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  • Cell Line  (55)
  • Time Factors  (46)
  • Cell Proliferation  (35)
  • Nature Publishing Group (NPG)  (130)
  • 2010-2014  (130)
  • 2014  (62)
  • 2010  (68)
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  • 2010-2014  (130)
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  • 1
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    Herbivores and nutrients control grassland plant diversity via light limitation (2014)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2014-03-29
    Description: Human alterations to nutrient cycles and herbivore communities are affecting global biodiversity dramatically. Ecological theory predicts these changes should be strongly counteractive: nutrient addition drives plant species loss through intensified competition for light, whereas herbivores prevent competitive exclusion by increasing ground-level light, particularly in productive systems. Here we use experimental data spanning a globally relevant range of conditions to test the hypothesis that herbaceous plant species losses caused by eutrophication may be offset by increased light availability due to herbivory. This experiment, replicated in 40 grasslands on 6 continents, demonstrates that nutrients and herbivores can serve as counteracting forces to control local plant diversity through light limitation, independent of site productivity, soil nitrogen, herbivore type and climate. Nutrient addition consistently reduced local diversity through light limitation, and herbivory rescued diversity at sites where it alleviated light limitation. Thus, species loss from anthropogenic eutrophication can be ameliorated in grasslands where herbivory increases ground-level light.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Borer, Elizabeth T -- Seabloom, Eric W -- Gruner, Daniel S -- Harpole, W Stanley -- Hillebrand, Helmut -- Lind, Eric M -- Adler, Peter B -- Alberti, Juan -- Anderson, T Michael -- Bakker, Jonathan D -- Biederman, Lori -- Blumenthal, Dana -- Brown, Cynthia S -- Brudvig, Lars A -- Buckley, Yvonne M -- Cadotte, Marc -- Chu, Chengjin -- Cleland, Elsa E -- Crawley, Michael J -- Daleo, Pedro -- Damschen, Ellen I -- Davies, Kendi F -- DeCrappeo, Nicole M -- Du, Guozhen -- Firn, Jennifer -- Hautier, Yann -- Heckman, Robert W -- Hector, Andy -- HilleRisLambers, Janneke -- Iribarne, Oscar -- Klein, Julia A -- Knops, Johannes M H -- La Pierre, Kimberly J -- Leakey, Andrew D B -- Li, Wei -- MacDougall, Andrew S -- McCulley, Rebecca L -- Melbourne, Brett A -- Mitchell, Charles E -- Moore, Joslin L -- Mortensen, Brent -- O'Halloran, Lydia R -- Orrock, John L -- Pascual, Jesus -- Prober, Suzanne M -- Pyke, David A -- Risch, Anita C -- Schuetz, Martin -- Smith, Melinda D -- Stevens, Carly J -- Sullivan, Lauren L -- Williams, Ryan J -- Wragg, Peter D -- Wright, Justin P -- Yang, Louie H -- England -- Nature. 2014 Apr 24;508(7497):517-20. doi: 10.1038/nature13144. Epub 2014 Mar 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Ecology, Evolution, and Behavior, University of Minnesota, St Paul, Minnesota 55108, USA. ; Department of Entomology, University of Maryland, College Park, Maryland 20742, USA. ; Department of Ecology, Evolution, and Organismal Biology, Iowa State University, Ames, Iowa 50011, USA. ; Institute for Chemistry and Biology of the Marine Environment, Carl-von- Ossietzky University, 26382 Wilhelmshaven, Oldenburg, Germany. ; Department of Wildland Resources and the Ecology Center, Utah State University, Logan, Utah 84322, USA. ; Instituto de Investigaciones Marinas y Costeras (IIMyC), Consejo Nacional de Investigaciones Cientificas y Tecnicas (CONICET), Mar del Plata 7600 , Argentina. ; Department of Biology, Wake Forest University, Winston-Salem, North Carolina 27109, USA. ; School of Environmental and Forest Sciences, University of Washington, Seattle, Washington 98195, USA. ; Agricultural Research Service (ARS), United States Department of Agriculture, Fort Collins, Colorado 80526, USA. ; Deptartment of Forest, Rangeland and Watershed Stewardship, Colorado State University, Fort Collins, Colorado 80523, USA. ; Department of Plant Biology, Michigan State University, East Lansing, Michigan 48824, USA. ; 1] ARC Centre of Excellence for Environmental Decisions, School of Biological Sciences, The University of Queensland, Queensland 4072, Australia [2] School of Natural Sciences, Trinity College Dublin, Dublin 2, Ireland. ; Department of Ecology and Evolutionary Biology, University of Toronto Scarborough, Ontario M1C 1A4, Canada. ; State Key Laboratory of Grassland and Agro-Ecosystems, Research Station of Alpine Meadow and Wetland Ecosystems, School of Life Sciences, Lanzhou University, Lanzhou, 730000 Gansu, China. ; Division of Biological Sciences, University of California, San Diego, California 92093, USA. ; Department of Biology, Imperial College at Silwood Park, Ascot, Berkshire SL5 7PY, UK. ; Department of Zoology, University of Wisconsin, Madison, Wisconsin 53706, USA. ; Department of Ecology and Evolutionary Biology, University of Colorado, Boulder Colorado 80309, USA. ; US Geological Survey, Forest and Rangeland Ecosystem Science Center, Corvallis, Oregon 97331, USA. ; Queensland University of Technology, Biogeosciences, Brisbane, Queensland 4001, Australia. ; Department of Biology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599, USA. ; Department of Plant Sciences, University of Oxford, Oxford OX1 3RB, UK. ; School of Biological Sciences, University of Nebraska, Lincoln, Nebraska 68588, USA. ; Berkeley Initiative for Global Change Biology, University of California, Berkeley 94704, USA. ; Department of Plant Biology, University of Illinois at Urbana-Champaign, llinois 61820, USA. ; Department of Integrative Biology, University of Guelph, Guelph, Ontario N1G 2W1, Canada. ; Department of Plant & Soil Sciences, University of Kentucky, Lexington, Kentucky 40546, USA. ; Australian Research Center for Urban Ecology, c/o School of Botany, University of Melbourne, Victoria 3010, Australia, and School of Biological Sciences, Monash University, Victoria 3800, Australia. ; Department of Zoology, Oregon State University, Corvallis, Oregon 97331, USA. ; CSIRO Ecosystem Sciences, Wembley, West Australia 6913, Australia. ; Swiss Federal Institute for Forest, Snow and Landscape Research, Birmensdorf 8903, Switzerland. ; Lancaster Environment Center, Lancaster University, Lancaster LA1 4YQ, UK. ; Department of Biology, Duke University, Durham, North Carolina 27708, USA. ; Department of Entomology, University of California, Davis, California 95616, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24670649" target="_blank"〉PubMed〈/a〉
