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  • *Ecosystem  (1,597)
  • Cells, Cultured  (1,353)
  • American Association for the Advancement of Science (AAAS)  (2,950)
  • American Association of Petroleum Geologists (AAPG)
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  • American Association for the Advancement of Science (AAAS)  (2,950)
  • American Association of Petroleum Geologists (AAPG)
  • Nature Publishing Group (NPG)  (682)
Years
  • 1
    Publication Date: 2016-02-26
    Description: Voltage-gated CaV1.2 channels (L-type calcium channel alpha1C subunits) are critical mediators of transcription-dependent neural plasticity. Whether these channels signal via the influx of calcium ion (Ca(2+)), voltage-dependent conformational change (VDeltaC), or a combination of the two has thus far been equivocal. We fused CaV1.2 to a ligand-gated Ca(2+)-permeable channel, enabling independent control of localized Ca(2+) and VDeltaC signals. This revealed an unexpected dual requirement: Ca(2+) must first mobilize actin-bound Ca(2+)/calmodulin-dependent protein kinase II, freeing it for subsequent VDeltaC-mediated accumulation. Neither signal alone sufficed to activate transcription. Signal order was crucial: Efficiency peaked when Ca(2+) preceded VDeltaC by 10 to 20 seconds. CaV1.2 VDeltaC synergistically augmented signaling by N-methyl-d-aspartate receptors. Furthermore, VDeltaC mistuning correlated with autistic symptoms in Timothy syndrome. Thus, nonionic VDeltaC signaling is vital to the function of CaV1.2 in synaptic and neuropsychiatric processes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Boxing -- Tadross, Michael R -- Tsien, Richard W -- New York, N.Y. -- Science. 2016 Feb 19;351(6275):863-7. doi: 10.1126/science.aad3647.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience and Physiology and New York University Neuroscience Institute, New York, NY 10016, USA. ; Department of Molecular and Cellular Physiology, Beckman Center, School of Medicine, Stanford University, Stanford, CA 94305, USA. Janelia Research Campus, Howard Hughes Medical Institute, Ashburn, VA 20147, USA. tadrossm@janelia.hhmi.org. ; Department of Neuroscience and Physiology and New York University Neuroscience Institute, New York, NY 10016, USA. Department of Molecular and Cellular Physiology, Beckman Center, School of Medicine, Stanford University, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26912895" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autistic Disorder/genetics/metabolism ; Calcium Channel Blockers/pharmacology ; Calcium Channels, L-Type/chemistry/*metabolism ; *Calcium Signaling ; Calcium-Calmodulin-Dependent Protein Kinase Type 2/*metabolism ; Cells, Cultured ; Cyclic AMP Response Element-Binding Protein/metabolism ; *Gene Expression Regulation ; HEK293 Cells ; Hippocampus/cytology ; Humans ; Long QT Syndrome/genetics/metabolism ; Neuronal Plasticity/*genetics ; Neurons/drug effects/*metabolism ; Nimodipine/pharmacology ; Protein Conformation/drug effects ; Rats ; Rats, Sprague-Dawley ; Receptors, N-Methyl-D-Aspartate/metabolism ; Synapses/metabolism ; Syndactyly/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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  • 2
    Publication Date: 2016-01-23
    Description: Differentiated macrophages can self-renew in tissues and expand long term in culture, but the gene regulatory mechanisms that accomplish self-renewal in the differentiated state have remained unknown. Here we show that in mice, the transcription factors MafB and c-Maf repress a macrophage-specific enhancer repertoire associated with a gene network that controls self-renewal. Single-cell analysis revealed that, in vivo, proliferating resident macrophages can access this network by transient down-regulation of Maf transcription factors. The network also controls embryonic stem cell self-renewal but is associated with distinct embryonic stem cell-specific enhancers. This indicates that distinct lineage-specific enhancer platforms regulate a shared network of genes that control self-renewal potential in both stem and mature cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Soucie, Erinn L -- Weng, Ziming -- Geirsdottir, Laufey -- Molawi, Kaaweh -- Maurizio, Julien -- Fenouil, Romain -- Mossadegh-Keller, Noushine -- Gimenez, Gregory -- VanHille, Laurent -- Beniazza, Meryam -- Favret, Jeremy -- Berruyer, Carole -- Perrin, Pierre -- Hacohen, Nir -- Andrau, J-C -- Ferrier, Pierre -- Dubreuil, Patrice -- Sidow, Arend -- Sieweke, Michael H -- P01AG036695/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2016 Feb 12;351(6274):aad5510. doi: 10.1126/science.aad5510. Epub 2016 Jan 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre d'Immunologie de Marseille-Luminy, Universite Aix-Marseille, UM2, Campus de Luminy, Case 906, 13288 Marseille Cedex 09, France. INSERM, U1104, Marseille, France. CNRS, UMR 7280, Marseille, France. Centre de Recherche en Cancerologie de Marseille, INSERM (U1068), CNRS (U7258), Universite Aix-Marseille (UM105), Marseille, France. sieweke@ciml.univ-mrs.fr erinn.soucie@inserm.fr arend@stanford.edu. ; Department of Pathology, Stanford University, Stanford, CA 94305-5324, USA. ; Centre d'Immunologie de Marseille-Luminy, Universite Aix-Marseille, UM2, Campus de Luminy, Case 906, 13288 Marseille Cedex 09, France. INSERM, U1104, Marseille, France. CNRS, UMR 7280, Marseille, France. ; Centre d'Immunologie de Marseille-Luminy, Universite Aix-Marseille, UM2, Campus de Luminy, Case 906, 13288 Marseille Cedex 09, France. INSERM, U1104, Marseille, France. CNRS, UMR 7280, Marseille, France. Max-Delbruck-Centrum fur Molekulare Medizin in der Helmholtz-Gemeinschaft, 10 Robert-Rossle-Strasse, 13125 Berlin, Germany. ; Broad Institute of Harvard University and MIT, Cambridge, MA 02142, USA. ; Centre d'Immunologie de Marseille-Luminy, Universite Aix-Marseille, UM2, Campus de Luminy, Case 906, 13288 Marseille Cedex 09, France. INSERM, U1104, Marseille, France. CNRS, UMR 7280, Marseille, France. Institut de Genetique Moleculaire de Montpellier, CNRS UMR 5535, 1919 Route de Mende, 34293 Montpellier, France. ; Centre de Recherche en Cancerologie de Marseille, INSERM (U1068), CNRS (U7258), Universite Aix-Marseille (UM105), Marseille, France. ; Department of Pathology, Stanford University, Stanford, CA 94305-5324, USA. Department of Genetics, Stanford University, Stanford, CA 94305, USA. sieweke@ciml.univ-mrs.fr erinn.soucie@inserm.fr arend@stanford.edu. ; Centre d'Immunologie de Marseille-Luminy, Universite Aix-Marseille, UM2, Campus de Luminy, Case 906, 13288 Marseille Cedex 09, France. INSERM, U1104, Marseille, France. CNRS, UMR 7280, Marseille, France. Max-Delbruck-Centrum fur Molekulare Medizin in der Helmholtz-Gemeinschaft, 10 Robert-Rossle-Strasse, 13125 Berlin, Germany. sieweke@ciml.univ-mrs.fr erinn.soucie@inserm.fr arend@stanford.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26797145" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation/*genetics ; Cell Lineage/*genetics ; Cell Proliferation ; Cells, Cultured ; Down-Regulation ; Embryonic Stem Cells/*cytology ; Enhancer Elements, Genetic/*physiology ; *Gene Expression Regulation ; Gene Regulatory Networks ; Macrophages/*cytology ; MafB Transcription Factor/metabolism ; Mice ; Proto-Oncogene Proteins c-maf/metabolism ; Single-Cell Analysis ; Transcriptional Activation
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
    Publication Date: 2016-02-26
    Description: Bruns and Taylor argue that our finding of widespread distribution among Glomeromycota "virtual taxa" is undermined by the species definition applied. Although identifying appropriate species concepts and accessing taxonomically informative traits are challenges for microorganism biogeography, the virtual taxa represent a pragmatic classification that corresponds approximately to the species rank of classical Glomeromycota taxonomy, yet is applicable to environmental DNA.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Opik, Maarja -- Davison, John -- Moora, Mari -- Partel, Meelis -- Zobel, Martin -- New York, N.Y. -- Science. 2016 Feb 19;351(6275):826. doi: 10.1126/science.aad5495.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Botany, University of Tartu, 40 Lai Street, 51005 Tartu, Estonia. maarja.opik@ut.ee. ; Department of Botany, University of Tartu, 40 Lai Street, 51005 Tartu, Estonia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26912890" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Ecosystem ; Humans ; *Mycorrhizae ; Plant Roots/*microbiology ; *Symbiosis
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
    Publication Date: 2016-02-26
    Description: Davison et al. (Reports, 28 August 2015, p. 970) claim that virtual taxa of Glomeromycota show little endemism and that endemism that exists is similar to the levels seen in plant families. We show that this is likely due to the conservative species definition rather than to any ecological pattern.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bruns, Thomas D -- Taylor, John W -- New York, N.Y. -- Science. 2016 Feb 19;351(6275):826. doi: 10.1126/science.aad4228.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Plant and Microbial Biology, 111 Koshland Hall, Berkeley, CA 94720-3102, USA. pogon@berkeley.edu. ; Department of Plant and Microbial Biology, 111 Koshland Hall, Berkeley, CA 94720-3102, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26912889" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Ecosystem ; Humans ; *Mycorrhizae ; Plant Roots/*microbiology ; *Symbiosis
    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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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2015-02-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dantzer, Ben -- New York, N.Y. -- Science. 2015 Feb 20;347(6224):822-3. doi: 10.1126/science.aaa6480.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychology and Department of Ecology and Evolutionary Biology, University of Michigan, Ann Arbor, MI 48109, USA. dantzer@umich.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25700499" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; *Competitive Behavior ; *Ecosystem ; Female ; Male ; *Maternal Behavior ; Songbirds/*physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
    Publication Date: 2015-04-11
    Description: Protein phosphorylation regulates virtually all biological processes. Although protein kinases are popular drug targets, targeting protein phosphatases remains a challenge. Here, we describe Sephin1 (selective inhibitor of a holophosphatase), a small molecule that safely and selectively inhibited a regulatory subunit of protein phosphatase 1 in vivo. Sephin1 selectively bound and inhibited the stress-induced PPP1R15A, but not the related and constitutive PPP1R15B, to prolong the benefit of an adaptive phospho-signaling pathway, protecting cells from otherwise lethal protein misfolding stress. In vivo, Sephin1 safely prevented the motor, morphological, and molecular defects of two otherwise unrelated protein-misfolding diseases in mice, Charcot-Marie-Tooth 1B, and amyotrophic lateral sclerosis. Thus, regulatory subunits of phosphatases are drug targets, a property exploited here to safely prevent two protein misfolding diseases.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4490275/" 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/PMC4490275/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Das, Indrajit -- Krzyzosiak, Agnieszka -- Schneider, Kim -- Wrabetz, Lawrence -- D'Antonio, Maurizio -- Barry, Nicholas -- Sigurdardottir, Anna -- Bertolotti, Anne -- 309516/European Research Council/International -- MC_U105185860/Medical Research Council/United Kingdom -- R01-NS55256/NS/NINDS NIH HHS/ -- Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2015 Apr 10;348(6231):239-42. doi: 10.1126/science.aaa4484.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council Laboratory of Molecular Biology, Francis Crick Avenue, Cambridge, CB2 0QH, UK. ; Division of Genetics and Cell Biology, San Raffaele Scientific Institute, 20132 Milan, Italy. ; Medical Research Council Laboratory of Molecular Biology, Francis Crick Avenue, Cambridge, CB2 0QH, UK. aberto@mrc-lmb.cam.ac.uk.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25859045" target="_blank"〉PubMed〈/a〉
    Keywords: Amyotrophic Lateral Sclerosis/drug therapy/metabolism/pathology ; Animals ; Cells, Cultured ; Charcot-Marie-Tooth Disease/drug therapy/metabolism/pathology ; Disease Models, Animal ; Endoplasmic Reticulum Stress/drug effects ; Enzyme Inhibitors/metabolism/pharmacokinetics/*pharmacology/toxicity ; Guanabenz/*analogs & derivatives/chemical ; synthesis/metabolism/pharmacology/toxicity ; HeLa Cells ; Humans ; Mice ; Mice, Transgenic ; Molecular Targeted Therapy ; Phosphorylation ; Protein Folding ; Protein Phosphatase 1/*antagonists & inhibitors ; Proteostasis Deficiencies/*drug therapy/*prevention & control ; Signal Transduction
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2015-12-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mervis, Jeffrey -- New York, N.Y. -- Science. 2015 Dec 18;350(6267):1454. doi: 10.1126/science.350.6267.1454.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26680170" target="_blank"〉PubMed〈/a〉
    Keywords: Contract Services/*economics ; Ecology/*economics ; *Ecosystem ; United States
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  • 8
    Publication Date: 2015-09-01
    Description: The global biogeography of microorganisms remains largely unknown, in contrast to the well-studied diversity patterns of macroorganisms. We used arbuscular mycorrhizal (AM) fungus DNA from 1014 plant-root samples collected worldwide to determine the global distribution of these plant symbionts. We found that AM fungal communities reflected local environmental conditions and the spatial distance between sites. However, despite AM fungi apparently possessing limited dispersal ability, we found 93% of taxa on multiple continents and 34% on all six continents surveyed. This contrasts with the high spatial turnover of other fungal taxa and with the endemism displayed by plants at the global scale. We suggest that the biogeography of AM fungi is driven by unexpectedly efficient dispersal, probably via both abiotic and biotic vectors, including humans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Davison, J -- Moora, M -- Opik, M -- Adholeya, A -- Ainsaar, L -- Ba, A -- Burla, S -- Diedhiou, A G -- Hiiesalu, I -- Jairus, T -- Johnson, N C -- Kane, A -- Koorem, K -- Kochar, M -- Ndiaye, C -- Partel, M -- Reier, U -- Saks, U -- Singh, R -- Vasar, M -- Zobel, M -- New York, N.Y. -- Science. 2015 Aug 28;349(6251):970-3. doi: 10.1126/science.aab1161.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Ecology and Earth Sciences, University of Tartu, Lai 40, Tartu 51005, Estonia. ; Centre for Mycorrhizal Research, The Energy and Resources Institute (TERI), India Habitat Centre, Lodhi Road, New Delhi 110 003, India. ; Laboratoire des Symbioses Tropicales et Mediterraneennes, Unite Mixte de Recherche 113, Laboratoire de Biologie et Physiologie Vegetales, Faculte des Sciences Exactes et Naturelles, Universite des Antilles, BP 592, 97159, Pointe-a-Pitre, Guadeloupe (French West Indies). ; Laboratoire Commun de Microbiologie de l'Institut de Recherche pour le Developpement-Institut Senegalais de Recherches Agricoles-Universite Cheikh Anta Diop (UCAD), Departement de Biologie Vegetale, UCAD, BP 5005 Dakar, Senegal. ; Institute of Ecology and Earth Sciences, University of Tartu, Lai 40, Tartu 51005, Estonia. Institute of Botany, Czech Academy of Sciences, Dukelska 135, 379 01 Trebon, Czech Republic. ; School of Earth Sciences and Environmental Sustainability, Northern Arizona University, Flagstaff, AZ 86011-5694, USA. ; Institute of Ecology and Earth Sciences, University of Tartu, Lai 40, Tartu 51005, Estonia. Netherlands Institute of Ecology, Droevendaalsesteeg 10, 6708 PB Wageningen, Netherlands. ; TERI-Deakin Nano Biotechnology Centre, Biotechnology and Management of Bioresources Division, TERI, India Habitat Centre, Lodhi Road, New Delhi 110 003, India.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26315436" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biodiversity ; DNA, Fungal/analysis ; *Ecosystem ; Environment ; Humans ; *Mycorrhizae/genetics/isolation & purification/physiology ; Phylogeny ; Phylogeography ; Plant Roots/*microbiology ; *Symbiosis ; Water ; Wind
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  • 9
    Publication Date: 2015-02-07
