slack, Frank J -- New York, N.Y. -- Science. 2014 Dec 19;346(6216):1459-60. doi: 10.1126/science.aaa4024.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, 330 Brookline Avenue, Boston, MA 02215, USA. ; Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, 330 Brookline Avenue, Boston, MA 02215, USA. fslack@bidmc.harvard.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25525233" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Humans ; Membrane Glycoproteins/*metabolism ; MicroRNAs/*blood ; Neoplasms/*blood ; RNA, Neoplasm/*blood ; Toll-Like Receptor 7/*metabolism ; Toll-Like Receptor 8/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
    Publication Date: 2014-08-29
    Description: The transcriptome is the readout of the genome. Identifying common features in it across distant species can reveal fundamental principles. To this end, the ENCODE and modENCODE consortia have generated large amounts of matched RNA-sequencing data for human, worm and fly. Uniform processing and comprehensive annotation of these data allow comparison across metazoan phyla, extending beyond earlier within-phylum transcriptome comparisons and revealing ancient, conserved features. Specifically, we discover co-expression modules shared across animals, many of which are enriched in developmental genes. Moreover, we use expression patterns to align the stages in worm and fly development and find a novel pairing between worm embryo and fly pupae, in addition to the embryo-to-embryo and larvae-to-larvae pairings. Furthermore, we find that the extent of non-canonical, non-coding transcription is similar in each organism, per base pair. Finally, we find in all three organisms that the gene-expression levels, both coding and non-coding, can be quantitatively predicted from chromatin features at the promoter using a 'universal model' based on a single set of organism-independent parameters.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4155737/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4155737/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gerstein, Mark B -- Rozowsky, Joel -- Yan, Koon-Kiu -- Wang, Daifeng -- Cheng, Chao -- Brown, James B -- Davis, Carrie A -- Hillier, LaDeana -- Sisu, Cristina -- Li, Jingyi Jessica -- Pei, Baikang -- Harmanci, Arif O -- Duff, Michael O -- Djebali, Sarah -- Alexander, Roger P -- Alver, Burak H -- Auerbach, Raymond -- Bell, Kimberly -- Bickel, Peter J -- Boeck, Max E -- Boley, Nathan P -- Booth, Benjamin W -- Cherbas, Lucy -- Cherbas, Peter -- Di, Chao -- Dobin, Alex -- Drenkow, Jorg -- Ewing, Brent -- Fang, Gang -- Fastuca, Megan -- Feingold, Elise A -- Frankish, Adam -- Gao, Guanjun -- Good, Peter J -- Guigo, Roderic -- Hammonds, Ann -- Harrow, Jen -- Hoskins, Roger A -- Howald, Cedric -- Hu, Long -- Huang, Haiyan -- Hubbard, Tim J P -- Huynh, Chau -- Jha, Sonali -- Kasper, Dionna -- Kato, Masaomi -- Kaufman, Thomas C -- Kitchen, Robert R -- Ladewig, Erik -- Lagarde, Julien -- Lai, Eric -- Leng, Jing -- Lu, Zhi -- MacCoss, Michael -- May, Gemma -- McWhirter, Rebecca -- Merrihew, Gennifer -- Miller, David M -- Mortazavi, Ali -- Murad, Rabi -- Oliver, Brian -- Olson, Sara -- Park, Peter J -- Pazin, Michael J -- Perrimon, Norbert -- Pervouchine, Dmitri -- Reinke, Valerie -- Reymond, Alexandre -- Robinson, Garrett -- Samsonova, Anastasia -- Saunders, Gary I -- Schlesinger, Felix -- Sethi, Anurag -- Slack, Frank J -- Spencer, William C -- Stoiber, Marcus H -- Strasbourger, Pnina -- Tanzer, Andrea -- Thompson, Owen A -- Wan, Kenneth H -- Wang, Guilin -- Wang, Huaien -- Watkins, Kathie L -- Wen, Jiayu -- Wen, Kejia -- Xue, Chenghai -- Yang, Li -- Yip, Kevin -- Zaleski, Chris -- Zhang, Yan -- Zheng, Henry -- Brenner, Steven E -- Graveley, Brenton R -- Celniker, Susan E -- Gingeras, Thomas R -- Waterston, Robert -- 1U01HG007031-01/HG/NHGRI NIH HHS/ -- 5U01HG004695-04/HG/NHGRI NIH HHS/ -- 5U54HG004555/HG/NHGRI NIH HHS/ -- HG007000/HG/NHGRI NIH HHS/ -- HG007355/HG/NHGRI NIH HHS/ -- K99 HG006698/HG/NHGRI NIH HHS/ -- P30 CA045508/CA/NCI NIH HHS/ -- R01 GM076655/GM/NIGMS NIH HHS/ -- RC2-HG005639/HG/NHGRI NIH HHS/ -- T15 LM007056/LM/NLM NIH HHS/ -- T32 HD060555/HD/NICHD NIH HHS/ -- U01 HG 004263/HG/NHGRI NIH HHS/ -- U01 HG004261/HG/NHGRI NIH HHS/ -- U01 HG004271/HG/NHGRI NIH HHS/ -- U01 HG007031/HG/NHGRI NIH HHS/ -- U01-HG004261/HG/NHGRI NIH HHS/ -- U01HG004258/HG/NHGRI NIH HHS/ -- U41 HG007000/HG/NHGRI NIH HHS/ -- U41 HG007234/HG/NHGRI NIH HHS/ -- U41 HG007355/HG/NHGRI NIH HHS/ -- U54 HG004555/HG/NHGRI NIH HHS/ -- U54 HG006944/HG/NHGRI NIH HHS/ -- U54 HG006994/HG/NHGRI NIH HHS/ -- U54 HG007004/HG/NHGRI NIH HHS/ -- U54 HG007005/HG/NHGRI NIH HHS/ -- U54HG007005/HG/NHGRI NIH HHS/ -- WT098051/Wellcome Trust/United Kingdom -- ZIA DK015600-18/Intramural NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2014 Aug 28;512(7515):445-8. doi: 10.1038/nature13424.