    Keywords: *Biodiversity ; Climate ; Eutrophication/drug effects/*radiation effects ; Geography ; Herbivory/*physiology ; Human Activities ; Internationality ; *Light ; Nitrogen/metabolism/pharmacology ; Plants/drug effects/*metabolism/*radiation effects ; *Poaceae/drug effects/physiology/radiation effects ; Time Factors
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 2
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    A promoter-level mammalian expression atlas (2014)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2014-03-29
    Description: Regulated transcription controls the diversity, developmental pathways and spatial organization of the hundreds of cell types that make up a mammal. Using single-molecule cDNA sequencing, we mapped transcription start sites (TSSs) and their usage in human and mouse primary cells, cell lines and tissues to produce a comprehensive overview of mammalian gene expression across the human body. We find that few genes are truly 'housekeeping', whereas many mammalian promoters are composite entities composed of several closely separated TSSs, with independent cell-type-specific expression profiles. TSSs specific to different cell types evolve at different rates, whereas promoters of broadly expressed genes are the most conserved. Promoter-based expression analysis reveals key transcription factors defining cell states and links them to binding-site motifs. The functions of identified novel transcripts can be predicted by coexpression and sample ontology enrichment analyses. The functional annotation of the mammalian genome 5 (FANTOM5) project provides comprehensive expression profiles and functional annotation of mammalian cell-type-specific transcriptomes with wide applications in biomedical research.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4529748/" 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/PMC4529748/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉FANTOM Consortium and the RIKEN PMI and CLST (DGT) -- Forrest, Alistair R R -- Kawaji, Hideya -- Rehli, Michael -- Baillie, J Kenneth -- de Hoon, Michiel J L -- Haberle, Vanja -- Lassmann, Timo -- Kulakovskiy, Ivan V -- Lizio, Marina -- Itoh, Masayoshi -- Andersson, Robin -- Mungall, Christopher J -- Meehan, Terrence F -- Schmeier, Sebastian -- Bertin, Nicolas -- Jorgensen, Mette -- Dimont, Emmanuel -- Arner, Erik -- Schmidl, Christian -- Schaefer, Ulf -- Medvedeva, Yulia A -- Plessy, Charles -- Vitezic, Morana -- Severin, Jessica -- Semple, Colin A -- Ishizu, Yuri -- Young, Robert S -- Francescatto, Margherita -- Alam, Intikhab -- Albanese, Davide -- Altschuler, Gabriel M -- Arakawa, Takahiro -- Archer, John A C -- Arner, Peter -- Babina, Magda -- Rennie, Sarah -- Balwierz, Piotr J -- Beckhouse, Anthony G -- Pradhan-Bhatt, Swati -- Blake, Judith A -- Blumenthal, Antje -- Bodega, Beatrice -- Bonetti, Alessandro -- Briggs, James -- Brombacher, Frank -- Burroughs, A Maxwell -- Califano, Andrea -- Cannistraci, Carlo V -- Carbajo, Daniel -- Chen, Yun -- Chierici, Marco -- Ciani, Yari -- Clevers, Hans C -- Dalla, Emiliano -- Davis, Carrie A -- Detmar, Michael -- Diehl, Alexander D -- Dohi, Taeko -- Drablos, Finn -- Edge, Albert S B -- Edinger, Matthias -- Ekwall, Karl -- Endoh, Mitsuhiro -- Enomoto, Hideki -- Fagiolini, Michela -- Fairbairn, Lynsey -- Fang, Hai -- Farach-Carson, Mary C -- Faulkner, Geoffrey J -- Favorov, Alexander V -- Fisher, Malcolm E -- Frith, Martin C -- Fujita, Rie -- Fukuda, Shiro -- Furlanello, Cesare -- Furino, Masaaki -- Furusawa, Jun-ichi -- Geijtenbeek, Teunis B -- Gibson, Andrew P -- Gingeras, Thomas -- Goldowitz, Daniel -- Gough, Julian -- Guhl, Sven -- Guler, Reto -- Gustincich, Stefano -- Ha, Thomas J -- Hamaguchi, Masahide -- Hara, Mitsuko -- Harbers, Matthias -- Harshbarger, Jayson -- Hasegawa, Akira -- Hasegawa, Yuki -- Hashimoto, Takehiro -- Herlyn, Meenhard -- Hitchens, Kelly J -- Ho Sui, Shannan J -- Hofmann, Oliver M -- Hoof, Ilka -- Hori, Furni -- Huminiecki, Lukasz -- Iida, Kei -- Ikawa, Tomokatsu -- Jankovic, Boris R -- Jia, Hui -- Joshi, Anagha -- Jurman, Giuseppe -- Kaczkowski, Bogumil -- Kai, Chieko -- Kaida, Kaoru -- Kaiho, Ai -- Kajiyama, Kazuhiro -- Kanamori-Katayama, Mutsumi -- Kasianov, Artem S -- Kasukawa, Takeya -- Katayama, Shintaro -- Kato, Sachi -- Kawaguchi, Shuji -- Kawamoto, Hiroshi -- Kawamura, Yuki I -- Kawashima, Tsugumi -- Kempfle, Judith S -- Kenna, Tony J -- Kere, Juha -- Khachigian, Levon M -- Kitamura, Toshio -- Klinken, S Peter -- Knox, Alan J -- Kojima, Miki -- Kojima, Soichi -- Kondo, Naoto -- Koseki, Haruhiko -- Koyasu, Shigeo -- Krampitz, Sarah -- Kubosaki, Atsutaka -- Kwon, Andrew T -- Laros, Jeroen F J -- Lee, Weonju -- Lennartsson, Andreas -- Li, Kang -- Lilje, Berit -- Lipovich, Leonard -- Mackay-Sim, Alan -- Manabe, Ri-ichiroh -- Mar, Jessica C -- Marchand, Benoit -- Mathelier, Anthony -- Mejhert, Niklas -- Meynert, Alison -- Mizuno, Yosuke -- de Lima Morais, David A -- Morikawa, Hiromasa -- Morimoto, Mitsuru -- Moro, Kazuyo -- Motakis, Efthymios -- Motohashi, Hozumi -- Mummery, Christine L -- Murata, Mitsuyoshi -- Nagao-Sato, Sayaka -- Nakachi, Yutaka -- Nakahara, Fumio -- Nakamura, Toshiyuki -- Nakamura, Yukio -- Nakazato, Kenichi -- van Nimwegen, Erik -- Ninomiya, Noriko -- Nishiyori, Hiromi -- Noma, Shohei -- Noazaki, Tadasuke -- Ogishima, Soichi -- Ohkura, Naganari -- Ohimiya, Hiroko -- Ohno, Hiroshi -- Ohshima, Mitsuhiro -- Okada-Hatakeyama, Mariko -- Okazaki, Yasushi -- Orlando, Valerio -- Ovchinnikov, Dmitry A -- Pain, Arnab -- Passier, Robert -- Patrikakis, Margaret -- Persson, Helena -- Piazza, Silvano -- Prendergast, James G D -- Rackham, Owen J L -- Ramilowski, Jordan A -- Rashid, Mamoon -- Ravasi, Timothy -- Rizzu, Patrizia -- Roncador, Marco -- Roy, Sugata -- Rye, Morten B -- Saijyo, Eri -- Sajantila, Antti -- Saka, Akiko -- Sakaguchi, Shimon -- Sakai, Mizuho -- Sato, Hiroki -- Savvi, Suzana -- Saxena, Alka -- Schneider, Claudio -- Schultes, Erik A -- Schulze-Tanzil, Gundula G -- Schwegmann, Anita -- Sengstag, Thierry -- Sheng, Guojun -- Shimoji, Hisashi -- Shimoni, Yishai -- Shin, Jay W -- Simon, Christophe -- Sugiyama, Daisuke -- Sugiyama, Takaai -- Suzuki, Masanori -- Suzuki, Naoko -- Swoboda, Rolf K -- 't Hoen, Peter A C -- Tagami, Michihira -- Takahashi, Naoko -- Takai, Jun -- Tanaka, Hiroshi -- Tatsukawa, Hideki -- Tatum, Zuotian -- Thompson, Mark -- Toyodo, Hiroo -- Toyoda, Tetsuro -- Valen, Elvind -- van de Wetering, Marc -- van den Berg, Linda M -- Verado, Roberto -- Vijayan, Dipti -- Vorontsov, Ilya E -- Wasserman, Wyeth W -- Watanabe, Shoko -- Wells, Christine A -- Winteringham, Louise N -- Wolvetang, Ernst -- Wood, Emily J -- Yamaguchi, Yoko -- Yamamoto, Masayuki -- Yoneda, Misako -- Yonekura, Yohei -- Yoshida, Shigehiro -- Zabierowski, Susan E -- Zhang, Peter G -- Zhao, Xiaobei -- Zucchelli, Silvia -- Summers, Kim M -- Suzuki, Harukazu -- Daub, Carsten O -- Kawai, Jun -- Heutink, Peter -- Hide, Winston -- Freeman, Tom C -- Lenhard, Boris -- Bajic, Vladimir B -- Taylor, Martin S -- Makeev, Vsevolod J -- Sandelin, Albin -- Hume, David A -- Carninci, Piero -- Hayashizaki, Yoshihide -- BB/F003722/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/G022771/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/I001107/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- MC_PC_U127597124/Medical Research Council/United Kingdom -- MC_UP_1102/1/Medical Research Council/United Kingdom -- R01 DE022969/DE/NIDCR NIH HHS/ -- R01 GM084875/GM/NIGMS NIH HHS/ -- England -- Nature. 2014 Mar 27;507(7493):462-70. doi: 10.1038/nature13182.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24670764" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Atlases as Topic ; Cell Line ; Cells, Cultured ; Cluster Analysis ; Conserved Sequence/genetics ; Gene Expression Regulation/genetics ; Gene Regulatory Networks/genetics ; Genes, Essential/genetics ; Genome/genetics ; Humans ; Mice ; *Molecular Sequence Annotation ; Open Reading Frames/genetics ; Organ Specificity ; Promoter Regions, Genetic/*genetics ; RNA, Messenger/analysis/genetics ; Transcription Factors/metabolism ; Transcription Initiation Site ; Transcription, Genetic/genetics ; Transcriptome/*genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 3
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    Rapid seeding of the viral reservoir prior to SIV viraemia in rhesus monkeys (2014)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2014-07-22
    Description: The viral reservoir represents a critical challenge for human immunodeficiency virus type 1 (HIV-1) eradication strategies. However, it remains unclear when and where the viral reservoir is seeded during acute infection and the extent to which it is susceptible to early antiretroviral therapy (ART). Here we show that the viral reservoir is seeded rapidly after mucosal simian immunodeficiency virus (SIV) infection of rhesus monkeys and before systemic viraemia. We initiated suppressive ART in groups of monkeys on days 3, 7, 10 and 14 after intrarectal SIVMAC251 infection. Treatment with ART on day 3 blocked the emergence of viral RNA and proviral DNA in peripheral blood and also substantially reduced levels of proviral DNA in lymph nodes and gastrointestinal mucosa as compared with treatment at later time points. In addition, treatment on day 3 abrogated the induction of SIV-specific humoral and cellular immune responses. Nevertheless, after discontinuation of ART following 24 weeks of fully suppressive therapy, virus rebounded in all animals, although the monkeys that were treated on day 3 exhibited a delayed viral rebound as compared with those treated on days 7, 10 and 14. The time to viral rebound correlated with total viraemia during acute infection and with proviral DNA at the time of ART discontinuation. These data demonstrate that the viral reservoir is seeded rapidly after intrarectal SIV infection of rhesus monkeys, during the 'eclipse' phase, and before detectable viraemia. This strikingly early seeding of the refractory viral reservoir raises important new challenges for HIV-1 eradication strategies.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4126858/" 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/PMC4126858/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Whitney, James B -- Hill, Alison L -- Sanisetty, Srisowmya -- Penaloza-MacMaster, Pablo -- Liu, Jinyan -- Shetty, Mayuri -- Parenteau, Lily -- Cabral, Crystal -- Shields, Jennifer -- Blackmore, Stephen -- Smith, Jeffrey Y -- Brinkman, Amanda L -- Peter, Lauren E -- Mathew, Sheeba I -- Smith, Kaitlin M -- Borducchi, Erica N -- Rosenbloom, Daniel I S -- Lewis, Mark G -- Hattersley, Jillian -- Li, Bei -- Hesselgesser, Joseph -- Geleziunas, Romas -- Robb, Merlin L -- Kim, Jerome H -- Michael, Nelson L -- Barouch, Dan H -- AI060354/AI/NIAID NIH HHS/ -- AI078526/AI/NIAID NIH HHS/ -- AI084794/AI/NIAID NIH HHS/ -- AI095985/AI/NIAID NIH HHS/ -- AI096040/AI/NIAID NIH HHS/ -- AI100645/AI/NIAID NIH HHS/ -- R01 AI084794/AI/NIAID NIH HHS/ -- R56 AI091514/AI/NIAID NIH HHS/ -- T32 AI007245/AI/NIAID NIH HHS/ -- U19 AI078526/AI/NIAID NIH HHS/ -- U19 AI095985/AI/NIAID NIH HHS/ -- U19 AI096040/AI/NIAID NIH HHS/ -- UM1 AI100645/AI/NIAID NIH HHS/ -- UM1 AI100663/AI/NIAID NIH HHS/ -- England -- Nature. 2014 Aug 7;512(7512):74-7. doi: 10.1038/nature13594. Epub 2014 Jul 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Center for Virology and Vaccine Research, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215, USA [2] Ragon Institute of MGH, MIT and Harvard, Cambridge, Massachusetts 02139, USA. ; Program for Evolutionary Dynamics, Harvard University, Cambridge, Massachusetts 02138 USA. ; Center for Virology and Vaccine Research, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215, USA. ; Bioqual, Rockville, Maryland 20852, USA. ; Gilead Sciences, Foster City, California 94404, USA. ; US Military HIV Research Program, Walter Reed Army Institute of Research, Silver Spring, Maryland 20910, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25042999" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anti-Retroviral Agents/administration & dosage/pharmacology/therapeutic use ; Carrier State/drug therapy/virology ; DNA, Viral/analysis/biosynthesis/blood ; Disease Models, Animal ; Female ; Kinetics ; Macaca mulatta/immunology/*virology ; Male ; Proviruses/genetics ; RNA, Viral/blood ; Rectum/virology ; Simian Acquired Immunodeficiency Syndrome/drug therapy/immunology/*virology ; Simian Immunodeficiency Virus/drug effects/*growth & ; development/immunology/physiology ; Time Factors ; Treatment Failure ; *Viral Load/drug effects ; Viremia/drug therapy/*virology ; Virus Replication/drug effects