    Description: Self-organized spatial vegetation patterning is widespread and has been described using models of scale-dependent feedback between plants and water on homogeneous substrates. As rainfall decreases, these models yield a characteristic sequence of patterns with increasingly sparse vegetation, followed by sudden collapse to desert. Thus, the final, spot-like pattern may provide early warning for such catastrophic shifts. In many arid ecosystems, however, termite nests impart substrate heterogeneity by altering soil properties, thereby enhancing plant growth. We show that termite-induced heterogeneity interacts with scale-dependent feedbacks to produce vegetation patterns at different spatial grains. Although the coarse-grained patterning resembles that created by scale-dependent feedback alone, it does not indicate imminent desertification. Rather, mound-field landscapes are more robust to aridity, suggesting that termites may help stabilize ecosystems under global change.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bonachela, Juan A -- Pringle, Robert M -- Sheffer, Efrat -- Coverdale, Tyler C -- Guyton, Jennifer A -- Caylor, Kelly K -- Levin, Simon A -- Tarnita, Corina E -- New York, N.Y. -- Science. 2015 Feb 6;347(6222):651-5. doi: 10.1126/science.1261487.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Ecology and Evolutionary Biology, Princeton University, Princeton, NJ 08544, USA. ; Department of Ecology and Evolutionary Biology, Princeton University, Princeton, NJ 08544, USA. Mpala Research Centre, Post Office Box 555, Nanyuki, Kenya. ; Mpala Research Centre, Post Office Box 555, Nanyuki, Kenya. Department of Civil and Environmental Engineering, Princeton University, Princeton, NJ 08544, USA. ; Department of Ecology and Evolutionary Biology, Princeton University, Princeton, NJ 08544, USA. Mpala Research Centre, Post Office Box 555, Nanyuki, Kenya. ctarnita@princeton.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25657247" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Climate Change ; Conservation of Natural Resources ; *Desert Climate ; *Ecosystem ; Feedback ; Isoptera/*physiology ; Models, Biological ; *Plant Development ; *Rain ; Soil ; *Water
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  • 10
    Publication Date: 2015-03-06
    Description: Sedimentary basins in eastern Africa preserve a record of continental rifting and contain important fossil assemblages for interpreting hominin evolution. However, the record of hominin evolution between 3 and 2.5 million years ago (Ma) is poorly documented in surface outcrops, particularly in Afar, Ethiopia. Here we present the discovery of a 2.84- to 2.58-million-year-old fossil and hominin-bearing sediments in the Ledi-Geraru research area of Afar, Ethiopia, that have produced the earliest record of the genus Homo. Vertebrate fossils record a faunal turnover indicative of more open and probably arid habitats than those reconstructed earlier in this region, which is in broad agreement with hypotheses addressing the role of environmental forcing in hominin evolution at this time. Geological analyses constrain depositional and structural models of Afar and date the LD 350-1 Homo mandible to 2.80 to 2.75 Ma.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉DiMaggio, Erin N -- Campisano, Christopher J -- Rowan, John -- Dupont-Nivet, Guillaume -- Deino, Alan L -- Bibi, Faysal -- Lewis, Margaret E -- Souron, Antoine -- Garello, Dominique -- Werdelin, Lars -- Reed, Kaye E -- Arrowsmith, J Ramon -- New York, N.Y. -- Science. 2015 Mar 20;347(6228):1355-9. doi: 10.1126/science.aaa1415. Epub 2015 Mar 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Geosciences, Pennsylvania State University, University Park, PA 16802, USA. dimaggio@psu.edu kreed@asu.edu. ; Institute of Human Origins, School of Human Evolution and Social Change, Arizona State University, Tempe, AZ 85287, USA. ; CNRS Geosciences Rennes, Campus de Beaulieu, 35042 Rennes, France. ; Berkeley Geochronology Center, 2455 Ridge Road, Berkeley, CA 94709, USA. ; Museum fur Naturkunde, Leibniz Institute for Evolution and Biodiversity Science, Invalidenstrasse 43, 10115 Berlin, Germany. ; Biology Program, Stockton University, 101 Vera King Farris Drive, Galloway, NJ 08205, USA. ; Human Evolution Research Center, University of California, Berkeley, 3101 Valley Life Sciences Building, Berkeley, CA, 94720-3160, USA. ; School of Earth and Space Exploration, Arizona State University, Tempe, AZ 85287, USA. ; Swedish Museum of Natural History, Department of Palaeobiology, Box 50007, SE-10405 Stockholm, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25739409" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; *Ecosystem ; Ethiopia ; Fossils ; *Geologic Sediments ; *Hominidae
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  • 11
    Publication Date: 2015-06-20
    Description: The inactive X chromosome (Xi) serves as a model to understand gene silencing on a global scale. Here, we perform "identification of direct RNA interacting proteins" (iDRiP) to isolate a comprehensive protein interactome for Xist, an RNA required for Xi silencing. We discover multiple classes of interactors-including cohesins, condensins, topoisomerases, RNA helicases, chromatin remodelers, and modifiers-that synergistically repress Xi transcription. Inhibiting two or three interactors destabilizes silencing. Although Xist attracts some interactors, it repels architectural factors. Xist evicts cohesins from the Xi and directs an Xi-specific chromosome conformation. Upon deleting Xist, the Xi acquires the cohesin-binding and chromosomal architecture of the active X. Our study unveils many layers of Xi repression and demonstrates a central role for RNA in the topological organization of mammalian chromosomes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Minajigi, Anand -- Froberg, John E -- Wei, Chunyao -- Sunwoo, Hongjae -- Kesner, Barry -- Colognori, David -- Lessing, Derek -- Payer, Bernhard -- Boukhali, Myriam -- Haas, Wilhelm -- Lee, Jeannie T -- R01-DA-38695/DA/NIDA NIH HHS/ -- R03-MH97478/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2015 Jul 17;349(6245). pii: aab2276. doi: 10.1126/science.aab2276. Epub 2015 Jun 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute; Department of Molecular Biology, Massachusetts General Hospital, Boston, MA, USA; Department of Genetics, Harvard Medical School, Boston, MA, USA. ; Massachusetts General Hospital Cancer Center, Charlestown, Boston, MA; Department of Medicine, Harvard Medical School, Boston, MA, USA. ; Howard Hughes Medical Institute; Department of Molecular Biology, Massachusetts General Hospital, Boston, MA, USA; Department of Genetics, Harvard Medical School, Boston, MA, USA. lee@molbio.mgh.harvard.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26089354" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphatases/metabolism ; Animals ; Cell Cycle Proteins/*metabolism ; Cells, Cultured ; Chromatin Assembly and Disassembly ; Chromosomal Proteins, Non-Histone/*metabolism ; DNA-Binding Proteins/metabolism ; Embryonic Stem Cells/metabolism ; Fibroblasts/metabolism ; Gene Knockdown Techniques ; Gene Silencing ; Mice ; Multiprotein Complexes/metabolism ; Nucleic Acid Conformation ; Proteomics ; RNA Helicases/metabolism ; RNA, Long Noncoding/*metabolism ; X Chromosome/chemistry/genetics/*metabolism ; *X Chromosome Inactivation
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  • 12
    Publication Date: 2015-02-24
    Description: An important question in ecology is how mechanistic processes occurring among individuals drive large-scale patterns of community formation and change. Here we show that in two species of bluebirds, cycles of replacement of one by the other emerge as an indirect consequence of maternal influence on offspring behavior in response to local resource availability. Sampling across broad temporal and spatial scales, we found that western bluebirds, the more competitive species, bias the birth order of offspring by sex in a way that influences offspring aggression and dispersal, setting the stage for rapid increases in population density that ultimately result in the replacement of their sister species. Our results provide insight into how predictable community dynamics can occur despite the contingency of local behavioral interactions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Duckworth, Renee A -- Belloni, Virginia -- Anderson, Samantha R -- New York, N.Y. -- Science. 2015 Feb 20;347(6224):875-7. doi: 10.1126/science.1260154.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Ecology and Evolutionary Biology, University of Arizona, Tucson, AZ 85721, USA. rad3@email.arizona.edu. ; Department of Ecology and Evolutionary Biology, University of Arizona, Tucson, AZ 85721, USA. Department of Tropical Medicine, School of Public Health and Tropical Medicine, Tulane University, New Orleans, LA 70112, USA. ; Department of Ecology and Evolutionary Biology, University of Arizona, Tucson, AZ 85721, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25700519" target="_blank"〉PubMed〈/a〉
    Keywords: Androgens/analysis ; Animals ; *Biological Evolution ; Clutch Size ; *Competitive Behavior ; *Ecosystem ; Egg Yolk/chemistry ; Female ; Fires ; Male ; *Maternal Behavior ; Population Density ; Songbirds/*physiology ; United States
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 13
    Publication Date: 2015-01-17
    Description: Vegetation structure is a key determinant of ecosystems and ecosystem function, but paleoecological techniques to quantify it are lacking. We present a method for reconstructing leaf area index (LAI) based on light-dependent morphology of leaf epidermal cells and phytoliths derived from them. Using this proxy, we reconstruct LAI for the Cenozoic (49 million to 11 million years ago) of middle-latitude Patagonia. Our record shows that dense forests opened up by the late Eocene; open forests and shrubland habitats then fluctuated, with a brief middle-Miocene regreening period. Furthermore, endemic herbivorous mammals show accelerated tooth crown height evolution during open, yet relatively grass-free, shrubland habitat intervals. Our Patagonian LAI record provides a high-resolution, sensitive tool with which to dissect terrestrial ecosystem response to changing Southern Ocean conditions during the Cenozoic.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dunn, Regan E -- Stromberg, Caroline A E -- Madden, Richard H -- Kohn, Matthew J -- Carlini, Alfredo A -- New York, N.Y. -- Science. 2015 Jan 16;347(6219):258-61. doi: 10.1126/science.1260947.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology and Burke Museum of Natural History and Culture, University of Washington, Seattle, WA 98195, USA. dunnr@u.washington.edu. ; Department of Biology and Burke Museum of Natural History and Culture, University of Washington, Seattle, WA 98195, USA. ; Department of Organismal Biology and Anatomy, University of Chicago, Chicago, IL 60637, USA. ; Department of Geosciences, Boise State University, Boise, ID 83725, USA. ; Paleontologia de Vertebrados, Universidad Nacional de La Plata, Consejo Nacional de Investigaciones Cientificas y Tecnicas (CONICET), La Plata, Argentina.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25593182" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Evolution ; Cell Shape ; Cell Size ; *Climate Change ; Costa Rica ; *Ecosystem ; *Forests ; Fossils ; Grassland ; Mammals/anatomy & histology ; Plant Epidermis/cytology ; *Plant Leaves/anatomy & histology ; *Plants ; South America ; Time ; Tooth Crown/anatomy & histology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 14
    Publication Date: 2015-05-23
    Description: Viruses influence ecosystems by modulating microbial population size, diversity, metabolic outputs, and gene flow. Here, we use quantitative double-stranded DNA (dsDNA) viral-fraction metagenomes (viromes) and whole viral community morphological data sets from 43 Tara Oceans expedition samples to assess viral community patterns and structure in the upper ocean. Protein cluster cataloging defined pelagic upper-ocean viral community pan and core gene sets and suggested that this sequence space is well-sampled. Analyses of viral protein clusters, populations, and morphology revealed biogeographic patterns whereby viral communities were passively transported on oceanic currents and locally structured by environmental conditions that affect host community structure. Together, these investigations establish a global ocean dsDNA viromic data set with analyses supporting the seed-bank hypothesis to explain how oceanic viral communities maintain high local diversity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brum, Jennifer R -- Ignacio-Espinoza, J Cesar -- Roux, Simon -- Doulcier, Guilhem -- Acinas, Silvia G -- Alberti, Adriana -- Chaffron, Samuel -- Cruaud, Corinne -- de Vargas, Colomban -- Gasol, Josep M -- Gorsky, Gabriel -- Gregory, Ann C -- Guidi, Lionel -- Hingamp, Pascal -- Iudicone, Daniele -- Not, Fabrice -- Ogata, Hiroyuki -- Pesant, Stephane -- Poulos, Bonnie T -- Schwenck, Sarah M -- Speich, Sabrina -- Dimier, Celine -- Kandels-Lewis, Stefanie -- Picheral, Marc -- Searson, Sarah -- Tara Oceans Coordinators -- Bork, Peer -- Bowler, Chris -- Sunagawa, Shinichi -- Wincker, Patrick -- Karsenti, Eric -- Sullivan, Matthew B -- New York, N.Y. -- Science. 2015 May 22;348(6237):1261498. doi: 10.1126/science.1261498.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Ecology and Evolutionary Biology, University of Arizona, Tucson, AZ 85721, USA. ; Department of Molecular and Cellular Biology, University of Arizona, Tucson, AZ 85721, USA. ; Department of Ecology and Evolutionary Biology, University of Arizona, Tucson, AZ 85721, USA. Environmental and Evolutionary Genomics Section, Institut de Biologie de l'Ecole Normale Superieure (IBENS), CNRS, UMR8197, INSERM U1024, 75230 Paris, France. ; Department of Marine Biology and Oceanography, Institute of Marine Sciences (ICM)-CSIC, Pg. Maritim de la Barceloneta 37-49, Barcelona, E08003, Spain. ; Genoscope, Commissariat a l'Energie Atomique (CEA)-Institut de Genomique, 2 rue Gaston Cremieux, 91057 Evry, France. ; Department of Microbiology and Immunology, Rega Institute, KU Leuven, Herestraat 49, 3000 Leuven, Belgium. Center for the Biology of Disease, VIB KU Leuven, Herestraat 49, 3000 Leuven, Belgium. Department of Applied Biological Sciences, Vrije Universiteit Brussel, Pleinlaan 2, 1050 Brussels, Belgium. ; CNRS, UMR 7144, Station Biologique de Roscoff, Place Georges Teissier, 29680 Roscoff, France. Sorbonne Universites, Universite Pierre et Marie Curie, Universite Paris 06, and UMR 7144, Station Biologique de Roscoff, Place Georges Teissier, 29680 Roscoff, France. ; CNRS, UMR 7093, Laboratoire d'oceanographie de Villefranche (LOV), Observatoire Oceanologique, 06230 Villefranche-sur-mer, France. Sorbonne Universites, Uiversite Pierre et Marie Curie, Universite Paris 06, UMR 7093, Laboratoire d'oceanographie de Villefranche (LOV), Observatoire Oceanologique, 06230 Villefranche-sur-mer, France. ; Soil, Water, and Environmental Science, University of Arizona, Tucson, AZ 85721, USA. ; Aix Marseille Universite, CNRS IGS UMR 7256, 13288 Marseille, France. ; Stazione Zoologica Anton Dohrn, Villa Comunale, 80121 Naples, Italy. ; Institute for Chemical Research, Kyoto University, Gokasho, Uji, Kyoto 611-0001, Japan. ; PANGAEA, Data Publisher for Earth and Environmental Science, University of Bremen, 28359 Bremen, Germany. MARUM, Center for Marine Environmental Sciences, University of Bremen, 28359 Bremen, Germany. ; Laboratoire de Physique des Oceans, Institut Universitaire Europeen de la Mer, Universite de Bretagne Occidentale (UBO-IUEM), Place Copernic, 29820 Plouzane, France. ; CNRS, UMR 7144, Station Biologique de Roscoff, Place Georges Teissier, 29680 Roscoff, France. Sorbonne Universites, Universite Pierre et Marie Curie, Universite Paris 06, and UMR 7144, Station Biologique de Roscoff, Place Georges Teissier, 29680 Roscoff, France. Institut de Biologie de l'Ecole Normale Superieure (IBENS), and INSERM U1024, and CNRS UMR 8197, Paris, 75005, France. ; Structural and Computational Biology, European Molecular Biology Laboratory, Meyerhofstrasse 1, 69117 Heidelberg, Germany. Directors' Research, European Molecular Biology Laboratory Meyerhofstrasse 1, 69117 Heidelberg, Germany. ; Structural and Computational Biology, European Molecular Biology Laboratory, Meyerhofstrasse 1, 69117 Heidelberg, Germany. Max-Delbruck-Centre for Molecular Medicine, 13092 Berlin, Germany. ; Institut de Biologie de l'Ecole Normale Superieure (IBENS), and INSERM U1024, and CNRS UMR 8197, Paris, 75005, France. ; Structural and Computational Biology, European Molecular Biology Laboratory, Meyerhofstrasse 1, 69117 Heidelberg, Germany. ; Genoscope, Commissariat a l'Energie Atomique (CEA)-Institut de Genomique, 2 rue Gaston Cremieux, 91057 Evry, France. CNRS, UMR 8030, CP5706, 91057 Evry, France. Universite d'Evry, UMR 8030, CP5706, 91057 Evry, France. ; Institut de Biologie de l'Ecole Normale Superieure (IBENS), and INSERM U1024, and CNRS UMR 8197, Paris, 75005, France. Directors' Research, European Molecular Biology Laboratory Meyerhofstrasse 1, 69117 Heidelberg, Germany. mbsulli@gmail.com karsenti@embl.de. ; Department of Ecology and Evolutionary Biology, University of Arizona, Tucson, AZ 85721, USA. Department of Molecular and Cellular Biology, University of Arizona, Tucson, AZ 85721, USA. Soil, Water, and Environmental Science, University of Arizona, Tucson, AZ 85721, USA. mbsulli@gmail.com karsenti@embl.de.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25999515" target="_blank"〉PubMed〈/a〉
    Keywords: Biodiversity ; DNA, Viral/genetics ; Ecological and Environmental Processes ; *Ecosystem ; Metagenome/genetics ; Microbiota/genetics ; Oceans and Seas ; Plankton/*classification/genetics ; Seawater/*virology ; Viral Proteins/genetics ; Viruses/*classification/genetics
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  • 15
    Publication Date: 2015-05-09