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Program in Computational Biology and Bioinformatics, Yale University, Bass 432, 266 Whitney Avenue, New Haven, Connecticut 06520, USA [2] Department of Molecular Biophysics and Biochemistry, Yale University, Bass 432, 266 Whitney Avenue, New Haven, Connecticut 06520, USA [3] Department of Computer Science, Yale University, 51 Prospect Street, New Haven, Connecticut 06511, USA [4] [5]. ; 1] Program in Computational Biology and Bioinformatics, Yale University, Bass 432, 266 Whitney Avenue, New Haven, Connecticut 06520, USA [2] Department of Molecular Biophysics and Biochemistry, Yale University, Bass 432, 266 Whitney Avenue, New Haven, Connecticut 06520, USA [3]. ; 1] Department of Genetics, Geisel School of Medicine at Dartmouth, Hanover, New Hampshire 03755, USA [2] Institute for Quantitative Biomedical Sciences, Norris Cotton Cancer Center, Geisel School of Medicine at Dartmouth, Lebanon, New Hampshire 03766, USA [3]. ; 1] Department of Genome Dynamics, Lawrence Berkeley National Laboratory, Berkeley, California 94720, USA [2] Department of Statistics, University of California, Berkeley, 367 Evans Hall, Berkeley, California 94720-3860, USA [3]. ; 1] Functional Genomics, Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724, USA [2]. ; 1] Department of Genome Sciences and University of Washington School of Medicine, William H. Foege Building S350D, 1705 Northeast Pacific Street, Box 355065 Seattle, Washington 98195-5065, USA [2]. ; 1] Department of Statistics, University of California, Berkeley, 367 Evans Hall, Berkeley, California 94720-3860, USA [2] Department of Statistics, University of California, Los Angeles, California 90095-1554, USA [3] Department of Human Genetics, University of California, Los Angeles, California 90095-7088, USA [4]. ; 1] Department of Genetics and Developmental Biology, Institute for Systems Genomics, University of Connecticut Health Center, 400 Farmington Avenue, Farmington, Connecticut 06030, USA [2]. ; 1] Centre for Genomic Regulation, Doctor Aiguader 88, 08003 Barcelona, Catalonia, Spain [2] Departament de Ciencies Experimentals i de la Salut, Universitat Pompeu Fabra, 08003 Barcelona, Catalonia, Spain [3]. ; 1] Program in Computational Biology and Bioinformatics, Yale University, Bass 432, 266 Whitney Avenue, New Haven, Connecticut 06520, USA [2] Department of Molecular Biophysics and Biochemistry, Yale University, Bass 432, 266 Whitney Avenue, New Haven, Connecticut 06520, USA. ; Center for Biomedical Informatics, Harvard Medical School, 10 Shattuck Street, Boston, Massachusetts 02115, USA. ; Functional Genomics, Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724, USA. ; Department of Statistics, University of California, Berkeley, 367 Evans Hall, Berkeley, California 94720-3860, USA. ; Department of Genome Sciences and University of Washington School of Medicine, William H. Foege Building S350D, 1705 Northeast Pacific Street, Box 355065 Seattle, Washington 98195-5065, USA. ; 1] Department of Genome Dynamics, Lawrence Berkeley National Laboratory, Berkeley, California 94720, USA [2] Department of Biostatistics, University of California, Berkeley, 367 Evans Hall, Berkeley, California 94720-3860, USA. ; Department of Genome Dynamics, Lawrence Berkeley National Laboratory, Berkeley, California 94720, USA. ; 1] Department of Biology, Indiana University, 1001 East 3rd Street, Bloomington, Indiana 47405-7005, USA [2] Center for Genomics and Bioinformatics, Indiana University, 1001 East 3rd Street, Bloomington, Indiana 47405-7005, USA. ; MOE Key Lab of