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 4
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    Eutrophication weakens stabilizing effects of diversity in natural grasslands (2014)
    Nature Publishing Group (NPG)
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    Publication Date: 2014-02-18
    Description: Studies of experimental grassland communities have demonstrated that plant diversity can stabilize productivity through species asynchrony, in which decreases in the biomass of some species are compensated for by increases in others. However, it remains unknown whether these findings are relevant to natural ecosystems, especially those for which species diversity is threatened by anthropogenic global change. Here we analyse diversity-stability relationships from 41 grasslands on five continents and examine how these relationships are affected by chronic fertilization, one of the strongest drivers of species loss globally. Unmanipulated communities with more species had greater species asynchrony, resulting in more stable biomass production, generalizing a result from biodiversity experiments to real-world grasslands. However, fertilization weakened the positive effect of diversity on stability. Contrary to expectations, this was not due to species loss after eutrophication but rather to an increase in the temporal variation of productivity in combination with a decrease in species asynchrony in diverse communities. Our results demonstrate separate and synergistic effects of diversity and eutrophication on stability, emphasizing the need to understand how drivers of global change interactively affect the reliable provisioning of ecosystem services in real-world systems.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hautier, Yann -- Seabloom, Eric W -- Borer, Elizabeth T -- Adler, Peter B -- Harpole, W Stanley -- Hillebrand, Helmut -- Lind, Eric M -- MacDougall, Andrew S -- Stevens, Carly J -- Bakker, Jonathan D -- Buckley, Yvonne M -- Chu, Chengjin -- Collins, Scott L -- Daleo, Pedro -- Damschen, Ellen I -- Davies, Kendi F -- Fay, Philip A -- Firn, Jennifer -- Gruner, Daniel S -- Jin, Virginia L -- Klein, Julia A -- Knops, Johannes M H -- La Pierre, Kimberly J -- Li, Wei -- McCulley, Rebecca L -- Melbourne, Brett A -- Moore, Joslin L -- O'Halloran, Lydia R -- Prober, Suzanne M -- Risch, Anita C -- Sankaran, Mahesh -- Schuetz, Martin -- Hector, Andy -- England -- Nature. 2014 Apr 24;508(7497):521-5. doi: 10.1038/nature13014. Epub 2014 Feb 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Department of Ecology, Evolution, and Behavior, University of Minnesota, St Paul, Minnesota 55108, USA [2] Institute of Evolutionary Biology and Environmental Studies, University of Zurich, 8057 Zurich, Switzerland. ; Department of Ecology, Evolution, and Behavior, University of Minnesota, St Paul, Minnesota 55108, USA. ; Department of Wildland Resources and the Ecology Center, Utah State University, Logan, Utah 84322, USA. ; Department of Ecology, Evolution, and Organismal Biology, Iowa State University, Ames, Iowa 50011, USA. ; Institute for Chemistry and Biology of the Marine Environment, Carl-von-Ossietzky University Oldenburg, D-26111 Oldenburg, Germany. ; Department of Integrative Biology, University of Guelph, Guelph, Ontario N1G 2W1, Canada. ; Lancaster Environment Centre, Lancaster University, Lancaster LA1 4YQ, UK. ; School of Environmental and Forest Sciences, University of Washington, Seattle, Washington 98195, USA. ; 1] Australian Research Council Centre of Excellence for Environmental Decisions, School of Biological Sciences, The University of Queensland, Queensland 4072, Australia [2] School of Natural Sciences, Department of Zoology, Trinity College Dublin, Dublin 2, Ireland. ; State Key Laboratory of Grassland and Agro-Ecosystems, Research Station of Alpine Meadow and Wetland Ecosystems, School of Life Sciences, Lanzhou University, Lanzhou 730000, China. ; Department of Biology, MSC03-2020, University of New Mexico, Albuquerque, New Mexico 87131, USA. ; Instituto de Investigaciones Marinas y Costeras (IIMyC) (CONICET-UNMdP), Mar del Plata 7600, Argentina. ; Department of Zoology, University of Wisconsin, Madison, Wisconsin 53706, USA. ; Department of Ecology and Evolutionary Biology, University of Colorado, Boulder, Colorado 80309, USA. ; United States Department of Agriculture Agricultural Research Service, Grassland Soil and Water Research Lab, Temple, Texas 76502, USA. ; Queensland University of Technology, School of Biological Sciences, Brisbane 4000, Australia. ; Department of Entomology, University of Maryland, College Park, Maryland 20742, USA. ; United States Department of Agriculture Agricultural Research Service, Agroecosystem Management Research Unit, Lincoln, Nebraska 68583, USA. ; Department of Forest, Rangeland and Watershed Stewardship, Colorado State University, Fort Collins, Colorado 80523, USA. ; School of Biological Sciences, University of Nebraska, Lincoln, Nebraska 68588, USA. ; Berkeley Initiative for Global Change Biology, University of California, Berkeley, California 94720, USA. ; Yunnan Academy of Biodiversity, Southwest Forestry University, Kunming 650224, China. ; Department of Plant and Soil Sciences, University of Kentucky, Lexington, Kentucky 40546, USA. ; 1] Australian Research Centre for Urban Ecology, Melbourne, c/o School of Botany, University of Melbourne, Victoria 3010, Australia [2] School of Biological Sciences, Monash University, Victoria 3800, Australia. ; Department of Zoology, Oregon State University, Corvallis, Oregon 97331, USA. ; CSIRO Ecosystem Sciences, Wembley, WA 6913, Australia. ; Swiss Federal Institute for Forest, Snow and Landscape Research, 8903 Birmensdorf, Switzerland. ; 1] School of Biology, University of Leeds, Leeds LS2 9JT, UK [2] National Centre for Biological Sciences, GKVK Campus, Bangalore 560065, India. ; Department of Plant Sciences, University of Oxford, Oxford OX1 3RB, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24531763" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biodiversity ; Biomass ; Climate ; *Eutrophication/drug effects ; Fertilizers/*adverse effects ; Geography ; International Cooperation ; *Poaceae/drug effects/physiology ; Time Factors