    Description: Efforts to identify host determinants for malaria have been hindered by the absence of a nucleus in erythrocytes, which precludes genetic manipulation in the cell in which the parasite replicates. We used cultured red blood cells derived from hematopoietic stem cells to carry out a forward genetic screen for Plasmodium falciparum host determinants. We found that CD55 is an essential host factor for P. falciparum invasion. CD55-null erythrocytes were refractory to invasion by all isolates of P. falciparum because parasites failed to attach properly to the erythrocyte surface. Thus, CD55 is an attractive target for the development of malaria therapeutics. Hematopoietic stem cell-based forward genetic screens may be valuable for the identification of additional host determinants of malaria pathogenesis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4465434/" 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/PMC4465434/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Egan, Elizabeth S -- Jiang, Rays H Y -- Moechtar, Mischka A -- Barteneva, Natasha S -- Weekes, Michael P -- Nobre, Luis V -- Gygi, Steven P -- Paulo, Joao A -- Frantzreb, Charles -- Tani, Yoshihiko -- Takahashi, Junko -- Watanabe, Seishi -- Goldberg, Jonathan -- Paul, Aditya S -- Brugnara, Carlo -- Root, David E -- Wiegand, Roger C -- Doench, John G -- Duraisingh, Manoj T -- 100140/Wellcome Trust/United Kingdom -- 1K08AI103034-01A1/AI/NIAID NIH HHS/ -- K01 DK098285/DK/NIDDK NIH HHS/ -- K01DK098285/DK/NIDDK NIH HHS/ -- K08 AI103034/AI/NIAID NIH HHS/ -- K12-HD000850/HD/NICHD NIH HHS/ -- R01AI091787/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2015 May 8;348(6235):711-4. doi: 10.1126/science.aaa3526.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology and Infectious Diseases, Harvard T. H. Chan School of Public Health, Boston, MA, USA. Division of Infectious Diseases, Boston Children's Hospital, Boston, MA, USA. ; Department of Immunology and Infectious Diseases, Harvard T. H. Chan School of Public Health, Boston, MA, USA. Department of Global Health and Center for Drug Discovery and Innovation, University of South Florida, Tampa, FL, USA. ; Department of Immunology and Infectious Diseases, Harvard T. H. Chan School of Public Health, Boston, MA, USA. ; Department of Pediatrics, Harvard Medical School and Program in Cellular and Molecular Medicine, Boston Children's Hospital, Boston, MA, USA. ; Cambridge Institute for Medical Research, University of Cambridge, Cambridge, UK. ; Department of Cell Biology, Harvard Medical School, Boston, MA, USA. ; Japanese Red Cross Kinki Block Blood Center, Osaka, Japan. ; Japanese Red Cross Kyushu Block Blood Center, Fukuoka, Japan. ; Department of Laboratory Medicine, Boston Children's Hospital and Harvard Medical School, Boston, MA, USA. ; The Broad Institute of Harvard and Massachussetts Insititute of Technology, Cambridge, MA, USAA. ; Department of Immunology and Infectious Diseases, Harvard T. H. Chan School of Public Health, Boston, MA, USA. The Broad Institute of Harvard and Massachussetts Insititute of Technology, Cambridge, MA, USAA. mduraisi@hsph.harvard.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25954012" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD44/genetics ; Antigens, CD55/*genetics ; Cell Differentiation/genetics ; Cells, Cultured ; Erythrocytes/cytology/metabolism/*parasitology ; Genetic Testing ; Hematopoietic Stem Cells/cytology ; Host-Parasite Interactions/*genetics ; Humans ; Malaria, Falciparum/*genetics/*parasitology ; Plasmodium falciparum/*pathogenicity ; RNA, Small Interfering/genetics
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  • 16
    Publication Date: 2015-09-01
    Description: Human mutations that truncate the massive sarcomere protein titin [TTN-truncating variants (TTNtvs)] are the most common genetic cause for dilated cardiomyopathy (DCM), a major cause of heart failure and premature death. Here we show that cardiac microtissues engineered from human induced pluripotent stem (iPS) cells are a powerful system for evaluating the pathogenicity of titin gene variants. We found that certain missense mutations, like TTNtvs, diminish contractile performance and are pathogenic. By combining functional analyses with RNA sequencing, we explain why truncations in the A-band domain of TTN cause DCM, whereas truncations in the I band are better tolerated. Finally, we demonstrate that mutant titin protein in iPS cell-derived cardiomyocytes results in sarcomere insufficiency, impaired responses to mechanical and beta-adrenergic stress, and attenuated growth factor and cell signaling activation. Our findings indicate that titin mutations cause DCM by disrupting critical linkages between sarcomerogenesis and adaptive remodeling.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4618316/" 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/PMC4618316/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hinson, John T -- Chopra, Anant -- Nafissi, Navid -- Polacheck, William J -- Benson, Craig C -- Swist, Sandra -- Gorham, Joshua -- Yang, Luhan -- Schafer, Sebastian -- Sheng, Calvin C -- Haghighi, Alireza -- Homsy, Jason -- Hubner, Norbert -- Church, George -- Cook, Stuart A -- Linke, Wolfgang A -- Chen, Christopher S -- Seidman, J G -- Seidman, Christine E -- EB017103/EB/NIBIB NIH HHS/ -- HG005550/HG/NHGRI NIH HHS/ -- HL007374/HL/NHLBI NIH HHS/ -- HL115553/HL/NHLBI NIH HHS/ -- HL125807/HL/NHLBI NIH HHS/ -- K08 HL125807/HL/NHLBI NIH HHS/ -- T32 HL007208/HL/NHLBI NIH HHS/ -- Department of Health/United Kingdom -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2015 Aug 28;349(6251):982-6. doi: 10.1126/science.aaa5458.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Cardiovascular Medicine, Brigham and Women's Hospital, Boston, MA 02115, USA. jthinson@partners.org cseidman@genetics.med.harvard.edu. ; Department of Biomedical Engineering, Boston University, Boston, MA 02215, USA. The Wyss Institute for Biologically Inspired Engineering at Harvard University, Boston, MA 02115, USA. ; Department of Genetics, Harvard Medical School, Boston, MA 02115, USA. ; Division of Cardiovascular Medicine, Beth Israel Deaconess Medical Center, Boston, MA 02215, USA. ; Department of Cardiovascular Physiology, Ruhr University Bochum, MA 3/56 D-44780, Bochum, Germany. ; The Wyss Institute for Biologically Inspired Engineering at Harvard University, Boston, MA 02115, USA. Department of Genetics, Harvard Medical School, Boston, MA 02115, USA. ; Cardiovascular and Metabolic Sciences, Max Delbruck Center for Molecular Medicine, Berlin, Germany. ; Division of Cardiovascular Medicine, Brigham and Women's Hospital, Boston, MA 02115, USA. Department of Genetics, Harvard Medical School, Boston, MA 02115, USA. Howard Hughes Medical Institute, Chevy Chase, MD 20815, USA. ; Cardiovascular and Metabolic Sciences, Max Delbruck Center for Molecular Medicine, Berlin, Germany. DZHK (German Center for Cardiovascular Research), Partner Site Berlin, Berlin, Germany. ; National Institute for Health Research (NIHR) Biomedical Research Unit in Cardiovascular Disease at Royal Brompton and Harefield National Health Service (NHS) Foundation Trust, Imperial College London, London, UK. National Heart Centre and Duke-National University, Singapore, Singapore. ; Division of Cardiovascular Medicine, Brigham and Women's Hospital, Boston, MA 02115, USA. Department of Genetics, Harvard Medical School, Boston, MA 02115, USA. Howard Hughes Medical Institute, Chevy Chase, MD 20815, USA. jthinson@partners.org cseidman@genetics.med.harvard.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26315439" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenergic beta-Agonists/pharmacology ; Cardiomyopathy, Dilated/*genetics/pathology/*physiopathology ; Cells, Cultured ; Connectin/chemistry/*genetics/*physiology ; Heart Rate ; Humans ; Induced Pluripotent Stem Cells/*physiology ; Isoproterenol/pharmacology ; Mutant Proteins/chemistry/physiology ; *Mutation, Missense ; Myocardial Contraction ; Myocytes, Cardiac/*physiology ; RNA/genetics/metabolism ; Sarcomeres/*physiology/ultrastructure ; Sequence Analysis, RNA ; Signal Transduction ; Stress, Physiological
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  • 17
    Publication Date: 2015-03-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Naeem, S -- Ingram, J C -- Varga, A -- Agardy, T -- Barten, P -- Bennett, G -- Bloomgarden, E -- Bremer, L L -- Burkill, P -- Cattau, M -- Ching, C -- Colby, M -- Cook, D C -- Costanza, R -- DeClerck, F -- Freund, C -- Gartner, T -- Goldman-Benner, R -- Gunderson, J -- Jarrett, D -- Kinzig, A P -- Kiss, A -- Koontz, A -- Kumar, P -- Lasky, J R -- Masozera, M -- Meyers, D -- Milano, F -- Naughton-Treves, L -- Nichols, E -- Olander, L -- Olmsted, P -- Perge, E -- Perrings, C -- Polasky, S -- Potent, J -- Prager, C -- Quetier, F -- Redford, K -- Saterson, K -- Thoumi, G -- Vargas, M T -- Vickerman, S -- Weisser, W -- Wilkie, D -- Wunder, S -- New York, N.Y. -- Science. 2015 Mar 13;347(6227):1206-7. doi: 10.1126/science.aaa1403. Epub 2015 Mar 12.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25766222" target="_blank"〉PubMed〈/a〉
    Keywords: *Conservation of Natural Resources/economics ; *Ecosystem ; *Environment ; Guidelines as Topic ; Policy
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  • 18
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2015-06-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hochberg, Yael V -- Fehder, Daniel C -- New York, N.Y. -- Science. 2015 Jun 12;348(6240):1202-3. doi: 10.1126/science.aab3351.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Rice University, Houston, TX 77251, USA. Massachusetts Institute of Technology, Cambridge, MA 02139, USA. National Bureau of Economic Research, Cambridge, MA 02138, USA. hochberg@rice.edu. ; Massachusetts Institute of Technology, Cambridge, MA 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26068829" target="_blank"〉PubMed〈/a〉
    Keywords: *Ecosystem ; *Entrepreneurship ; Software
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  • 19
    Publication Date: 2015-06-06
    Description: Aneuploidy in human eggs is the leading cause of pregnancy loss and several genetic disorders such as Down syndrome. Most aneuploidy results from chromosome segregation errors during the meiotic divisions of an oocyte, the egg's progenitor cell. The basis for particularly error-prone chromosome segregation in human oocytes is not known. We analyzed meiosis in more than 100 live human oocytes and identified an error-prone chromosome-mediated spindle assembly mechanism as a major contributor to chromosome segregation defects. Human oocytes assembled a meiotic spindle independently of either centrosomes or other microtubule organizing centers. Instead, spindle assembly was mediated by chromosomes and the small guanosine triphosphatase Ran in a process requiring ~16 hours. This unusually long spindle assembly period was marked by intrinsic spindle instability and abnormal kinetochore-microtubule attachments, which favor chromosome segregation errors and provide a possible explanation for high rates of aneuploidy in human eggs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4477045/" 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/PMC4477045/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Holubcova, Zuzana -- Blayney, Martyn -- Elder, Kay -- Schuh, Melina -- MC_U105192711/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2015 Jun 5;348(6239):1143-7. doi: 10.1126/science.aaa9529.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council, Laboratory of Molecular Biology, Francis Crick Avenue, Cambridge Biomedical Campus, Cambridge CB2 0QH, UK. ; Bourn Hall Clinic, Bourn, Cambridge CB23 2TN, UK. ; Medical Research Council, Laboratory of Molecular Biology, Francis Crick Avenue, Cambridge Biomedical Campus, Cambridge CB2 0QH, UK. mschuh@mrc-lmb.cam.ac.uk.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26045437" target="_blank"〉PubMed〈/a〉
    Keywords: Anaphase ; *Aneuploidy ; Animals ; Cells, Cultured ; *Chromosome Segregation ; Female ; Green Fluorescent Proteins/genetics/metabolism ; Humans ; Kinetochores/metabolism ; *Meiosis ; Mice ; Microtubule-Associated Proteins/genetics/metabolism ; Microtubule-Organizing Center/metabolism ; Oocytes/*pathology ; Spindle Apparatus/*metabolism ; ran GTP-Binding Protein/metabolism
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  • 20
    Publication Date: 2015-09-05
    Description: Growing up on a dairy farm protects children from allergy, hay fever, and asthma. A mechanism linking exposure to this endotoxin (bacterial lipopolysaccharide)-rich environment with protection has remained elusive. Here we show that chronic exposure to low-dose endotoxin or farm dust protects mice from developing house dust mite (HDM)-induced asthma. Endotoxin reduced epithelial cell cytokines that activate dendritic cells (DCs), thus suppressing type 2 immunity to HDMs. Loss of the ubiquitin-modifying enzyme A20 in lung epithelium abolished the protective effect. A single-nucleotide polymorphism in the gene encoding A20 was associated with allergy and asthma risk in children growing up on farms. Thus, the farming environment protects from allergy by modifying the communication between barrier epithelial cells and DCs through A20 induction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schuijs, Martijn J -- Willart, Monique A -- Vergote, Karl -- Gras, Delphine -- Deswarte, Kim -- Ege, Markus J -- Madeira, Filipe Branco -- Beyaert, Rudi -- van Loo, Geert -- Bracher, Franz -- von Mutius, Erika -- Chanez, Pascal -- Lambrecht, Bart N -- Hammad, Hamida -- New York, N.Y. -- Science. 2015 Sep 4;349(6252):1106-10. doi: 10.1126/science.aac6623.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Immunoregulation, VIB Inflammation Research Center, Ghent, Belgium. Department of Internal Medicine, Ghent University, Ghent, Belgium. ; Department of Respiratory Medicine, Assistance Publique Hopitaux de Marseille, UMR INSERM U1067 CNRS 7333, Aix Marseille University, Marseille, France. ; Dr. von Hauner Children's Hospital, Ludwig-Maximilians-Universitat, Munich, Germany. ; Unit of Molecular Signal Transduction, VIB Inflammation Research Center, Ghent, Belgium. Department of Biomedical Molecular Biology, Ghent University, Ghent, Belgium. ; Center for Drug Research, Department of Pharmacy, Ludwig Maximilians University, Butenandtstrasse 5-13, D-81377 Munich, Germany. ; Laboratory of Immunoregulation, VIB Inflammation Research Center, Ghent, Belgium. Department of Internal Medicine, Ghent University, Ghent, Belgium. Department of Pulmonary Medicine, Erasmus Medical Center, Rotterdam, Netherlands. hamida.hammad@ugent.be bart.lambrecht@ugent.be. ; Laboratory of Immunoregulation, VIB Inflammation Research Center, Ghent, Belgium. Department of Internal Medicine, Ghent University, Ghent, Belgium. hamida.hammad@ugent.be bart.lambrecht@ugent.be.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26339029" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Asthma/immunology/prevention & control ; Cells, Cultured ; Child ; DNA-Binding Proteins/*biosynthesis ; Dairying ; Dendritic Cells/immunology ; Dust/*immunology ; Female ; Humans ; Hygiene Hypothesis ; Hypersensitivity/enzymology/immunology/*prevention & control ; Inhalation Exposure ; Intracellular Signaling Peptides and Proteins/*biosynthesis ; Lipopolysaccharides/*immunology ; Lung/*enzymology/immunology ; Mice ; Mice, Inbred C57BL ; Nuclear Proteins/*biosynthesis ; Pyroglyphidae/*immunology ; Respiratory Mucosa/*enzymology/immunology
    Print ISSN: 0036-8075
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  • 21
    Publication Date: 2015-08-08
    Description: Cytoplasmic aggregation of TDP-43, accompanied by its nuclear clearance, is a key common pathological hallmark of amyotrophic lateral sclerosis and frontotemporal dementia (ALS-FTD). However, a limited understanding of this RNA-binding protein (RBP) impedes the clarification of pathogenic mechanisms underlying TDP-43 proteinopathy. In contrast to RBPs that regulate splicing of conserved exons, we found that TDP-43 repressed the splicing of nonconserved cryptic exons, maintaining intron integrity. When TDP-43 was depleted from mouse embryonic stem cells, these cryptic exons were spliced into messenger RNAs, often disrupting their translation and promoting nonsense-mediated decay. Moreover, enforced repression of cryptic exons prevented cell death in TDP-43-deficient cells. Furthermore, repression of cryptic exons was impaired in ALS-FTD cases, suggesting that this splicing defect could potentially underlie TDP-43 proteinopathy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ling, Jonathan P -- Pletnikova, Olga -- Troncoso, Juan C -- Wong, Philip C -- P50AG05146/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2015 Aug 7;349(6248):650-5. doi: 10.1126/science.aab0983.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21205-2196, USA. ; Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21205-2196, USA. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD 21205-2196, USA. ; Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21205-2196, USA. Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205-2196, USA. wong@jhmi.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26250685" target="_blank"〉PubMed〈/a〉
    Keywords: Amyotrophic Lateral Sclerosis/*genetics ; Animals ; Base Sequence ; Cells, Cultured ; Cysteine Endopeptidases/genetics ; DNA-Binding Proteins/genetics/*physiology ; Embryonic Stem Cells ; Exons/*genetics ; Frontotemporal Dementia/*genetics ; Gene Knockout Techniques ; HeLa Cells ; Humans ; Mice ; Molecular Sequence Data ; Protein Isoforms/genetics ; *RNA Splicing ; RNA Stability ; RNA, Messenger/metabolism ; Sequence Analysis, DNA