Bioinformatics, School of Life Sciences, Tsinghua University, Beijing 100084, China. ; National Human Genome Research Institute, National Institutes of Health, 5635 Fishers Lane, Bethesda, Maryland 20892-9307, USA. ; Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge CB10 1SA, UK. ; 1] Centre for Genomic Regulation, Doctor Aiguader 88, 08003 Barcelona, Catalonia, Spain [2] Departament de Ciencies Experimentals i de la Salut, Universitat Pompeu Fabra, 08003 Barcelona, Catalonia, Spain. ; 1] Center for Integrative Genomics, University of Lausanne, Genopode building, Lausanne 1015, Switzerland [2] Swiss Institute of Bioinformatics, Genopode building, Lausanne 1015, Switzerland. ; 1] Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge CB10 1SA, UK [2] Medical and Molecular Genetics, King's College London, London WC2R 2LS, UK. ; Department of Genetics, Yale University School of Medicine, New Haven, Connecticut 06520-8005, USA. ; Department of Molecular, Cellular and Developmental Biology, PO Box 208103, Yale University, New Haven, Connecticut 06520, USA. ; Department of Biology, Indiana University, 1001 East 3rd Street, Bloomington, Indiana 47405-7005, USA. ; Sloan-Kettering Institute, 1275 York Avenue, Box 252, New York, New York 10065, USA. ; 1] Department of Genetics and Developmental Biology, Institute for Systems Genomics, University of Connecticut Health Center, 400 Farmington Avenue, Farmington, Connecticut 06030, USA [2] Department of Biological Sciences, Carnegie Mellon University, Pittsburgh, Pennsylvania 15213 USA. ; Department of Cell and Developmental Biology, Vanderbilt University, 465 21st Avenue South, Nashville, Tennessee 37232-8240, USA. ; 1] Developmental and Cell Biology, University of California, Irvine, California 92697, USA [2] Center for Complex Biological Systems, University of California, Irvine, California 92697, USA. ; Section of Developmental Genomics, Laboratory of Cellular and Developmental Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA. ; Department of Genetics and Developmental Biology, Institute for Systems Genomics, University of Connecticut Health Center, 400 Farmington Avenue, Farmington, Connecticut 06030, USA. ; 1] Department of Genetics and Drosophila RNAi Screening Center, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, Massachusetts 02115, USA [2] Howard Hughes Medical Institute, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, Massachusetts 02115, USA. ; Center for Integrative Genomics, University of Lausanne, Genopode building, Lausanne 1015, Switzerland. ; 1] Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge CB10 1SA, UK [2] European Bioinformatics Institute, Wellcome Trust Genome Campus, Hinxton, CB10 1SD, UK. ; 1] Bioinformatics and Genomics Programme, Center for Genomic Regulation, Universitat Pompeu Fabra (CRG-UPF), 08003 Barcelona, Catalonia, Spain [2] Institute for Theoretical Chemistry, Theoretical Biochemistry Group (TBI), University of Vienna, Wahringerstrasse 17/3/303, A-1090 Vienna, Austria. ; 1] Department of Genetics and Developmental Biology, Institute for Systems Genomics, University of Connecticut Health Center, 400 Farmington Avenue, Farmington, Connecticut 06030, USA [2] Key Laboratory of Computational Biology, CAS-MPG Partner Institute for Computational Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China. ; 1] Hong Kong Bioinformatics Centre, The Chinese University of Hong Kong, Shatin, New Territories, Hong Kong [2] 5 CUHK-BGI Innovation Institute of Trans-omics, The Chinese University of Hong Kong, Shatin, New Territories, Hong Kong. ; 1] Department of Molecular and Cell Biology, University of California, Berkeley, California 94720, USA [2] Department of Plant and Microbial Biology, University of California, Berkeley, California 94720, USA [3]. ; 1] Department of Genome Dynamics, Lawrence Berkeley National Laboratory, Berkeley, California 94720, USA [2].〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25164755" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caenorhabditis elegans/embryology/*genetics/growth & development ; Chromatin/genetics ; Cluster Analysis ; Drosophila melanogaster/*genetics/growth & development ; *Gene Expression Profiling ; Gene Expression Regulation, Developmental/genetics ; Histones/metabolism ; Humans ; Larva/genetics/growth & development ; Models, Genetic ; Molecular Sequence Annotation ; Promoter Regions, Genetic/genetics ; Pupa/genetics/growth & development ; RNA, Untranslated/genetics ; Sequence Analysis, RNA ; Transcriptome/*genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 7