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
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    A population-specific HTR2B stop codon predisposes to severe impulsivity (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-12-24
    Description: Impulsivity, describing action without foresight, is an important feature of several psychiatric diseases, suicidality and violent behaviour. The complex origins of impulsivity hinder identification of the genes influencing it and the diseases with which it is associated. Here we perform exon-focused sequencing of impulsive individuals in a founder population, targeting fourteen genes belonging to the serotonin and dopamine domain. A stop codon in HTR2B was identified that is common (minor allele frequency 〉 1%) but exclusive to Finnish people. Expression of the gene in the human brain was assessed, as well as the molecular functionality of the stop codon, which was associated with psychiatric diseases marked by impulsivity in both population and family-based analyses. Knockout of Htr2b increased impulsive behaviours in mice, indicative of predictive validity. Our study shows the potential for identifying and tracing effects of rare alleles in complex behavioural phenotypes using founder populations, and indicates a role for HTR2B in impulsivity.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3183507/" 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/PMC3183507/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bevilacqua, Laura -- Doly, Stephane -- Kaprio, Jaakko -- Yuan, Qiaoping -- Tikkanen, Roope -- Paunio, Tiina -- Zhou, Zhifeng -- Wedenoja, Juho -- Maroteaux, Luc -- Diaz, Silvina -- Belmer, Arnaud -- Hodgkinson, Colin A -- Dell'osso, Liliana -- Suvisaari, Jaana -- Coccaro, Emil -- Rose, Richard J -- Peltonen, Leena -- Virkkunen, Matti -- Goldman, David -- AA-09203/AA/NIAAA NIH HHS/ -- AA-12502/AA/NIAAA NIH HHS/ -- Z01 AA000301-09/Intramural NIH HHS/ -- Z01 AA000301-10/Intramural NIH HHS/ -- Z99 AA999999/Intramural NIH HHS/ -- England -- Nature. 2010 Dec 23;468(7327):1061-6. doi: 10.1038/nature09629.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Neurogenetics, National Institute on Alcohol Abuse and Alcoholism, NIH, Rockville, Maryland 20852, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21179162" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/metabolism ; Case-Control Studies ; Cell Line ; Female ; Finland ; Founder Effect ; Gene Expression Regulation ; Gene Knockout Techniques ; Genotype ; Humans ; Impulsive Behavior/*genetics ; Male ; Mental Disorders/genetics ; Mice ; Mice, 129 Strain ; Mice, Knockout ; Pedigree ; Polymorphism, Single Nucleotide/genetics ; Receptor, Serotonin, 5-HT2B/*genetics/*metabolism ; Testosterone/blood/cerebrospinal fluid
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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    N-myristoyltransferase inhibitors as new leads to treat sleeping sickness (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-04-03
    Description: African sleeping sickness or human African trypanosomiasis, caused by Trypanosoma brucei spp., is responsible for approximately 30,000 deaths each year. Available treatments for this disease are poor, with unacceptable efficacy and safety profiles, particularly in the late stage of the disease when the parasite has infected the central nervous system. Here we report the validation of a molecular target and the discovery of associated lead compounds with the potential to address this lack of suitable treatments. Inhibition of this target-T. brucei N-myristoyltransferase-leads to rapid killing of trypanosomes both in vitro and in vivo and cures trypanosomiasis in mice. These high-affinity inhibitors bind into the peptide substrate pocket of the enzyme and inhibit protein N-myristoylation in trypanosomes. The compounds identified have promising pharmaceutical properties and represent an opportunity to develop oral drugs to treat this devastating disease. Our studies validate T. brucei N-myristoyltransferase as a promising therapeutic target for human African trypanosomiasis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2917743/" 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/PMC2917743/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Frearson, Julie A -- Brand, Stephen -- McElroy, Stuart P -- Cleghorn, Laura A T -- Smid, Ondrej -- Stojanovski, Laste -- Price, Helen P -- Guther, M Lucia S -- Torrie, Leah S -- Robinson, David A -- Hallyburton, Irene -- Mpamhanga, Chidochangu P -- Brannigan, James A -- Wilkinson, Anthony J -- Hodgkinson, Michael -- Hui, Raymond -- Qiu, Wei -- Raimi, Olawale G -- van Aalten, Daan M F -- Brenk, Ruth -- Gilbert, Ian H -- Read, Kevin D -- Fairlamb, Alan H -- Ferguson, Michael A J -- Smith, Deborah F -- Wyatt, Paul G -- 077503/Wellcome Trust/United Kingdom -- 077705/Wellcome Trust/United Kingdom -- 085622/Wellcome Trust/United Kingdom -- 087590/Wellcome Trust/United Kingdom -- 1097737/Canadian Institutes of Health Research/Canada -- G0900138/Medical Research Council/United Kingdom -- G0900138(90614)/Medical Research Council/United Kingdom -- WT077503/Wellcome Trust/United Kingdom -- WT077705/Wellcome Trust/United Kingdom -- WT083481,/Wellcome Trust/United Kingdom -- WT085622/Wellcome Trust/United Kingdom -- England -- Nature. 2010 Apr 1;464(7289):728-32. doi: 10.1038/nature08893.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Drug Discovery Unit, Division of Biological Chemistry and Drug Discovery, University of Dundee, Dundee DD1 5EH, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20360736" target="_blank"〉PubMed〈/a〉