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  • 22
    Publication Date: 2015-07-18
    Description: Secretion of the cytokine interleukin-1beta (IL-1beta) by macrophages, a major driver of pathogenesis in atherosclerosis, requires two steps: Priming signals promote transcription of immature IL-1beta, and then endogenous "danger" signals activate innate immune signaling complexes called inflammasomes to process IL-1beta for secretion. Although cholesterol crystals are known to act as danger signals in atherosclerosis, what primes IL-1beta transcription remains elusive. Using a murine model of atherosclerosis, we found that cholesterol crystals acted both as priming and danger signals for IL-1beta production. Cholesterol crystals triggered neutrophils to release neutrophil extracellular traps (NETs). NETs primed macrophages for cytokine release, activating T helper 17 (TH17) cells that amplify immune cell recruitment in atherosclerotic plaques. Therefore, danger signals may drive sterile inflammation, such as that seen in atherosclerosis, through their interactions with neutrophils.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Warnatsch, Annika -- Ioannou, Marianna -- Wang, Qian -- Papayannopoulos, Venizelos -- MC_UP_1202/13/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2015 Jul 17;349(6245):316-20. doi: 10.1126/science.aaa8064. Epub 2015 Jul 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Mill Hill Laboratory, Francis Crick Institute, London NW7 1AA, UK. ; Mill Hill Laboratory, Francis Crick Institute, London NW7 1AA, UK. veni.p@crick.ac.uk.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26185250" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apolipoproteins E/genetics ; Atherosclerosis/*immunology ; Cells, Cultured ; Cholesterol/chemistry/immunology ; Disease Models, Animal ; Extracellular Traps/*immunology ; Humans ; Inflammasomes/immunology ; Inflammation/immunology ; Interleukin-1beta/*biosynthesis/genetics ; Macrophages/*immunology ; Mice ; Mice, Mutant Strains ; Neutrophils/*immunology ; Signal Transduction ; Th17 Cells/immunology ; Transcription, Genetic
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  • 23
    Publication Date: 2015-07-04
    Description: The ocean moderates anthropogenic climate change at the cost of profound alterations of its physics, chemistry, ecology, and services. Here, we evaluate and compare the risks of impacts on marine and coastal ecosystems-and the goods and services they provide-for growing cumulative carbon emissions under two contrasting emissions scenarios. The current emissions trajectory would rapidly and significantly alter many ecosystems and the associated services on which humans heavily depend. A reduced emissions scenario-consistent with the Copenhagen Accord's goal of a global temperature increase of less than 2 degrees C-is much more favorable to the ocean but still substantially alters important marine ecosystems and associated goods and services. The management options to address ocean impacts narrow as the ocean warms and acidifies. Consequently, any new climate regime that fails to minimize ocean impacts would be incomplete and inadequate.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gattuso, J-P -- Magnan, A -- Bille, R -- Cheung, W W L -- Howes, E L -- Joos, F -- Allemand, D -- Bopp, L -- Cooley, S R -- Eakin, C M -- Hoegh-Guldberg, O -- Kelly, R P -- Portner, H-O -- Rogers, A D -- Baxter, J M -- Laffoley, D -- Osborn, D -- Rankovic, A -- Rochette, J -- Sumaila, U R -- Treyer, S -- Turley, C -- New York, N.Y. -- Science. 2015 Jul 3;349(6243):aac4722. doi: 10.1126/science.aac4722.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratoire d'Oceanographie de Villefranche, CNRS-Institut National des Sciences de l'Univers, F-06230 Villefranche-sur-mer, France. Sorbonne Universites, Universite Pierre et Marie Curie, Univ Paris 06, Observatoire Oceanologique, F-06230 Villefranche-sur-mer, France. Institute for Sustainable Development and International Relations, Sciences Po, 27 rue Saint Guillaume, F-75007 Paris, France. gattuso@obs-vlfr.fr. ; Institute for Sustainable Development and International Relations, Sciences Po, 27 rue Saint Guillaume, F-75007 Paris, France. ; Secretariat of the Pacific Community, B.P. D5, 98848 Noumea Cedex, New Caledonia. ; Nippon Foundation-UBC Nereus Program, University of British Columbia (UBC), Vancouver, BC V6T 1Z4, Canada. ; Alfred Wegener Institute, Helmholtz Centre for Polar and Marine Research, Am Handelshafen 12, D-27570, Bremenrhaven, Germany. ; Climate and Environmental Physics, Physics Institute and Oeschger Centre for Climate Change Research, University of Bern, Sidlerstrasse 5, CH-3012 Bern, Switzerland. ; Centre Scientifique de Monaco, 8 Quai Antoine Ier, MC-98000 Monaco, Principality of Monaco. Institut Pierre Simon Laplace/Laboratoire des Science du Climat et de l'Environnement, UMR8212, CNRS-Commissariat a l'Energie Atomique et aux Energies Alternatives-Universite de Versailles Saint-Quentin-en-Yvelines, Gif sur Yvette, France. ; Ocean Conservancy, 1300 19th Street NW, 8th Floor, Washington, DC 20036, USA. ; Coral Reef Watch, National Oceanic and Atmospheric Administration, College Park, MD 20740, USA. ; Global Change Institute and Australian Research Council Centre for Excellence in Coral Reef Studies, University of Queensland, Building 20, St Lucia, 4072 Queensland, Australia. ; School of Marine and Environmental Affairs, University of Washington, 3707 Brooklyn Avenue NE, Seattle, WA 98105, USA. ; Department of Zoology, University of Oxford, South Parks Road, Oxford OX1 3PS, UK. ; Scottish Natural Heritage, 231 Corstorphine Road, Edinburgh EH12 7AT, Scotland. ; IUCN, Rue Mauverney 28, CH-1196 Gland, Switzerland. ; Environment Laboratories, International Atomic Energy Agency, 4a Quai Antoine 1er, MC-98000 Monaco, Principality of Monaco. ; Program on Science, Technology, and Society, John F. Kennedy School of Government, Harvard University, 79 John F. Kennedy Street, Cambridge, MA 02138, USA. ; Institute for Sustainable Development and International Relations, Sciences Po, 27 rue Saint Guillaume, F-75007 Paris, France. Fisheries Economics Research Unit, University of British Columbia, Vancouver, BC V6T 1Z4, Canada. ; Plymouth Marine Laboratory, Prospect Place, The Hoe, Plymouth PL1 3DH, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26138982" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aquaculture ; *Aquatic Organisms ; *Carbon Dioxide ; *Ecosystem ; *Global Warming ; *Greenhouse Effect ; Health ; Humans ; Oceans and Seas ; Risk ; Travel
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  • 24
    Publication Date: 2015-04-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Allred, Brady W -- Smith, W Kolby -- Twidwell, Dirac -- Haggerty, Julia H -- Running, Steven W -- Naugle, David E -- Fuhlendorf, Samuel D -- New York, N.Y. -- Science. 2015 Apr 24;348(6233):401-2. doi: 10.1126/science.aaa4785. Epub 2015 Apr 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉College of Forestry and Conservation, University of Montana, Missoula, MT 59812, USA. brady.allred@umontana.edu. ; College of Forestry and Conservation, University of Montana, Missoula, MT 59812, USA. Institute on the Environment, University of Minnesota, St. Paul, MN 55108, USA. ; Department of Agronomy and Horticulture, University of Nebraska-Lincoln, Lincoln, NE 68583, USA. ; Department of Earth Sciences, Montana State University, Bozeman, MT 59717, USA. ; College of Forestry and Conservation, University of Montana, Missoula, MT 59812, USA. ; Department of Natural Resource Ecology and Management, Oklahoma State University, Stillwater, OK 74078, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25908812" target="_blank"〉PubMed〈/a〉
    Keywords: Canada ; *Crops, Agricultural ; *Ecosystem ; *Extraction and Processing Industry ; *Oil and Gas Fields ; United States
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  • 25
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2015-12-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennisi, Elizabeth -- New York, N.Y. -- Science. 2015 Dec 18;350(6267):1452. doi: 10.1126/science.350.6267.1452.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26680168" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Ecosystem ; *Extinction, Biological ; *Human Activities ; Humans ; Paleontology ; Plants
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  • 26
    Publication Date: 2015-01-24
    Description: The 26S proteasome is a key player in eukaryotic protein quality control and in the regulation of numerous cellular processes. Here, we describe quantitative in situ structural studies of this highly dynamic molecular machine in intact hippocampal neurons. We used electron cryotomography with the Volta phase plate, which allowed high fidelity and nanometer precision localization of 26S proteasomes. We undertook a molecular census of single- and double-capped proteasomes and assessed the conformational states of individual complexes. Under the conditions of the experiment-that is, in the absence of proteotoxic stress-only 20% of the 26S proteasomes were engaged in substrate processing. The remainder was in the substrate-accepting ground state. These findings suggest that in the absence of stress, the capacity of the proteasome system is not fully used.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Asano, Shoh -- Fukuda, Yoshiyuki -- Beck, Florian -- Aufderheide, Antje -- Forster, Friedrich -- Danev, Radostin -- Baumeister, Wolfgang -- New York, N.Y. -- Science. 2015 Jan 23;347(6220):439-42. doi: 10.1126/science.1261197.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Structural Biology, Max-Planck Institute of Biochemistry, 82152 Martinsried, Germany. ; Department of Molecular Structural Biology, Max-Planck Institute of Biochemistry, 82152 Martinsried, Germany. baumeist@biochem.mpg.de.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25613890" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Hippocampus/*cytology/enzymology ; Neurons/*enzymology/*ultrastructure ; Proteasome Endopeptidase Complex/*chemistry ; Protein Conformation ; Rats ; Stress, Physiological
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  • 27
    Publication Date: 2015-09-26
    Description: Cellular senescence is a terminal stress-activated program controlled by the p53 and p16(INK4a) tumor suppressor proteins. A striking feature of senescence is the senescence-associated secretory phenotype (SASP), a pro-inflammatory response linked to tumor promotion and aging. We have identified the transcription factor GATA4 as a senescence and SASP regulator. GATA4 is stabilized in cells undergoing senescence and is required for the SASP. Normally, GATA4 is degraded by p62-mediated selective autophagy, but this regulation is suppressed during senescence, thereby stabilizing GATA4. GATA4 in turn activates the transcription factor NF-kappaB to initiate the SASP and facilitate senescence. GATA4 activation depends on the DNA damage response regulators ATM and ATR, but not on p53 or p16(INK4a). GATA4 accumulates in multiple tissues, including the aging brain, and could contribute to aging and its associated inflammation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kang, Chanhee -- Xu, Qikai -- Martin, Timothy D -- Li, Mamie Z -- Demaria, Marco -- Aron, Liviu -- Lu, Tao -- Yankner, Bruce A -- Campisi, Judith -- Elledge, Stephen J -- AG009909/AG/NIA NIH HHS/ -- AG017242/AG/NIA NIH HHS/ -- AG046174/AG/NIA NIH HHS/ -- DP1 OD006849/OD/NIH HHS/ -- DP1OD006849/OD/NIH HHS/ -- GM44664/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2015 Sep 25;349(6255):aaa5612. doi: 10.1126/science.aaa5612.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Harvard Medical School, Division of Genetics, Brigham and Women's Hospital, Howard Hughes Medical Institute, Boston, MA 02115, USA. ; Buck Institute for Research on Aging, Novato, CA 94945, USA. ; Department of Genetics, Harvard Medical School, Boston, MA 02115, USA. ; Department of Genetics, Harvard Medical School, Division of Genetics, Brigham and Women's Hospital, Howard Hughes Medical Institute, Boston, MA 02115, USA. selledge@genetics.med.harvard.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26404840" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/*genetics/metabolism ; Animals ; Ataxia Telangiectasia Mutated Proteins/metabolism ; Autophagy/*genetics ; Brain/metabolism ; Cell Aging/*genetics ; Cell Cycle/genetics ; Cells, Cultured ; Cyclin-Dependent Kinase Inhibitor p16 ; *DNA Damage ; Fibroblasts ; GATA4 Transcription Factor/genetics/*metabolism ; Gene Expression Profiling ; Humans ; Inflammation/*genetics ; Interleukin-1alpha/genetics/metabolism ; Mice ; Mice, Inbred C57BL ; MicroRNAs/genetics/metabolism ; NF-kappa B/metabolism ; Phenotype ; Promoter Regions, Genetic ; Tumor Necrosis Factor Receptor-Associated Peptides and ; Proteins/genetics/metabolism ; Tumor Suppressor Protein p53/metabolism
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  • 28
    Publication Date: 2015-02-24
    Description: Pancreatic beta cells lower insulin release in response to nutrient depletion. The question of whether starved beta cells induce macroautophagy, a predominant mechanism maintaining energy homeostasis, remains poorly explored. We found that, in contrast to many mammalian cells, macroautophagy in pancreatic beta cells was suppressed upon starvation. Instead, starved beta cells induced lysosomal degradation of nascent secretory insulin granules, which was controlled by protein kinase D (PKD), a key player in secretory granule biogenesis. Starvation-induced nascent granule degradation triggered lysosomal recruitment and activation of mechanistic target of rapamycin that suppressed macroautophagy. Switching from macroautophagy to insulin granule degradation was important to keep insulin secretion low upon fasting. Thus, beta cells use a PKD-dependent mechanism to adapt to nutrient availability and couple autophagy flux to secretory function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Goginashvili, Alexander -- Zhang, Zhirong -- Erbs, Eric -- Spiegelhalter, Coralie -- Kessler, Pascal -- Mihlan, Michael -- Pasquier, Adrien -- Krupina, Ksenia -- Schieber, Nicole -- Cinque, Laura -- Morvan, Joelle -- Sumara, Izabela -- Schwab, Yannick -- Settembre, Carmine -- Ricci, Romeo -- New York, N.Y. -- Science. 2015 Feb 20;347(6224):878-82. doi: 10.1126/science.aaa2628.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut de Genetique et de Biologie Moleculaire et Cellulaire (IGBMC), INSERM, CNRS, Universite de Strasbourg, 67404 Illkirch, France. ; Cell Biology and Biophysics Unit, European Molecular Biology Laboratory (EMBL), 69117 Heidelberg, Germany. ; Dulbecco Telethon Institute and Telethon Institute of Genetics and Medicine (TIGEM), 80131 Naples, Italy. ; Dulbecco Telethon Institute and Telethon Institute of Genetics and Medicine (TIGEM), 80131 Naples, Italy. Medical Genetics, Department of Medical and Translational Science Unit, Federico II University, Via Pansini 5, 80131 Naples, Italy. ; Institut de Genetique et de Biologie Moleculaire et Cellulaire (IGBMC), INSERM, CNRS, Universite de Strasbourg, 67404 Illkirch, France. Nouvel Hopital Civil, Laboratoire de Biochimie et de Biologie Moleculaire, Universite de Strasbourg, 67091 Strasbourg, France. romeo.ricci@igbmc.fr.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25700520" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Autophagy ; Cells, Cultured ; Fasting ; Humans ; Insulin/*secretion ; Insulin-Secreting Cells/*physiology/secretion/ultrastructure ; Mice ; Mice, Mutant Strains ; Mice, Transgenic ; Mitogen-Activated Protein Kinase 13/genetics ; Protein Kinase C/physiology ; Secretory Vesicles/*physiology/secretion
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  • 29
    Publication Date: 2015-02-24