    ISSN: 1365-2958
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology , Medicine
    Notes: Two previously identified Bacillus subtilis DNA segments, dciA and dciB, whose transcripts accumulate very rapidly after induction of sporulation, were found in the same 6.2 kb transcription unit, now known as the dciA operon. Analysis of the sequence of the dciA operon showed that its putative products are homologous to bacterial peptide transport systems. The product of the fifth gene, DciAE, is similar to peptide-binding proteins from Escherichia coli and Salmonella typhimurium (DppA and OppA) and B. subtilis (OppA). A null mutation in dciAE abolished the ability of a proline auxotroph to grow in a medium containing the dipeptide Pro–Gly as sole proline source, suggesting that the dciA operon encodes a dipeptide transport system.
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Molecular microbiology 5 (1991), S. 0 
    ISSN: 1365-2958
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology , Medicine
    Notes: The Bacillus subtilis dciA operon, which encodes a dipeptide transport system, was induced rapidly by several conditions that caused the cells to enter stationary phase and initiate sporulation. The in vivo start point of transcription was mapped precisely and shown to correspond to a site of transcription initiation in vitro by the major vegetative form of RNA polymerase. Post-exponential expression was prevented by a mutation in the spo0A gene (whose product is a known regulator of early sporulation genes) but was restored in a spo0A abrB double mutant. This implicated AbrB, another known regulator, as a repressor of dciA. In fact, purified AbrB protein bound to a portion of the dciA promoter region, protecting it against DNase I digestion. Expression of dciA in growing cells was also repressed independently by glucose and by a mixture of amino acids; neither of these effects was mediated by AbrB.
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  • 9
    Publication Date: 2012-06-08
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
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  • 10
    Publication Date: 2015-02-10
    Description: SMARCA4 is the catalytic subunit of the SWI/SNF chromatin-remodeling complex, which alters the interactions between DNA and histones and modifies the availability of the DNA for transcription. The latest deep sequencing of tumor genomes has reinforced the important and ubiquitous tumor suppressor role of the SWI/SNF complex in cancer. However, although SWI/SNF complex plays a key role in gene expression, the regulation of this complex itself is poorly understood. Significantly, an understanding of the regulation of SMARCA4 expression has gained in importance due to recent proposals incorporating it in therapeutic strategies that use synthetic lethal interactions between SMARCA4-MAX and SMARCA4-SMARCA2 . In this report, we found that the loss of expression of SMARCA4 observed in some primary lung tumors, whose mechanism was largely unknown, can be explained, at least partially by the activity of microRNAs (miRNAs). We reveal that SMARCA4 expression is regulated by miR-101, miR-199 and especially miR-155 through their binding to two alternative 3'UTRs. Importantly, our experiments suggest that the oncogenic properties of miR-155 in lung cancer can be largely explained by its role inhibiting SMARCA4 . This new discovered functional relationship could explain the poor prognosis displayed by patients that independently have high miR-155 and low SMARCA4 expression levels. In addition, these results could lead to application of incipient miRNA technology to the aforementioned synthetic lethal therapeutic strategies.
    Print ISSN: 0964-6906
    Electronic ISSN: 1460-2083
    Topics: Biology , Medicine
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