    Keywords: Acyltransferases/*antagonists & inhibitors/metabolism ; Aminopyridines/chemistry/metabolism/pharmacology/therapeutic use ; Animals ; Antiparasitic Agents/chemistry/metabolism/*pharmacology/*therapeutic use ; Enzyme Assays ; Enzyme Inhibitors/chemistry/metabolism/pharmacology/therapeutic use ; Female ; Humans ; Mice ; Molecular Structure ; Pyrazoles/chemistry/metabolism/pharmacology/therapeutic use ; Rats ; Sulfonamides/chemistry/metabolism/pharmacology/therapeutic use ; Time Factors ; Trypanosoma brucei brucei/*drug effects/*enzymology/growth & development ; Trypanosomiasis, African/*drug therapy/*parasitology
    Print ISSN: 0028-0836
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 7
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    C11orf95-RELA fusions drive oncogenic NF-kappaB signalling in ependymoma (2014)
    Nature Publishing Group (NPG)
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    Publication Date: 2014-02-21
    Description: Members of the nuclear factor-kappaB (NF-kappaB) family of transcriptional regulators are central mediators of the cellular inflammatory response. Although constitutive NF-kappaB signalling is present in most human tumours, mutations in pathway members are rare, complicating efforts to understand and block aberrant NF-kappaB activity in cancer. Here we show that more than two-thirds of supratentorial ependymomas contain oncogenic fusions between RELA, the principal effector of canonical NF-kappaB signalling, and an uncharacterized gene, C11orf95. In each case, C11orf95-RELA fusions resulted from chromothripsis involving chromosome 11q13.1. C11orf95-RELA fusion proteins translocated spontaneously to the nucleus to activate NF-kappaB target genes, and rapidly transformed neural stem cells--the cell of origin of ependymoma--to form these tumours in mice. Our data identify a highly recurrent genetic alteration of RELA in human cancer, and the C11orf95-RELA fusion protein as a potential therapeutic target in supratentorial ependymoma.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4050669/" 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/PMC4050669/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Parker, Matthew -- Mohankumar, Kumarasamypet M -- Punchihewa, Chandanamali -- Weinlich, Ricardo -- Dalton, James D -- Li, Yongjin -- Lee, Ryan -- Tatevossian, Ruth G -- Phoenix, Timothy N -- Thiruvenkatam, Radhika -- White, Elsie -- Tang, Bo -- Orisme, Wilda -- Gupta, Kirti -- Rusch, Michael -- Chen, Xiang -- Li, Yuxin -- Nagahawhatte, Panduka -- Hedlund, Erin -- Finkelstein, David -- Wu, Gang -- Shurtleff, Sheila -- Easton, John -- Boggs, Kristy -- Yergeau, Donald -- Vadodaria, Bhavin -- Mulder, Heather L -- Becksfort, Jared -- Gupta, Pankaj -- Huether, Robert -- Ma, Jing -- Song, Guangchun -- Gajjar, Amar -- Merchant, Thomas -- Boop, Frederick -- Smith, Amy A -- Ding, Li -- Lu, Charles -- Ochoa, Kerri -- Zhao, David -- Fulton, Robert S -- Fulton, Lucinda L -- Mardis, Elaine R -- Wilson, Richard K -- Downing, James R -- Green, Douglas R -- Zhang, Jinghui -- Ellison, David W -- Gilbertson, Richard J -- P01 CA096832/CA/NCI NIH HHS/ -- P01CA96832/CA/NCI NIH HHS/ -- P30 CA021765/CA/NCI NIH HHS/ -- P30CA021765/CA/NCI NIH HHS/ -- R01 CA129541/CA/NCI NIH HHS/ -- R01CA129541/CA/NCI NIH HHS/ -- England -- Nature. 2014 Feb 27;506(7489):451-5. doi: 10.1038/nature13109. Epub 2014 Feb 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] St. Jude Children's Research Hospital - Washington University Pediatric Cancer Genome Project, Memphis, Tennessee 38105, USA [2] Department of Computational Biology and Bioinformatics, St. Jude Children's Research Hospital, Memphis, Tennessee 38105, USA [3]. ; 1] Department of Developmental Neurobiology, St. Jude Children's Research Hospital, Memphis, Tennessee 38105, USA [2]. ; 1] Department of Pathology, St. Jude Children's Research Hospital, Memphis, Tennessee 38105, USA [2]. ; 1] Department of Immunology, St. Jude Children's Research Hospital, Memphis, Tennessee 38105, USA [2]. ; 1] St. Jude Children's Research Hospital - Washington University Pediatric Cancer Genome Project, Memphis, Tennessee 38105, USA [2] Department of Pathology, St. Jude Children's Research Hospital, Memphis, Tennessee 38105, USA. ; 1] St. Jude Children's Research Hospital - Washington University Pediatric Cancer Genome Project, Memphis, Tennessee 38105, USA [2] Department of Computational Biology and Bioinformatics, St. Jude Children's Research Hospital, Memphis, Tennessee 38105, USA. ; Department of Pathology, St. Jude Children's Research Hospital, Memphis, Tennessee 38105, USA. ; Department of Developmental Neurobiology, St. Jude Children's Research Hospital, Memphis, Tennessee 38105, USA. ; Department of Computational Biology and Bioinformatics, St. Jude Children's Research Hospital, Memphis, Tennessee 38105, USA. ; 1] Department of Computational Biology and Bioinformatics, St. Jude Children's Research Hospital, Memphis, Tennessee 38105, USA [2] Structural Biology, St. Jude Children's Research Hospital, Memphis, Tennessee 38105, USA. ; St. Jude Children's Research Hospital - Washington University Pediatric Cancer Genome Project, Memphis, Tennessee 38105, USA. ; Structural Biology, St. Jude Children's Research Hospital, Memphis, Tennessee 38105, USA. ; 1] St. Jude Children's Research Hospital - Washington University Pediatric Cancer Genome Project, Memphis, Tennessee 38105, USA [2] Department of Oncology, St. Jude Children's Research Hospital, Memphis, Tennessee 38105, USA. ; Department of Radiological Sciences, St. Jude Children's Research Hospital, Memphis, Tennessee 38105, USA. ; Department of Surgery, St. Jude Children's Research Hospital, Memphis, Tennessee 38105, USA. ; MD Anderson Cancer Center Orlando, Pediatric Hematology/Oncology, 92 West Miller MP 318, Orlando, Florida 32806, USA. ; 1] St. Jude Children's Research Hospital - Washington University Pediatric Cancer Genome Project, Memphis, Tennessee 38105, USA [2] The Genome Institute, Washington University School of Medicine in St Louis, St Louis, Missouri 63108, USA [3] Department of Genetics, Washington University School of Medicine in St Louis, St Louis, Missouri 63108, USA. ; 1] St. Jude Children's Research Hospital - Washington University Pediatric Cancer Genome Project, Memphis, Tennessee 38105, USA [2] The Genome Institute, Washington University School of Medicine in St Louis, St Louis, Missouri 63108, USA. ; 1] St. Jude Children's Research Hospital - Washington University Pediatric Cancer Genome