    Description: Mutations in sunlight-induced melanoma arise from cyclobutane pyrimidine dimers (CPDs), DNA photoproducts that are typically created picoseconds after an ultraviolet (UV) photon is absorbed at thymine or cytosine. We found that in melanocytes, CPDs are generated for 〉3 hours after exposure to UVA, a major component of the radiation in sunlight and in tanning beds. These "dark CPDs" constitute the majority of CPDs and include the cytosine-containing CPDs that initiate UV-signature C--〉T mutations. Dark CPDs arise when UV-induced reactive oxygen and nitrogen species combine to excite an electron in fragments of the pigment melanin. This creates a quantum triplet state that has the energy of a UV photon but induces CPDs by energy transfer to DNA in a radiation-independent manner. Melanin may thus be carcinogenic as well as protective against cancer. These findings also validate the long-standing suggestion that chemically generated excited electronic states are relevant to mammalian biology.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4432913/" 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/PMC4432913/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Premi, Sanjay -- Wallisch, Silvia -- Mano, Camila M -- Weiner, Adam B -- Bacchiocchi, Antonella -- Wakamatsu, Kazumasa -- Bechara, Etelvino J H -- Halaban, Ruth -- Douki, Thierry -- Brash, Douglas E -- 2 P50 CA121974/CA/NCI NIH HHS/ -- P30 DK034989/DK/NIDDK NIH HHS/ -- P30 DK34989/DK/NIDDK NIH HHS/ -- P50 CA121974/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2015 Feb 20;347(6224):842-7. doi: 10.1126/science.1256022.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Therapeutic Radiology, Yale University School of Medicine, New Haven, CT 06520, USA. ; Department of Therapeutic Radiology, Yale University School of Medicine, New Haven, CT 06520, USA. Departamento de Bioquimica, Instituto de Quimica, Universidade de Sao Paulo, Sao Paulo 05513-970 SP, Brazil. ; Department of Dermatology, Yale University School of Medicine, New Haven, CT 06520, USA. ; Department of Chemistry, Fujita Health University School of Health Sciences, Toyoake, Aichi 470-1192, Japan. ; Departamento de Bioquimica, Instituto de Quimica, Universidade de Sao Paulo, Sao Paulo 05513-970 SP, Brazil. Departamento de Ciencias Exatas e da Terra, Universidade Federal de Sao Paulo, Diadema, Sao Paulo 09972-270 SP, Brazil. ; Department of Dermatology, Yale University School of Medicine, New Haven, CT 06520, USA. Yale Comprehensive Cancer Center, Yale University School of Medicine, New Haven, CT 06520, USA. ; INAC/LCIB UMR-E3 CEA-UJF/Commissariat a l'Energie Atomique (CEA), 38054 Grenoble Cedex 9, France. ; Department of Therapeutic Radiology, Yale University School of Medicine, New Haven, CT 06520, USA. Yale Comprehensive Cancer Center, Yale University School of Medicine, New Haven, CT 06520, USA. douglas.brash@yale.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25700512" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Cytosine/metabolism ; DNA/chemistry/genetics/*radiation effects ; DNA Damage/*genetics ; Energy Transfer ; Humans ; Melanins/chemistry/*metabolism ; Melanocytes/metabolism/*radiation effects ; Melanoma/*genetics ; Mice ; Mice, Inbred C57BL ; Mutagenesis ; Mutation ; Neoplasms, Radiation-Induced/*genetics ; Photons ; Pyrimidine Dimers/*metabolism ; Receptor, Melanocortin, Type 1/genetics ; Skin Neoplasms/*genetics ; Sunlight/adverse effects ; Thymine/metabolism ; Ultraviolet Rays
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  • 30
    Publication Date: 2015-01-17
    Description: Marine defaunation, or human-caused animal loss in the oceans, emerged forcefully only hundreds of years ago, whereas terrestrial defaunation has been occurring far longer. Though humans have caused few global marine extinctions, we have profoundly affected marine wildlife, altering the functioning and provisioning of services in every ocean. Current ocean trends, coupled with terrestrial defaunation lessons, suggest that marine defaunation rates will rapidly intensify as human use of the oceans industrializes. Though protected areas are a powerful tool to harness ocean productivity, especially when designed with future climate in mind, additional management strategies will be required. Overall, habitat degradation is likely to intensify as a major driver of marine wildlife loss. Proactive intervention can avert a marine defaunation disaster of the magnitude observed on land.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McCauley, Douglas J -- Pinsky, Malin L -- Palumbi, Stephen R -- Estes, James A -- Joyce, Francis H -- Warner, Robert R -- New York, N.Y. -- Science. 2015 Jan 16;347(6219):1255641. doi: 10.1126/science.1255641.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Ecology, Evolution, and Marine Biology, University of California, Santa Barbara, CA 93106, USA. douglas.mccauley@lifesci.ucsb.edu. ; Department of Ecology, Evolution, and Natural Resources, Institute of Marine and Coastal Sciences, Rutgers University, New Brunswick, NJ 08901, USA. ; Department of Biology, Stanford University, Hopkins Marine Station, Pacific Grove, CA 93950, USA. ; Department of Ecology and Evolutionary Biology, University of California, Santa Cruz, CA 95060, USA. ; Department of Ecology, Evolution, and Marine Biology, University of California, Santa Barbara, CA 93106, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25593191" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Animals, Wild ; *Aquatic Organisms ; Biodiversity ; Climate Change ; *Ecosystem ; *Endangered Species ; *Extinction, Biological ; Human Activities ; Humans ; Oceans and Seas ; Population Dynamics ; *Seawater
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2015-09-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stone, Richard -- New York, N.Y. -- Science. 2015 Sep 4;349(6252):1046-7. doi: 10.1126/science.349.6252.1046.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26339010" target="_blank"〉PubMed〈/a〉
    Keywords: Acinonyx ; Animals ; *Droughts ; *Ecosystem ; *Environmental Restoration and Remediation ; Extinction, Biological ; Iran ; *Lakes
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  • 32
    Publication Date: 2015-03-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Groner, Maya -- Breyta, Rachel -- Dobson, Andy -- Friedman, Carolyn S -- Froelich, Brett -- Garren, Melissa -- Gulland, Frances -- Maynard, Jeffrey -- Weil, Ernesto -- Wyllie-Echeverria, Sandy -- Harvell, Drew -- New York, N.Y. -- Science. 2015 Mar 13;347(6227):1210. doi: 10.1126/science.347.6227.1210-a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre for Veterinary and Epidemiological Research, Department of Health Management, Atlantic Veterinary College, University of Prince Edward Island, Charlottetown, PE, C1A 4P3, Canada. mgroner@upei.ca. ; School of Aquatic and Fishery Sciences, University of Washington, Seattle, WA 98195, USA. ; Department of Ecology and Evolutionary Biology, Princeton, NJ 08544, USA. ; Department of Marine Science, University of North Carolina, Chapel Hill, NC 27599, USA. ; Department of Civil and Environmental Engineering, Massachusetts Institute of Technology, Cambridge, MA 02139, USA. ; The Marine Mammal Center, Sausalito, CA 94965, USA. ; Department of Ecology and Evolutionary Biology, Cornell University, Ithaca, NY 14853, USA. ; Department of Marine Sciences, University of Puerto Rico, Mayaguez, Mayaguez, PR 00680, USA. ; Friday Harbor Laboratories, University of Washington, Friday Harbor, WA 98250, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25766223" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aquatic Organisms/*microbiology ; *Ecosystem ; Oceans and Seas ; *Plant Diseases ; *Seawater
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 33
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2015-08-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kintisch, Eli -- New York, N.Y. -- Science. 2015 Aug 7;349(6248):578-81. doi: 10.1126/science.349.6248.578.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26250666" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arctic Regions ; *Ecosystem ; Fishes ; *Global Warming ; *Ice Cover ; Oceans and Seas ; Plankton ; Species Specificity
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  • 34
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2015-09-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rau, Greg H -- Greene, Charles H -- New York, N.Y. -- Science. 2015 Sep 25;349(6255):1459. doi: 10.1126/science.349.6255.1459-b.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Marine Sciences, University of California, Santa Cruz, CA 95064, USA. ghrau@sbcglobal.net. ; Ocean Resources and Ecosystems Program, Cornell University, Ithaca, NY 14853, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26404817" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Aquatic Organisms ; *Carbon Dioxide ; *Ecosystem ; *Global Warming ; *Greenhouse Effect ; Humans
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  • 35
    Publication Date: 2015-11-07
    Description: In a classical view of hematopoiesis, the various blood cell lineages arise via a hierarchical scheme starting with multipotent stem cells that become increasingly restricted in their differentiation potential through oligopotent and then unipotent progenitors. We developed a cell-sorting scheme to resolve myeloid (My), erythroid (Er), and megakaryocytic (Mk) fates from single CD34(+) cells and then mapped the progenitor hierarchy across human development. Fetal liver contained large numbers of distinct oligopotent progenitors with intermingled My, Er, and Mk fates. However, few oligopotent progenitor intermediates were present in the adult bone marrow. Instead, only two progenitor classes predominate, multipotent and unipotent, with Er-Mk lineages emerging from multipotent cells. The developmental shift to an adult "two-tier" hierarchy challenges current dogma and provides a revised framework to understand normal and disease states of human hematopoiesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Notta, Faiyaz -- Zandi, Sasan -- Takayama, Naoya -- Dobson, Stephanie -- Gan, Olga I -- Wilson, Gavin -- Kaufmann, Kerstin B -- McLeod, Jessica -- Laurenti, Elisa -- Dunant, Cyrille F -- McPherson, John D -- Stein, Lincoln D -- Dror, Yigal -- Dick, John E -- Canadian Institutes of Health Research/Canada -- Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2016 Jan 8;351(6269):aab2116. doi: 10.1126/science.aab2116. Epub 2015 Nov 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Princess Margaret Cancer Centre, University Health Network, University of Toronto, Toronto, Ontario, Canada. Department of Molecular Genetics, University of Toronto, Toronto, Ontario, Canada. ; Princess Margaret Cancer Centre, University Health Network, University of Toronto, Toronto, Ontario, Canada. ; Department of Molecular Genetics, University of Toronto, Toronto, Ontario, Canada. Ontario Institute for Cancer Research, Toronto, Ontario, Canada. ; Wellcome Trust, Medical Research Council Cambridge Stem Cell Institute, Department of Haematology, University of Cambridge, Cambridge, UK. ; Ecole Polytechnique Federale de Lausanne, LMC, Station 12, Lausanne, CH-1015, Switzerland. ; Medical Biophysics, University of Toronto, Toronto, Ontario, Canada. Ontario Institute for Cancer Research, Toronto, Ontario, Canada. ; The Hospital for Sick Children Research Institute, University of Toronto, Ontario, Canada. ; Princess Margaret Cancer Centre, University Health Network, University of Toronto, Toronto, Ontario, Canada. Department of Molecular Genetics, University of Toronto, Toronto, Ontario, Canada. jdick@uhnres.utoronto.ca.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26541609" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Antigens, CD34/analysis ; Cell Lineage/genetics/*physiology ; Cell Separation ; Cells, Cultured ; Erythroid Cells/*cytology ; Fetal Blood/cytology ; Gene Expression Profiling ; Hematopoiesis/genetics/*physiology ; Humans ; Liver/cytology/embryology ; Megakaryocyte Progenitor Cells/*cytology ; Megakaryocytes/*cytology ; Multipotent Stem Cells/cytology ; Myeloid Cells/*cytology ; Transcription, Genetic
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  • 36
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-07-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Woodroffe, Rosie -- Hedges, Simon -- Durant, Sarah -- New York, N.Y. -- Science. 2014 Jul 25;345(6195):389-90. doi: 10.1126/science.345.6195.389-b. Epub 2014 Jul 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Zoology, Zoological Society of London, London, NW1 4RY, UK. rosie.woodroffe@ioz.ac.uk. ; Wildlife Conservation Society, Bronx, NY 10460, USA. ; Institute of Zoology, Zoological Society of London, London, NW1 4RY, UK. Wildlife Conservation Society, Bronx, NY 10460, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25061195" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Animals, Wild ; *Biodiversity ; *Conservation of Natural Resources ; *Ecosystem ; Humans
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  • 37
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-06-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennisi, Elizabeth -- New York, N.Y. -- Science. 2014 Jun 27;344(6191):1470-1. doi: 10.1126/science.344.6191.1470.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24970076" target="_blank"〉PubMed〈/a〉
    Keywords: Biodiversity ; *Ecosystem ; Geologic Sediments/*microbiology ; *Natural Gas ; Oil and Gas Fields/*microbiology
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  • 38
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-04-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Woodroffe, Rosie -- Hedges, Simon -- Durant, Sarah M -- New York, N.Y. -- Science. 2014 Apr 4;344(6179):46-8. doi: 10.1126/science.1246251.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Zoology, Regent's Park, London NW1 4RY, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24700847" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Animals, Wild ; *Biodiversity ; *Conservation of Natural Resources ; *Ecosystem ; Humans
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  • 39
    Publication Date: 2014-06-28
    Description: Reef-building in metazoans represents an important ecological innovation whereby individuals collectively enhance feeding efficiency and gain protection from competitors and predation. The appearance of metazoan reefs in the fossil record therefore indicates an adaptive response to complex ecological pressures. In the Nama Group, Namibia, we found evidence of reef-building by the earliest known skeletal metazoan, the globally distributed Cloudina, ~548 million years ago. These Cloudina reefs formed open frameworks without a microbial component but with mutual attachment and cementation between individuals. Orientated growth implies a passive suspension-feeding habit into nutrient-rich currents. The characteristics of Cloudina support the view that metazoan reef-building was promoted by the rise of substrate competitors and predators.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Penny, A M -- Wood, R -- Curtis, A -- Bowyer, F -- Tostevin, R -- Hoffman, K-H -- New York, N.Y. -- Science. 2014 Jun 27;344(6191):1504-6. doi: 10.1126/science.1253393.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of GeoSciences, University of Edinburgh, West Mains Road, Edinburgh EH9 3JW, UK. a.m.penny@ed.ac.uk. ; School of GeoSciences, University of Edinburgh, West Mains Road, Edinburgh EH9 3JW, UK. ; Department of Earth Sciences, University College London, Gower Street, London WC1E 6BT, UK. ; Geological Survey of Namibia, Private Bag 13297, Windhoek, Namibia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24970084" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carbonates ; *Ecosystem ; *Fossils ; Invertebrates/anatomy & histology/*growth & development/physiology ; Namibia ; Predatory Behavior
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  • 40
    Publication Date: 2014-09-23
    Description: Reported trends in the mean and variability of coastal upwelling in eastern boundary currents have raised concerns about the future of these highly productive and biodiverse marine ecosystems. However, the instrumental records on which these estimates are based are insufficiently long to determine whether such trends exceed preindustrial limits. In the California Current, a 576-year reconstruction of climate variables associated with winter upwelling indicates that variability increased over the latter 20th century to levels equaled only twice during the past 600 years. This modern trend in variance may be unique, because it appears to be driven by an unprecedented succession of extreme, downwelling-favorable, winter climate conditions that profoundly reduce productivity for marine predators of commercial and conservation interest.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Black, Bryan A -- Sydeman, William J -- Frank, David C -- Griffin, Daniel -- Stahle, David W -- Garcia-Reyes, Marisol -- Rykaczewski, Ryan R -- Bograd, Steven J -- Peterson, William T -- New York, N.Y. -- Science. 2014 Sep 19;345(6203):1498-502. doi: 10.1126/science.1253209.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of Texas Marine Science Institute, 750 Channel View Drive, Port Aransas, TX 78373, USA. bryan.black@utexas.edu. ; Farallon Institute for Advanced Ecosystem Research, 101 H Street, Suite Q, Petaluma, CA 94952, USA. ; Swiss Federal Research Institute WSL, Zurcherstrasse 111, CH-8903 Birmensdorf, Switzerland and Oeschger Centre for Climate Change Research, University of Bern, Zahringerstrasse 25, CH-3012 Bern, Switzerland. ; Department of Geology and Geophysics, Woods Hole Oceanographic Institution, 266 Woods Hole Road, Woods Hole, MA 02543, USA. ; Department of Geosciences, University of Arkansas, 216 Ozark Hall, Fayetteville, AR 72701, USA. ; Department of Biological Sciences and Marine Science Program, University of South Carolina, 701 Sumter Street, Columbia, SC 29208, USA. ; Environmental Research Division, Southwest Fisheries Science Center, National Oceanic and Atmospheric Administration (NOAA), 1352 Lighthouse Avenue, Pacific Grove, CA 93950, USA. ; Northwest Fisheries Science Center, Hatfield Marine Science Center, NOAA, 2030 Southeast Marine Science Drive, Newport, OR 97365, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25237100" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Aquatic Organisms ; Biodiversity ; Climate Change ; *Ecosystem ; Food Chain ; *Oceans and Seas ; Seasons
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  • 41
    Publication Date: 2014-08-30
    Description: Cells use actomyosin contractility to move through three-dimensional (3D) extracellular matrices. Contractility affects the type of protrusions cells use to migrate in 3D, but the mechanisms are unclear. In this work, we found that contractility generated high-pressure lobopodial protrusions in human cells migrating in a 3D matrix. In these cells, the nucleus physically divided the cytoplasm into forward and rear compartments. Actomyosin contractility with the nucleoskeleton-intermediate filament linker protein nesprin-3 pulled the nucleus forward and pressurized the front of the cell. Reducing expression of nesprin-3 decreased and equalized the intracellular pressure. Thus, the nucleus can act as a piston that physically compartmentalizes the cytoplasm and increases the hydrostatic pressure between the nucleus and the leading edge of the cell to drive lamellipodia-independent 3D cell migration.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Petrie, Ryan J -- Koo, Hyun -- Yamada, Kenneth M -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2014 Aug 29;345(6200):1062-5. doi: 10.1126/science.1256965.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Cell and Developmental Biology, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD 20892-4370, USA. petrier@mail.nih.gov kyamada@mail.nih.gov. ; Laboratory of Cell and Developmental Biology, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD 20892-4370, USA. Center for Oral Biology, Department of Microbiology and Immunology, University of Rochester Medical Center, Rochester, NY 14642, USA. Biofilm Research Labs, Levy Center for Oral Health, Department of Orthodontics, University of Pennsylvania School of Dental Medicine, Philadelphia, PA 19104-6030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25170155" target="_blank"〉PubMed〈/a〉
    Keywords: Actomyosin/physiology ; Cell Movement/*physiology ; Cell Nucleus/*physiology ; Cells, Cultured ; Cytoplasm/physiology ; Extracellular Matrix/*physiology/ultrastructure ; Fibroblasts/*physiology ; Humans ; Hydrostatic Pressure ; Microfilament Proteins ; Pseudopodia/*physiology ; Vimentin/metabolism
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  • 42
    Publication Date: 2014-07-06
    Description: In 1990, Andrew Bakun proposed that increasing greenhouse gas concentrations would force intensification of upwelling-favorable winds in eastern boundary current systems that contribute substantial services to society. Because there is considerable disagreement about whether contemporary wind trends support Bakun's hypothesis, we performed a meta-analysis of the literature on upwelling-favorable wind intensification. The preponderance of published analyses suggests that winds have intensified in the California, Benguela, and Humboldt upwelling systems and weakened in the Iberian system over time scales ranging up to 60 years; wind change is equivocal in the Canary system. Stronger intensification signals are observed at higher latitudes, consistent with the warming pattern associated with climate change. Overall, reported changes in coastal winds, although subtle and spatially variable, support Bakun's hypothesis of upwelling intensification in eastern boundary current systems.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sydeman, W J -- Garcia-Reyes, M -- Schoeman, D S -- Rykaczewski, R R -- Thompson, S A -- Black, B A -- Bograd, S J -- New York, N.Y. -- Science. 2014 Jul 4;345(6192):77-80. doi: 10.1126/science.1251635.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Farallon Institute for Advanced Ecosystem Research, Suite Q, 101 H Street, Petaluma, CA 94952, USA. wsydeman@comcast.net. ; Farallon Institute for Advanced Ecosystem Research, Suite Q, 101 H Street, Petaluma, CA 94952, USA. ; Faculty of Science, Health, Education and Engineering, University of the Sunshine Coast, Locked Bag 4, Maroochydore DC, Queensland 4558, Australia. ; Department of Biological Sciences and Marine Science Program, University of South Carolina, 701 Sumter Street, Columbia, SC 29208, USA. ; Farallon Institute for Advanced Ecosystem Research, Suite Q, 101 H Street, Petaluma, CA 94952, USA. Climate Impacts Group, University of Washington, Box 355674, Seattle, WA 98195, USA. ; Marine Science Institute, University of Texas, 750 Channel View Drive, Port Aransas, TX 78373, USA. ; Environmental Research Division, National Oceanic and Atmospheric Administration (NOAA) Southwest Fisheries Science Center, 1352 Lighthouse Avenue, Pacific Grove, CA 93950-2097, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24994651" target="_blank"〉PubMed〈/a〉
    Keywords: California ; *Climate Change ; *Ecosystem ; Greenhouse Effect ; *Wind
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-05-03
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gramling, Carolyn -- New York, N.Y. -- Science. 2014 May 2;344(6183):463. doi: 10.1126/science.344.6183.463.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24786058" target="_blank"〉PubMed〈/a〉
    Keywords: *Aquatic Organisms ; Copper ; *Ecosystem ; Gold ; Mining/*economics ; Papua New Guinea ; *Seawater
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  • 44
    Publication Date: 2014-11-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ferreira, J -- Aragao, L E O C -- Barlow, J -- Barreto, P -- Berenguer, E -- Bustamante, M -- Gardner, T A -- Lees, A C -- Lima, A -- Louzada, J -- Pardini, R -- Parry, L -- Peres, C A -- Pompeu, P S -- Tabarelli, M -- Zuanon, J -- New York, N.Y. -- Science. 2014 Nov 7;346(6210):706-7. doi: 10.1126/science.1260194.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉See the supplementary materials for author af liations. joice.ferreira@embrapa.br. ; See the supplementary materials for author af liations.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25378611" target="_blank"〉PubMed〈/a〉
    Keywords: Biodiversity ; Brazil ; Conservation of Natural Resources/*trends ; *Ecosystem ; Federal Government ; *Mining ; Risk
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  • 45
    Publication Date: 2014-07-26
    Description: In theoretical ecology, traditional studies based on dynamical stability and numerical simulations have not found a unified answer to the effect of network architecture on community persistence. Here, we introduce a mathematical framework based on the concept of structural stability to explain such a disparity of results. We investigated the range of conditions necessary for the stable coexistence of all species in mutualistic systems. We show that the apparently contradictory conclusions reached by previous studies arise as a consequence of overseeing either the necessary conditions for persistence or its dependence on model parameterization. We show that observed network architectures maximize the range of conditions for species coexistence. We discuss the applicability of structural stability to study other types of interspecific interactions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rohr, Rudolf P -- Saavedra, Serguei -- Bascompte, Jordi -- New York, N.Y. -- Science. 2014 Jul 25;345(6195):1253497. doi: 10.1126/science.1253497.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Integrative Ecology Group, Estacion Biologica de Donana-Consejo Superior de Investigaciones Cientificas (EBD-CSIC), Calle Americo Vespucio s/n, E-41092 Sevilla, Spain. Unit of Ecology and Evolution, Department of Biology, University of Fribourg, Chemin du Musee 10, CH-1700 Fribourg, Switzerland. ; Integrative Ecology Group, Estacion Biologica de Donana-Consejo Superior de Investigaciones Cientificas (EBD-CSIC), Calle Americo Vespucio s/n, E-41092 Sevilla, Spain. ; Integrative Ecology Group, Estacion Biologica de Donana-Consejo Superior de Investigaciones Cientificas (EBD-CSIC), Calle Americo Vespucio s/n, E-41092 Sevilla, Spain. bascompte@ebd.csic.es.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25061214" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Computer Simulation ; *Ecosystem ; *Models, Biological ; Plants ; *Symbiosis
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  • 46
    Publication Date: 2014-03-01
    Description: Understanding the spatial organization of gene expression with single-nucleotide resolution requires localizing the sequences of expressed RNA transcripts within a cell in situ. Here, we describe fluorescent in situ RNA sequencing (FISSEQ), in which stably cross-linked complementary DNA (cDNA) amplicons are sequenced within a biological sample. Using 30-base reads from 8102 genes in situ, we examined RNA expression and localization in human primary fibroblasts with a simulated wound-healing assay. FISSEQ is compatible with tissue sections and whole-mount embryos and reduces the limitations of optical resolution and noisy signals on single-molecule detection. Our platform enables massively parallel detection of genetic elements, including gene transcripts and molecular barcodes, and can be used to investigate cellular phenotype, gene regulation, and environment in situ.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4140943/" 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/PMC4140943/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, Je Hyuk -- Daugharthy, Evan R -- Scheiman, Jonathan -- Kalhor, Reza -- Yang, Joyce L -- Ferrante, Thomas C -- Terry, Richard -- Jeanty, Sauveur S F -- Li, Chao -- Amamoto, Ryoji -- Peters, Derek T -- Turczyk, Brian M -- Marblestone, Adam H -- Inverso, Samuel A -- Bernard, Amy -- Mali, Prashant -- Rios, Xavier -- Aach, John -- Church, George M -- GM080177/GM/NIGMS NIH HHS/ -- MH098977/MH/NIMH NIH HHS/ -- P50 HG005550/HG/NHGRI NIH HHS/ -- RC2 HL102815/HL/NHLBI NIH HHS/ -- RC2HL102815/HL/NHLBI NIH HHS/ -- T32 GM007753/GM/NIGMS NIH HHS/ -- T32 GM080177/GM/NIGMS NIH HHS/ -- U01 MH098977/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2014 Mar 21;343(6177):1360-3. doi: 10.1126/science.1250212. Epub 2014 Feb 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wyss Institute, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24578530" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Cell Line ; Cells, Cultured ; DNA, Complementary ; Fluorescence ; Gene Expression Profiling/*methods ; Humans ; Induced Pluripotent Stem Cells ; RNA, Messenger/genetics/metabolism ; Sequence Analysis, RNA/*methods ; Single-Cell Analysis ; Transcription Initiation Site ; *Transcriptome ; Wound Healing
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  • 47
    Publication Date: 2014-01-25
    Description: The physical manifestation of learning and memory formation in the brain can be expressed by strengthening or weakening of synaptic connections through morphological changes. Local actin remodeling underlies some forms of plasticity and may be facilitated by local beta-actin synthesis, but dynamic information is lacking. In this work, we use single-molecule in situ hybridization to demonstrate that dendritic beta-actin messenger RNA (mRNA) and ribosomes are in a masked, neuron-specific form. Chemically induced long-term potentiation prompts transient mRNA unmasking, which depends on factors active during synaptic activity. Ribosomes and single beta-actin mRNA motility increase after stimulation, indicative of release from complexes. Hence, the single-molecule assays we developed allow for the quantification of activity-induced unmasking and availability for active translation. Further, our work demonstrates that beta-actin mRNA and ribosomes are in a masked state that is alleviated by stimulation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4121734/" 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/PMC4121734/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Buxbaum, Adina R -- Wu, Bin -- Singer, Robert H -- GM84364/GM/NIGMS NIH HHS/ -- NS083085-19/NS/NINDS NIH HHS/ -- R01 NS083085/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2014 Jan 24;343(6169):419-22. doi: 10.1126/science.1242939.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy and Structural Biology, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24458642" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/*biosynthesis/genetics ; Animals ; Cells, Cultured ; Dendrites/metabolism ; In Situ Hybridization, Fluorescence/methods ; Long-Term Potentiation/drug effects/*physiology ; Memory/physiology ; Mice ; Mice, Transgenic ; Neuronal Plasticity/drug effects/physiology ; Neurons/*metabolism ; *Protein Biosynthesis ; RNA, Messenger/analysis/*biosynthesis ; RNA, Ribosomal/metabolism ; Ribosomes/*metabolism ; Synapses/metabolism
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  • 48
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-06-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cardinale, Bradley -- New York, N.Y. -- Science. 2014 Jun 6;344(6188):1098. doi: 10.1126/science.344.6188.1098-a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Natural Resources and Environment, University of Michigan, Ann Arbor, MI 48103, USA. bradcard@umich.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24904146" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biodiversity ; *Birds ; *Ecosystem ; *Fishes ; *Invertebrates ; *Mammals ; *Plants
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  • 49
    Publication Date: 2014-02-01
    Description: Ecologists have long sought to understand the factors controlling the structure of savanna vegetation. Using data from 2154 sites in savannas across Africa, Australia, and South America, we found that increasing moisture availability drives increases in fire and tree basal area, whereas fire reduces tree basal area. However, among continents, the magnitude of these effects varied substantially, so that a single model cannot adequately represent savanna woody biomass across these regions. Historical and environmental differences drive the regional variation in the functional relationships between woody vegetation, fire, and climate. These same differences will determine the regional responses of vegetation to future climates, with implications for global carbon stocks.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lehmann, Caroline E R -- Anderson, T Michael -- Sankaran, Mahesh -- Higgins, Steven I -- Archibald, Sally -- Hoffmann, William A -- Hanan, Niall P -- Williams, Richard J -- Fensham, Roderick J -- Felfili, Jeanine -- Hutley, Lindsay B -- Ratnam, Jayashree -- San Jose, Jose -- Montes, Ruben -- Franklin, Don -- Russell-Smith, Jeremy -- Ryan, Casey M -- Durigan, Giselda -- Hiernaux, Pierre -- Haidar, Ricardo -- Bowman, David M J S -- Bond, William J -- New York, N.Y. -- Science. 2014 Jan 31;343(6170):548-52. doi: 10.1126/science.1247355.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, Macquarie University, New South Wales 2109, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24482480" target="_blank"〉PubMed〈/a〉
    Keywords: Africa ; Australia ; *Climate ; *Ecosystem ; *Fires ; Humidity ; Models, Biological ; South America ; *Trees
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  • 50
    Publication Date: 2014-08-12
    Description: Spinal muscular atrophy (SMA) is a genetic disease caused by mutation or deletion of the survival of motor neuron 1 (SMN1) gene. A paralogous gene in humans, SMN2, produces low, insufficient levels of functional SMN protein due to alternative splicing that truncates the transcript. The decreased levels of SMN protein lead to progressive neuromuscular degeneration and high rates of mortality. Through chemical screening and optimization, we identified orally available small molecules that shift the balance of SMN2 splicing toward the production of full-length SMN2 messenger RNA with high selectivity. Administration of these compounds to Delta7 mice, a model of severe SMA, led to an increase in SMN protein levels, improvement of motor function, and protection of the neuromuscular circuit. These compounds also extended the life span of the mice. Selective SMN2 splicing modifiers may have therapeutic potential for patients with SMA.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Naryshkin, Nikolai A -- Weetall, Marla -- Dakka, Amal -- Narasimhan, Jana -- Zhao, Xin -- Feng, Zhihua -- Ling, Karen K Y -- Karp, Gary M -- Qi, Hongyan -- Woll, Matthew G -- Chen, Guangming -- Zhang, Nanjing -- Gabbeta, Vijayalakshmi -- Vazirani, Priya -- Bhattacharyya, Anuradha -- Furia, Bansri -- Risher, Nicole -- Sheedy, Josephine -- Kong, Ronald -- Ma, Jiyuan -- Turpoff, Anthony -- Lee, Chang-Sun -- Zhang, Xiaoyan -- Moon, Young-Choon -- Trifillis, Panayiota -- Welch, Ellen M -- Colacino, Joseph M -- Babiak, John -- Almstead, Neil G -- Peltz, Stuart W -- Eng, Loren A -- Chen, Karen S -- Mull, Jesse L -- Lynes, Maureen S -- Rubin, Lee L -- Fontoura, Paulo -- Santarelli, Luca -- Haehnke, Daniel -- McCarthy, Kathleen D -- Schmucki, Roland -- Ebeling, Martin -- Sivaramakrishnan, Manaswini -- Ko, Chien-Ping -- Paushkin, Sergey V -- Ratni, Hasane -- Gerlach, Irene -- Ghosh, Anirvan -- Metzger, Friedrich -- New York, N.Y. -- Science. 2014 Aug 8;345(6197):688-93. doi: 10.1126/science.1250127.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉PTC Therapeutics, 100 Corporate Court, South Plainfield, NJ 07080, USA. ; Section of Neurobiology, Department of Biological Sciences, University of Southern California, Los Angeles, CA 90089, USA. ; PTC Therapeutics, 100 Corporate Court, South Plainfield, NJ 07080, USA. friedrich.metzger@roche.com speltz@ptcbio.com. ; SMA Foundation, 888 Seventh Avenue, Suite 400, New York, NY 10019, USA. ; Department of Stem Cell and Regenerative Biology and the Harvard Stem Cell Institute, Harvard University, Cambridge, MA 02138, USA. ; Roche Pharmaceutical Research and Early Development, Roche Innovation Center Basel, F. Hoffmann-La Roche, Grenzacherstrasse 124, 4070 Basel, Switzerland. ; Roche Pharmaceutical Research and Early Development, Roche Innovation Center Basel, F. Hoffmann-La Roche, Grenzacherstrasse 124, 4070 Basel, Switzerland. friedrich.metzger@roche.com speltz@ptcbio.com.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25104390" target="_blank"〉PubMed〈/a〉