Project, Memphis, Tennessee 38105, USA [2] The Genome Institute, Washington University School of Medicine in St Louis, St Louis, Missouri 63108, USA [3] Department of Genetics, Washington University School of Medicine in St Louis, St Louis, Missouri 63108, USA [4] Siteman Cancer Center, Washington University School of Medicine in St Louis, St Louis, Missouri 63108, USA. ; Department of Immunology, St. Jude Children's Research Hospital, Memphis, Tennessee 38105, USA. ; 1] St. Jude Children's Research Hospital - Washington University Pediatric Cancer Genome Project, Memphis, Tennessee 38105, USA [2] Department of Developmental Neurobiology, St. Jude Children's Research Hospital, Memphis, Tennessee 38105, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24553141" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing/genetics/metabolism ; Animals ; Base Sequence ; Brain Neoplasms/genetics/metabolism/pathology ; Cell Line ; Cell Nucleus/metabolism ; *Cell Transformation, Neoplastic/genetics ; Chromosomes, Human, Pair 11/genetics ; Ependymoma/*genetics/*metabolism/pathology ; Female ; Humans ; Mice ; Models, Genetic ; Molecular Sequence Data ; NF-kappa B/genetics/*metabolism ; Neural Stem Cells/metabolism/pathology ; Oncogene Proteins, Fusion/genetics/metabolism ; Phosphoproteins/genetics/metabolism ; Proteins/genetics/*metabolism ; *Signal Transduction ; Transcription Factor RelA/genetics/*metabolism ; Translocation, Genetic/genetics
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 8
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    Comprehensive methylome map of lineage commitment from haematopoietic progenitors (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-08-20
    Description: Epigenetic modifications must underlie lineage-specific differentiation as terminally differentiated cells express tissue-specific genes, but their DNA sequence is unchanged. Haematopoiesis provides a well-defined model to study epigenetic modifications during cell-fate decisions, as multipotent progenitors (MPPs) differentiate into progressively restricted myeloid or lymphoid progenitors. Although DNA methylation is critical for myeloid versus lymphoid differentiation, as demonstrated by the myeloerythroid bias in Dnmt1 hypomorphs, a comprehensive DNA methylation map of haematopoietic progenitors, or of any multipotent/oligopotent lineage, does not exist. Here we examined 4.6 million CpG sites throughout the genome for MPPs, common lymphoid progenitors (CLPs), common myeloid progenitors (CMPs), granulocyte/macrophage progenitors (GMPs), and thymocyte progenitors (DN1, DN2, DN3). Marked epigenetic plasticity accompanied both lymphoid and myeloid restriction. Myeloid commitment involved less global DNA methylation than lymphoid commitment, supported functionally by myeloid skewing of progenitors following treatment with a DNA methyltransferase inhibitor. Differential DNA methylation correlated with gene expression more strongly at CpG island shores than CpG islands. Many examples of genes and pathways not previously known to be involved in choice between lymphoid/myeloid differentiation have been identified, such as Arl4c and Jdp2. Several transcription factors, including Meis1, were methylated and silenced during differentiation, indicating a role in maintaining an undifferentiated state. Additionally, epigenetic modification of modifiers of the epigenome seems to be important in haematopoietic differentiation. Our results directly demonstrate that modulation of DNA methylation occurs during lineage-specific differentiation and defines a comprehensive map of the methylation and transcriptional changes that accompany myeloid versus lymphoid fate decisions.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2956609/" 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/PMC2956609/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ji, Hong -- Ehrlich, Lauren I R -- Seita, Jun -- Murakami, Peter -- Doi, Akiko -- Lindau, Paul -- Lee, Hwajin -- Aryee, Martin J -- Irizarry, Rafael A -- Kim, Kitai -- Rossi, Derrick J -- Inlay, Matthew A -- Serwold, Thomas -- Karsunky, Holger -- Ho, Lena -- Daley, George Q -- Weissman, Irving L -- Feinberg, Andrew P -- CA09151/CA/NCI NIH HHS/ -- F32 AI058521/AI/NIAID NIH HHS/ -- F32 AI058521-02/AI/NIAID NIH HHS/ -- F32AI058521/AI/NIAID NIH HHS/ -- P50 HG003233/HG/NHGRI NIH HHS/ -- P50 HG003233-07/HG/NHGRI NIH HHS/ -- P50 HG003233-08/HG/NHGRI NIH HHS/ -- P50HG003233/HG/NHGRI NIH HHS/ -- R00 AG029760/AG/NIA NIH HHS/ -- R00 AG029760-04/AG/NIA NIH HHS/ -- R00AGO29760/PHS HHS/ -- R01 AI047457/AI/NIAID NIH HHS/ -- R01 AI047457-04/AI/NIAID NIH HHS/ -- R01 AI047457-05/AI/NIAID NIH HHS/ -- R01 AI047458/AI/NIAID NIH HHS/ -- R01 CA086065/CA/NCI NIH HHS/ -- R01 GM083084/GM/NIGMS NIH HHS/ -- R01 GM083084-04/GM/NIGMS NIH HHS/ -- R01AI047457/AI/NIAID NIH HHS/ -- R01AI047458/AI/NIAID NIH HHS/ -- R37 CA054358/CA/NCI NIH HHS/ -- R37 CA054358-18/CA/NCI NIH HHS/ -- R37 CA054358-19/CA/NCI NIH HHS/ -- R37CA053458/CA/NCI NIH HHS/ -- England -- Nature. 2010 Sep 16;467(7313):338-42. doi: 10.1038/nature09367. Epub 2010 Aug 15.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Epigenetics and Department of Medicine, Johns Hopkins University School of Medicine, 570 Rangos, 725 N. Wolfe St., Baltimore, Maryland 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20720541" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; *Cell Lineage/genetics ; CpG Islands/genetics ; *DNA Methylation/genetics ; Epigenesis, Genetic ; Gene Expression Profiling ; Genome/genetics ; *Hematopoiesis/genetics ; Hematopoietic Stem Cells/*cytology/*metabolism ; Lymphocytes/cytology/metabolism ; Metabolome ; Metabolomics ; Mice ; Myeloid Cells/cytology/metabolism ; Pluripotent Stem Cells/cytology/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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    TAp63 suppresses metastasis through coordinate regulation of Dicer and miRNAs (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-10-22
    Description: Aberrant expression of microRNAs (miRNAs) and the enzymes that control their processing have been reported in multiple biological processes including primary and metastatic tumours, but the mechanisms governing this are not clearly understood. Here we show that TAp63, a p53 family member, suppresses tumorigenesis and metastasis, and coordinately regulates Dicer and miR-130b to suppress metastasis. Metastatic mouse and human tumours deficient in TAp63 express Dicer at very low levels, and we found that modulation of expression of Dicer and miR-130b markedly affected the metastatic potential of cells lacking TAp63. TAp63 binds to and transactivates the Dicer promoter, demonstrating direct transcriptional regulation of Dicer by TAp63. These data provide a novel understanding of the roles of TAp63 in tumour and metastasis suppression through the coordinate transcriptional regulation of Dicer and miR-130b and may have implications for the many processes regulated by miRNAs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3055799/" 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/PMC3055799/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Su, Xiaohua -- Chakravarti, Deepavali -- Cho, Min Soon -- Liu, Lingzhi -- Gi, Young Jin -- Lin, Yu-Li -- Leung, Marco L -- El-Naggar, Adel -- Creighton, Chad J -- Suraokar, Milind B -- Wistuba, Ignacio -- Flores, Elsa R -- 01DE019765/DE/NIDCR NIH HHS/ -- CA16672/CA/NCI NIH HHS/ -- P30 CA016672-27/CA/NCI NIH HHS/ -- P50 CA070907/CA/NCI NIH HHS/ -- P50 CA070907-10/CA/NCI NIH HHS/ -- P50 CA091846/CA/NCI NIH HHS/ -- P50 CA091846-10/CA/NCI NIH HHS/ -- P50CA070907/CA/NCI NIH HHS/ -- P50CA091846/CA/NCI NIH HHS/ -- U01 DE019765/DE/NIDCR NIH HHS/ -- U01 DE019765-03/DE/NIDCR NIH HHS/ -- England -- Nature. 2010 Oct 21;467(7318):986-90. doi: 10.1038/nature09459.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Oncology, The University of Texas M. D. Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, Texas 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20962848" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Aging ; Cell Line ; Cell Line, Tumor ; DEAD-box RNA Helicases/biosynthesis/deficiency/genetics/*metabolism ; Endoribonucleases/genetics/*metabolism ; Female ; *Gene Expression Regulation, Neoplastic ; Genes, Tumor Suppressor/physiology ; Genomic Instability ; Humans ; Male ; Mice ; Mice, Inbred C57BL ; MicroRNAs/*biosynthesis/genetics/metabolism ; Neoplasm Metastasis/*genetics ; Neoplasms/genetics/pathology/secretion ; Phosphoproteins/deficiency/genetics/*metabolism ; Promoter Regions, Genetic/genetics ; Ribonuclease III/biosynthesis/deficiency/genetics/*metabolism ; Trans-Activators/deficiency/genetics/*metabolism ; Transcription Factors ; Transcriptional Activation ; Tumor Suppressor Proteins/deficiency/genetics/*metabolism
    Print ISSN: 0028-0836
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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    Patient-specific induced pluripotent stem-cell-derived models of LEOPARD syndrome (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-06-11
    Description: The generation of reprogrammed induced pluripotent stem cells (iPSCs) from patients with defined genetic disorders holds the promise of increased understanding of the aetiologies of complex diseases and may also facilitate the development of novel therapeutic interventions. We have generated iPSCs from patients with LEOPARD syndrome (an acronym formed from its main features; that is, lentigines, electrocardiographic abnormalities, ocular hypertelorism, pulmonary valve stenosis, abnormal genitalia, retardation of growth and deafness), an autosomal-dominant developmental disorder belonging to a relatively prevalent class of inherited RAS-mitogen-activated protein kinase signalling diseases, which also includes Noonan syndrome, with pleomorphic effects on several tissues and organ systems. The patient-derived cells have a mutation in the PTPN11 gene, which encodes the SHP2 phosphatase. The iPSCs have been extensively characterized and produce multiple differentiated cell lineages. A major disease phenotype in patients with LEOPARD syndrome is hypertrophic cardiomyopathy. We show that in vitro-derived cardiomyocytes from LEOPARD syndrome iPSCs are larger, have a higher degree of sarcomeric organization and preferential localization of NFATC4 in the nucleus when compared with cardiomyocytes derived from human embryonic stem cells or wild-type iPSCs derived from a healthy brother of one of the LEOPARD syndrome patients. These features correlate with a potential hypertrophic state. We also provide molecular insights into signalling pathways that may promote the disease phenotype.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2885001/" 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/PMC2885001/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Carvajal-Vergara, Xonia -- Sevilla, Ana -- D'Souza, Sunita L -- Ang, Yen-Sin -- Schaniel, Christoph -- Lee, Dung-Fang -- Yang, Lei -- Kaplan, Aaron D -- Adler, Eric D -- Rozov, Roye -- Ge, Yongchao -- Cohen, Ninette -- Edelmann, Lisa J -- Chang, Betty -- Waghray, Avinash -- Su, Jie -- Pardo, Sherly -- Lichtenbelt, Klaske D -- Tartaglia, Marco -- Gelb, Bruce D -- Lemischka, Ihor R -- 5R01GM078465/GM/NIGMS NIH HHS/ -- R01 GM078465/GM/NIGMS NIH HHS/ -- R01 GM078465-03/GM/NIGMS NIH HHS/ -- England -- Nature. 2010 Jun 10;465(7299):808-12. doi: 10.1038/nature09005.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Gene and Cell Medicine, Black Family Stem Cell Institute, Mount Sinai School of Medicine, New York, New York 10029, USA. xcarvajal@gmail.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20535210" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Cell Differentiation ; Cell Line ; Cell Lineage ; Cells, Cultured ; Embryonic Stem Cells/metabolism ; Enzyme Activation ; Female ; Fibroblasts/metabolism/pathology ; Gene Expression Profiling ; Homeodomain Proteins/genetics ; Humans ; Induced Pluripotent Stem Cells/enzymology/metabolism/*pathology ; LEOPARD Syndrome/drug therapy/metabolism/*pathology ; Male ; Mitogen-Activated Protein Kinases/metabolism ; *Models, Biological ; Myocytes, Cardiac/metabolism/pathology ; NFATC Transcription Factors/genetics/metabolism ; Octamer Transcription Factor-3/genetics ; Phosphoproteins/analysis ; Polymerase Chain Reaction ; *Precision Medicine ; Protein Tyrosine Phosphatase, Non-Receptor Type 11/genetics/metabolism ; SOXB1 Transcription Factors/genetics
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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