    Keywords: Administration, Oral ; Alternative Splicing/*drug effects ; Animals ; Cells, Cultured ; Coumarins/*administration & dosage/chemistry ; Disease Models, Animal ; Drug Evaluation, Preclinical ; Humans ; Isocoumarins/*administration & dosage/chemistry ; Longevity/*drug effects ; Mice ; Muscular Atrophy, Spinal/*drug therapy/genetics/metabolism ; Pyrimidinones/*administration & dosage/chemistry ; RNA, Messenger/genetics ; Sequence Deletion ; Small Molecule Libraries/*administration & dosage/chemistry ; Survival of Motor Neuron 2 Protein/*genetics/metabolism
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  • 51
    Publication Date: 2014-04-05
    Description: Adrenal Cushing's syndrome is caused by excess production of glucocorticoid from adrenocortical tumors and hyperplasias, which leads to metabolic disorders. We performed whole-exome sequencing of 49 blood-tumor pairs and RNA sequencing of 44 tumors from cortisol-producing adrenocortical adenomas (ACAs), adrenocorticotropic hormone-independent macronodular adrenocortical hyperplasias (AIMAHs), and adrenocortical oncocytomas (ADOs). We identified a hotspot in the PRKACA gene with a L205R mutation in 69.2% (27 out of 39) of ACAs and validated in 65.5% of a total of 87 ACAs. Our data revealed that the activating L205R mutation, which locates in the P+1 loop of the protein kinase A (PKA) catalytic subunit, promoted PKA substrate phosphorylation and target gene expression. Moreover, we discovered the recurrently mutated gene DOT1L in AIMAHs and CLASP2 in ADOs. Collectively, these data highlight potentially functional mutated genes in adrenal Cushing's syndrome.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cao, Yanan -- He, Minghui -- Gao, Zhibo -- Peng, Ying -- Li, Yanli -- Li, Lin -- Zhou, Weiwei -- Li, Xiangchun -- Zhong, Xu -- Lei, Yiming -- Su, Tingwei -- Wang, Hang -- Jiang, Yiran -- Yang, Lin -- Wei, Wei -- Yang, Xu -- Jiang, Xiuli -- Liu, Li -- He, Juan -- Ye, Junna -- Wei, Qing -- Li, Yingrui -- Wang, Weiqing -- Wang, Jun -- Ning, Guang -- New York, N.Y. -- Science. 2014 May 23;344(6186):913-7. doi: 10.1126/science.1249480. Epub 2014 Apr 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Shanghai Clinical Center for Endocrine and Metabolic Diseases, Shanghai Key Laboratory for Endocrine Tumors, Rui-Jin Hospital, Shanghai Jiao-Tong University School of Medicine, Shanghai, China. ; BGI-Shanghai, BGI-Shenzhen, Shenzhen, China. ; Department of Pathology, Rui-Jin Hospital, Shanghai Jiao-Tong University School of Medicine, Shanghai, China. ; Shanghai Clinical Center for Endocrine and Metabolic Diseases, Shanghai Key Laboratory for Endocrine Tumors, Rui-Jin Hospital, Shanghai Jiao-Tong University School of Medicine, Shanghai, China. guangning@medmail.com.cn wangj@genomics.org.cn wqingw@hotmail.com. ; BGI-Shanghai, BGI-Shenzhen, Shenzhen, China. Department of Biology, University of Copenhagen, Copenhagen, Denmark. King Abdulaziz University, Jeddah, Saudi Arabia. Macau University of Science and Technology, Macau, China. Department of Medicine, University of Hong Kong, Hong Kong. guangning@medmail.com.cn wangj@genomics.org.cn wqingw@hotmail.com. ; Shanghai Clinical Center for Endocrine and Metabolic Diseases, Shanghai Key Laboratory for Endocrine Tumors, Rui-Jin Hospital, Shanghai Jiao-Tong University School of Medicine, Shanghai, China. Laboratory of Endocrinology and Metabolism, Institute of Health Sciences, Shanghai Institutes for Biological Sciences (SIBS), Chinese Academy of Sciences (CAS), and Shanghai Jiao Tong University School of Medicine (SJTUSM), Shanghai, China. guangning@medmail.com.cn wangj@genomics.org.cn wqingw@hotmail.com.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24700472" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenal Cortex Neoplasms/*genetics/*metabolism ; Adrenocortical Adenoma/*genetics/*metabolism ; Amino Acid Substitution ; Arginine/genetics ; Catalytic Domain/genetics ; Cells, Cultured ; Cushing Syndrome/*genetics ; Cyclic AMP-Dependent Protein Kinase Catalytic Subunits/chemistry/*genetics ; Glucocorticoids/metabolism ; Humans ; Hydrocortisone/*metabolism ; Leucine/genetics ; Methyltransferases/genetics ; Microtubule-Associated Proteins/genetics ; Mutation
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  • 52
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-07-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pawar, Samraat -- New York, N.Y. -- Science. 2014 Jul 25;345(6195):383. doi: 10.1126/science.1256466.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Life Sciences, Imperial College London, Silwood Park, Ascot, Berkshire SL5 7PY, U K. s.pawar@imperial.ac.uk.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25061191" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Ecosystem ; *Models, Biological ; *Symbiosis
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  • 53
    Publication Date: 2014-04-05
    Description: Animal migrations span the globe, involving immense numbers of individuals from a wide range of taxa. Migrants transport nutrients, energy, and other organisms as they forage and are preyed upon throughout their journeys. These highly predictable, pulsed movements across large spatial scales render migration a potentially powerful yet underappreciated dimension of biodiversity that is intimately embedded within resident communities. We review examples from across the animal kingdom to distill fundamental processes by which migratory animals influence communities and ecosystems, demonstrating that they can uniquely alter energy flow, food-web topology and stability, trophic cascades, and the structure of metacommunities. Given the potential for migration to alter ecological networks worldwide, we suggest an integrative framework through which community dynamics and ecosystem functioning may explicitly consider animal migrations.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bauer, S -- Hoye, B J -- New York, N.Y. -- Science. 2014 Apr 4;344(6179):1242552. doi: 10.1126/science.1242552.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Bird Migration, Swiss Ornithological Institute, 6204 Sempach, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24700862" target="_blank"〉PubMed〈/a〉
    Keywords: *Animal Migration ; Animals ; *Biodiversity ; *Ecosystem ; Food Chain ; Herbivory ; Parasites/physiology ; Predatory Behavior
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  • 54
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-03-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stokstad, Erik -- New York, N.Y. -- Science. 2014 Mar 21;343(6177):1301. doi: 10.1126/science.343.6177.1301.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24653015" target="_blank"〉PubMed〈/a〉
    Keywords: Colorado ; *Ecosystem ; *Floods ; Groundwater ; Mexico ; *Rivers ; Salinity ; Trees/*growth & development ; United States
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  • 55
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-03-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McNutt, Marcia -- New York, N.Y. -- Science. 2014 Mar 21;343(6177):1289. doi: 10.1126/science.1253412.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Marcia McNutt is Editor-in-Chief of Science.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24653006" target="_blank"〉PubMed〈/a〉
    Keywords: Alaska ; *Aquatic Organisms ; *Ecosystem ; Environmental Monitoring ; Environmental Restoration and Remediation ; Gulf of Mexico ; *Petroleum Pollution
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  • 56
    Publication Date: 2014-06-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kelly, Ryan P -- Port, Jesse A -- Yamahara, Kevan M -- Martone, Rebecca G -- Lowell, Natalie -- Thomsen, Philip Francis -- Mach, Megan E -- Bennett, Meredith -- Prahler, Erin -- Caldwell, Margaret R -- Crowder, Larry B -- New York, N.Y. -- Science. 2014 Jun 27;344(6191):1455-6. doi: 10.1126/science.1251156. Epub 2014 Jun 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Marine and Environmental Affairs, University of Washington, Seattle, WA 98103, USA. Center for Ocean Solutions, Stanford University, Stanford, CA 94305, USA. rpkelly@uw.edu. ; Center for Ocean Solutions, Stanford University, Stanford, CA 94305, USA. ; School of Marine and Environmental Affairs, University of Washington, Seattle, WA 98103, USA. ; Centre for GeoGenetics, Natural History Museum of Denmark, University of Copenhagen, Copenhagen, Denmark.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24970068" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Aquatic Organisms/genetics ; DNA/*analysis ; Ecological Parameter Monitoring/*methods ; *Ecosystem ; Environmental Monitoring/*methods ; *Environmental Policy/legislation & jurisprudence ; Introduced Species
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  • 57
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-02-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennisi, Elizabeth -- New York, N.Y. -- Science. 2014 Jan 31;343(6170):472-3. doi: 10.1126/science.343.6170.472.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24482456" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Ants ; Biomass ; Butterflies ; Carnivory ; *Ecosystem ; Male ; *Salts ; *Sodium Chloride ; Soil/*chemistry ; Trees
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  • 58
    Publication Date: 2014-07-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pfeifer, M -- Packer, C -- Burton, A C -- Garnett, S T -- Loveridge, A J -- MacNulty, D -- Platts, P J -- New York, N.Y. -- Science. 2014 Jul 25;345(6195):389. doi: 10.1126/science.345.6195.389-a. Epub 2014 Jul 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Forest Ecology and Conservation Lab, Department of Life Sciences, Imperial College London, Ascot, SL5 7PY, UK. York Institute for Tropical Ecosystems, Environment Department, University of York, York, YO10 5DD, UK. m.pfeifer@imperial.ac.uk. ; Department of Ecology, Evolution and Behavior, University of Minnesota, St. Paul, MN 55108, USA. ; Alberta Innovates Technology Futures, Victoria, BC V8Z 7X8, Canada. Department of Biology, University of Victoria, Victoria, BC V8W 2Y2, Canada. ; Research Institute for the Environment and Livelihoods, Charles Darwin University, Darwin, NT 0909, Australia. ; Wildlife Conservation Research Unit, Department of Zoology, Oxford University, Oxford, OX13 5QL, UK. ; Department of Wildland Resources, Utah State University, Logan, UT 84322, USA. ; York Institute for Tropical Ecosystems, Environment Department, University of York, York, YO10 5DD, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25061194" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Animals, Wild ; *Biodiversity ; *Conservation of Natural Resources ; *Ecosystem ; Humans
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  • 59
    Publication Date: 2014-08-02
    Description: Many RNA regulatory proteins controlling pre-messenger RNA splicing contain serine:arginine (SR) repeats. Here, we found that these SR domains bound hydrogel droplets composed of fibrous polymers of the low-complexity domain of heterogeneous ribonucleoprotein A2 (hnRNPA2). Hydrogel binding was reversed upon phosphorylation of the SR domain by CDC2-like kinases 1 and 2 (CLK1/2). Mutated variants of the SR domains changing serine to glycine (SR-to-GR variants) also bound to hnRNPA2 hydrogels but were not affected by CLK1/2. When expressed in mammalian cells, these variants bound nucleoli. The translation products of the sense and antisense transcripts of the expansion repeats associated with the C9orf72 gene altered in neurodegenerative disease encode GRn and PRn repeat polypeptides. Both peptides bound to hnRNPA2 hydrogels independent of CLK1/2 activity. When applied to cultured cells, both peptides entered cells, migrated to the nucleus, bound nucleoli, and poisoned RNA biogenesis, which caused cell death.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4459787/" 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/PMC4459787/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kwon, Ilmin -- Xiang, Siheng -- Kato, Masato -- Wu, Leeju -- Theodoropoulos, Pano -- Wang, Tao -- Kim, Jiwoong -- Yun, Jonghyun -- Xie, Yang -- McKnight, Steven L -- U01 GM107623/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2014 Sep 5;345(6201):1139-45. doi: 10.1126/science.1254917. Epub 2014 Jul 31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, UT Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390-9152, USA. ; Quantitative Biomedical Research Center, Department of Clinical Sciences, UT Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390-9152, USA. ; Department of Biochemistry, UT Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390-9152, USA. steven.mcknight@utsouthwestern.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25081482" target="_blank"〉PubMed〈/a〉
    Keywords: Alternative Splicing ; Amyotrophic Lateral Sclerosis/genetics/*metabolism/pathology ; Astrocytes/*metabolism/pathology ; Cell Death ; Cell Nucleolus/*metabolism ; Cells, Cultured ; Dipeptides/genetics/*metabolism/pharmacology ; Frontotemporal Dementia/genetics/*metabolism/pathology ; Glutamate Plasma Membrane Transport Proteins/genetics ; Heterogeneous-Nuclear Ribonucleoprotein Group A-B/*metabolism ; Humans ; Hydrogel ; Phosphorylation ; Protein Biosynthesis ; Protein Structure, Tertiary ; Protein-Serine-Threonine Kinases/metabolism ; Protein-Tyrosine Kinases/metabolism ; Proteins/*genetics ; RNA, Antisense/antagonists & inhibitors/biosynthesis ; RNA, Messenger/antagonists & inhibitors/biosynthesis ; RNA, Ribosomal/antagonists & inhibitors/biosynthesis ; Repetitive Sequences, Amino Acid ; Transcription, Genetic
    Print ISSN: 0036-8075
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  • 60
    Publication Date: 2014-06-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dornelas, Maria -- Gotelli, Nicholas J -- McGill, Brian -- Magurran, Anne E -- New York, N.Y. -- Science. 2014 Jun 6;344(6188):1098-9. doi: 10.1126/science.344.6188.1098-b.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre for Biological Diversity and Scottish Oceans Institute, School of Biology, University of St. Andrews, St. Andrews, Fife, KY16 9TH, UK. maadd@st-andrews.ac.uk. ; Department of Biology, University of Vermont, Burlington, VT 05405, USA. ; School of Biology and Ecology, Sustainability Solutions Initiative, University of Maine, Orono, ME 04469, USA. ; Centre for Biological Diversity and Scottish Oceans Institute, School of Biology, University of St. Andrews, St. Andrews, Fife, KY16 9TH, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24904147" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biodiversity ; *Birds ; *Ecosystem ; *Fishes ; *Invertebrates ; *Mammals ; *Plants
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  • 61
    Publication Date: 2014-04-20
    Description: The extent to which biodiversity change in local assemblages contributes to global biodiversity loss is poorly understood. We analyzed 100 time series from biomes across Earth to ask how diversity within assemblages is changing through time. We quantified patterns of temporal alpha diversity, measured as change in local diversity, and temporal beta diversity, measured as change in community composition. Contrary to our expectations, we did not detect systematic loss of alpha diversity. However, community composition changed systematically through time, in excess of predictions from null models. Heterogeneous rates of environmental change, species range shifts associated with climate change, and biotic homogenization may explain the different patterns of temporal alpha and beta diversity. Monitoring and understanding change in species composition should be a conservation priority.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dornelas, Maria -- Gotelli, Nicholas J -- McGill, Brian -- Shimadzu, Hideyasu -- Moyes, Faye -- Sievers, Caya -- Magurran, Anne E -- New York, N.Y. -- Science. 2014 Apr 18;344(6181):296-9. doi: 10.1126/science.1248484.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre for Biological Diversity and Scottish Oceans Institute, School of Biology, University of St. Andrews, St. Andrews, Fife KY16 9TH, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24744374" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biodiversity ; *Birds ; *Ecosystem ; Extinction, Biological ; *Fishes ; Introduced Species ; *Invertebrates ; *Mammals ; *Plants ; Population Dynamics ; Time Factors
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  • 62
    Publication Date: 2014-01-11
    Description: Large carnivores face serious threats and are experiencing massive declines in their populations and geographic ranges around the world. We highlight how these threats have affected the conservation status and ecological functioning of the 31 largest mammalian carnivores on Earth. Consistent with theory, empirical studies increasingly show that large carnivores have substantial effects on the structure and function of diverse ecosystems. Significant cascading trophic interactions, mediated by their prey or sympatric mesopredators, arise when some of these carnivores are extirpated from or repatriated to ecosystems. Unexpected effects of trophic cascades on various taxa and processes include changes to bird, mammal, invertebrate, and herpetofauna abundance or richness; subsidies to scavengers; altered disease dynamics; carbon sequestration; modified stream morphology; and crop damage. Promoting tolerance and coexistence with large carnivores is a crucial societal challenge that will ultimately determine the fate of Earth's largest carnivores and all that depends upon them, including humans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ripple, William J -- Estes, James A -- Beschta, Robert L -- Wilmers, Christopher C -- Ritchie, Euan G -- Hebblewhite, Mark -- Berger, Joel -- Elmhagen, Bodil -- Letnic, Mike -- Nelson, Michael P -- Schmitz, Oswald J -- Smith, Douglas W -- Wallach, Arian D -- Wirsing, Aaron J -- New York, N.Y. -- Science. 2014 Jan 10;343(6167):1241484. doi: 10.1126/science.1241484.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Trophic Cascades Program, Department of Forest Ecosystems and Society, Oregon State University, Corvallis, OR 97331, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24408439" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Carnivora/anatomy & histology/classification/physiology ; *Ecological and Environmental Phenomena ; *Ecosystem ; *Extinction, Biological ; Humans ; Meat Products/statistics & numerical data ; Oceans and Seas ; Plants ; Population Dynamics
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 63
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-07-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Law, Kara Lavender -- Thompson, Richard C -- New York, N.Y. -- Science. 2014 Jul 11;345(6193):144-5. doi: 10.1126/science.1254065. Epub 2014 Jul 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Oceanography, Sea Education Association, Woods Hole, MA 02543, USA. klavender@sea.edu. ; School of Marine Science and Engineering, Plymouth University, Plymouth PL4 8AA, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25013051" target="_blank"〉PubMed〈/a〉
    Keywords: Aquatic Organisms/*drug effects ; *Ecosystem ; Oceans and Seas ; Particle Size ; Plastics/*toxicity ; *Seawater ; Water Pollutants, Chemical/*toxicity ; Water Pollution, Chemical/*prevention & control
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  • 64
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-03-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chapron, Guillaume -- Lopez-Bao, Jose Vicente -- New York, N.Y. -- Science. 2014 Mar 14;343(6176):1199-200. doi: 10.1126/science.343.6176.1199-b.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Grimso Wildlife Research Station, Swedish University of Agricultural Sciences, SE-73091 Riddarhyttan, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24626913" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Carnivora ; *Ecological and Environmental Phenomena ; *Ecosystem ; *Extinction, Biological ; Humans
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  • 65
    Publication Date: 2014-06-28
    Description: Lassa virus spreads from a rodent to humans and can lead to lethal hemorrhagic fever. Despite its broad tropism, chicken cells were reported 30 years ago to resist infection. We found that Lassa virus readily engaged its cell-surface receptor alpha-dystroglycan in avian cells, but virus entry in susceptible species involved a pH-dependent switch to an intracellular receptor, the lysosome-resident protein LAMP1. Iterative haploid screens revealed that the sialyltransferase ST3GAL4 was required for the interaction of the virus glycoprotein with LAMP1. A single glycosylated residue in LAMP1, present in susceptible species but absent in birds, was essential for interaction with the Lassa virus envelope protein and subsequent infection. The resistance of Lamp1-deficient mice to Lassa virus highlights the relevance of this receptor switch in vivo.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4239993/" 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/PMC4239993/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jae, Lucas T -- Raaben, Matthijs -- Herbert, Andrew S -- Kuehne, Ana I -- Wirchnianski, Ariel S -- Soh, Timothy K -- Stubbs, Sarah H -- Janssen, Hans -- Damme, Markus -- Saftig, Paul -- Whelan, Sean P -- Dye, John M -- Brummelkamp, Thijn R -- AI081842/AI/NIAID NIH HHS/ -- AI109740/AI/NIAID NIH HHS/ -- R01 AI081842/AI/NIAID NIH HHS/ -- T32 AI007245/AI/NIAID NIH HHS/ -- U19 AI109740/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2014 Jun 27;344(6191):1506-10. doi: 10.1126/science.1252480.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX, Amsterdam, Netherlands. ; Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX, Amsterdam, Netherlands. Department of Microbiology and Immunobiology, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, MA 02115, USA. ; U.S. Army Medical Research Institute of Infectious Diseases, 1425 Porter Street, Fort Detrick, MD 21702-5011, USA. ; Department of Microbiology and Immunobiology, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, MA 02115, USA. ; Biochemisches Institut, Christian Albrechts-Universitat Kiel, 24118 Kiel, Germany. ; Department of Microbiology and Immunobiology, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, MA 02115, USA. t.brummelkamp@nki.nl john.m.dye1.civ@mail.mil sean_whelan@hms.harvard.edu. ; U.S. Army Medical Research Institute of Infectious Diseases, 1425 Porter Street, Fort Detrick, MD 21702-5011, USA. t.brummelkamp@nki.nl john.m.dye1.civ@mail.mil sean_whelan@hms.harvard.edu. ; Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX, Amsterdam, Netherlands. CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, 1090 Vienna, Austria. Cancer Genomics Center (CGC.nl), Plesmanlaan 121, 1066 CX, Amsterdam, Netherlands. t.brummelkamp@nki.nl john.m.dye1.civ@mail.mil sean_whelan@hms.harvard.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24970085" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cell Line ; Cell Membrane/metabolism/virology ; Cells, Cultured ; Chickens ; Dystroglycans/genetics/metabolism ; Glycosylation ; Humans ; Hydrogen-Ion Concentration ; Lassa Fever/virology ; Lassa virus/*physiology ; Lysosomal-Associated Membrane Protein 1/chemistry/*metabolism ; Lysosomes/metabolism/virology ; Mice ; Mice, Knockout ; Molecular Sequence Data ; Protein Binding ; Receptors, Virus/*metabolism ; Sialyltransferases/metabolism ; Viral Envelope Proteins/*metabolism ; *Virus Internalization
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  • 66
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-09-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mace, Georgina M -- New York, N.Y. -- Science. 2014 Sep 26;345(6204):1558-60. doi: 10.1126/science.1254704.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre for Biodiversity and Environment Research, Department of Genetics, Evolution and Environment, University College London, London WC1E 6BT, UK. g.mace@ucl.ac.uk.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25258063" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Conservation of Natural Resources ; Ecological and Environmental Processes ; *Ecosystem ; Humans
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  • 67
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-02-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Machovina, Brian -- Feeley, Kenneth J -- New York, N.Y. -- Science. 2014 Feb 21;343(6173):838. doi: 10.1126/science.343.6173.838-a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Florida International University, Miami, FL 33199, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24558143" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Carnivora ; *Ecological and Environmental Phenomena ; *Ecosystem ; *Extinction, Biological ; Humans
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  • 68
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-02-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Servick, Kelly -- New York, N.Y. -- Science. 2014 Feb 21;343(6173):834-7. doi: 10.1126/science.343.6173.834.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24558142" target="_blank"〉PubMed〈/a〉
    Keywords: Acoustics ; Animals ; Computer Systems ; Ecological Parameter Monitoring/*methods ; *Ecosystem ; Software ; *Sound ; *Vocalization, Animal
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  • 69
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-03-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Alexander, Kathleen A -- Sanderson, Claire E -- New York, N.Y. -- Science. 2014 Mar 14;343(6176):1199. doi: 10.1126/science.343.6176.1199-a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Fisheries and Wildlife Conservation, Virginia Tech University, Blacksburg, VA 24061, USA and CARACAL, Centre for Conservation of African Resources: Animals, Communities, and Land Use, Kasane, Botswana.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24626912" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Carnivora ; *Ecological and Environmental Phenomena ; *Ecosystem ; *Extinction, Biological ; Humans
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  • 70
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-04-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pandolfi, John M -- Lovelock, Catherine E -- New York, N.Y. -- Science. 2014 Apr 18;344(6181):266-7. doi: 10.1126/science.1252963.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Biological Sciences, ARC Centre of Excellence for Coral Reef Studies, University of Queensland, St. Lucia, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24744366" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biodiversity ; *Birds ; *Ecosystem ; *Fishes ; *Invertebrates ; *Mammals ; *Plants
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  • 71
    Publication Date: 2014-01-25
    Description: The transcription and transport of messenger RNA (mRNA) are critical steps in regulating the spatial and temporal components of gene expression, but it has not been possible to observe the dynamics of endogenous mRNA in primary mammalian tissues. We have developed a transgenic mouse in which all beta-actin mRNA is fluorescently labeled. We found that beta-actin mRNA in primary fibroblasts localizes predominantly by diffusion and trapping as single mRNAs. In cultured neurons and acute brain slices, we found that multiple beta-actin mRNAs can assemble together, travel by active transport, and disassemble upon depolarization by potassium chloride. Imaging of brain slices revealed immediate early induction of beta-actin transcription after depolarization. Studying endogenous mRNA in live mouse tissues provides insight into its dynamic regulation within the context of the cellular and tissue microenvironment.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4111226/" 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/PMC4111226/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Park, Hye Yoon -- Lim, Hyungsik -- Yoon, Young J -- Follenzi, Antonia -- Nwokafor, Chiso -- Lopez-Jones, Melissa -- Meng, Xiuhua -- Singer, Robert H -- EB13571/EB/NIBIB NIH HHS/ -- F32-GM87122/GM/NIGMS NIH HHS/ -- GM84364/GM/NIGMS NIH HHS/ -- NS083085-19/NS/NINDS NIH HHS/ -- R01 EB013571/EB/NIBIB NIH HHS/ -- R01 NS083085/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2014 Jan 24;343(6169):422-4. doi: 10.1126/science.1239200.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy and Structural Biology, Albert Einstein College of Medicine, Bronx, NY 10461, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24458643" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/*biosynthesis/genetics ; Animals ; Brain/cytology/metabolism ; Cells, Cultured ; Fibroblasts/metabolism ; Fluorescent Dyes/chemistry ; Mice ; Mice, Transgenic ; Neuroimaging/*methods ; Neurons/metabolism ; Protein Biosynthesis ; RNA, Messenger/analysis/biosynthesis/*metabolism ; Staining and Labeling
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  • 72
    Publication Date: 2014-11-29
    Description: Norovirus gastroenteritis is a major public health burden worldwide. Although fecal shedding is important for transmission of enteric viruses, little is known about the immune factors that restrict persistent enteric infection. We report here that although the cytokines interferon-alpha (IFN-alpha) and IFN-beta prevented the systemic spread of murine norovirus (MNoV), only IFN-lambda controlled persistent enteric infection. Infection-dependent induction of IFN-lambda was governed by the MNoV capsid protein and correlated with diminished enteric persistence. Treatment of established infection with IFN-lambda cured mice in a manner requiring nonhematopoietic cell expression of the IFN-lambda receptor, Ifnlr1, and independent of adaptive immunity. These results suggest the therapeutic potential of IFN-lambda for curing virus infections in the gastrointestinal tract.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4398891/" 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/PMC4398891/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nice, Timothy J -- Baldridge, Megan T -- McCune, Broc T -- Norman, Jason M -- Lazear, Helen M -- Artyomov, Maxim -- Diamond, Michael S -- Virgin, Herbert W -- 5T32A100716334/PHS HHS/ -- 5T32AI007163/AI/NIAID NIH HHS/ -- 5T32CA009547/CA/NCI NIH HHS/ -- F31 CA177194/CA/NCI NIH HHS/ -- F31CA177194-01/CA/NCI NIH HHS/ -- R01 AI084887/AI/NIAID NIH HHS/ -- T32 AI007163/AI/NIAID NIH HHS/ -- T32 CA009547/CA/NCI NIH HHS/ -- U19 AI083019/AI/NIAID NIH HHS/ -- U19 AI106772/AI/NIAID NIH HHS/ -- U19 AI109725/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2015 Jan 16;347(6219):269-73. doi: 10.1126/science.1258100. Epub 2014 Nov 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA. ; Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA. ; Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA. Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA. Department of Molecular Microbiology, Washington University School of Medicine, St. Louis, MO 63110, USA. ; Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA. virgin@wustl.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25431489" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptive Immunity ; Animals ; Caliciviridae Infections/*drug therapy/*immunology/virology ; Capsid Proteins/immunology/metabolism ; Cells, Cultured ; Cytokines/biosynthesis/*immunology/*therapeutic use ; Feces/virology ; Gastroenteritis/drug therapy/*immunology/virology ; Immunity, Innate ; Interferon-alpha/biosynthesis/immunology ; Interferon-beta/biosynthesis/immunology ; Mice ; Mice, Inbred C57BL ; Norovirus/*immunology/*physiology ; Virus Replication ; Virus Shedding
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  • 73
    Publication Date: 2014-12-06
    Description: Distinct types of CD4(+) T cells protect the host against different classes of pathogens. However, it is unclear whether a given pathogen induces a single type of polarized T cell. By combining antigenic stimulation and T cell receptor deep sequencing, we found that human pathogen- and vaccine-specific T helper 1 (T(H)1), T(H)2, and T(H)17 memory cells have different frequencies but comparable diversity and comprise not only clones polarized toward a single fate, but also clones whose progeny have acquired multiple fates. Single naive T cells primed by a pathogen in vitro could also give rise to multiple fates. Our results unravel an unexpected degree of interclonal and intraclonal functional heterogeneity of the human T cell response and suggest that polarized responses result from preferential expansion rather than priming.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Becattini, Simone -- Latorre, Daniela -- Mele, Federico -- Foglierini, Mathilde -- De Gregorio, Corinne -- Cassotta, Antonino -- Fernandez, Blanca -- Kelderman, Sander -- Schumacher, Ton N -- Corti, Davide -- Lanzavecchia, Antonio -- Sallusto, Federica -- New York, N.Y. -- Science. 2015 Jan 23;347(6220):400-6. doi: 10.1126/science.1260668. Epub 2014 Dec 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Research in Biomedicine, Bellinzona, Universita della Svizzera Italiana, Lugano, Switzerland. Institute of Microbiology, ETH Zurich, Zurich, Switzerland. ; Institute for Research in Biomedicine, Bellinzona, Universita della Svizzera Italiana, Lugano, Switzerland. ; Division of Immunology, Netherlands Cancer Institute, Amsterdam, Netherlands. ; Institute for Research in Biomedicine, Bellinzona, Universita della Svizzera Italiana, Lugano, Switzerland. federica.sallusto@irb.usi.ch.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25477212" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; CD4-Positive T-Lymphocytes/*immunology ; Candida albicans/*immunology ; Cells, Cultured ; Clone Cells ; High-Throughput Nucleotide Sequencing ; Host-Pathogen Interactions/*immunology ; Humans ; *Immunologic Memory ; Lymphocyte Activation ; Molecular Sequence Data ; Mycobacterium tuberculosis/*immunology ; Receptors, Antigen, T-Cell/genetics ; T-Lymphocyte Subsets/*immunology ; Th1 Cells/immunology ; Th17 Cells/immunology ; Th2 Cells/immunology ; Vaccines/*immunology
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  • 74
    Publication Date: 2013-12-07
    Description: The skin is a classical example of a tissue maintained by stem cells. However, the identity of the stem cells that maintain the interfollicular epidermis and the source of the signals that control their activity remain unclear. Using mouse lineage tracing and quantitative clonal analyses, we showed that the Wnt target gene Axin2 marks interfollicular epidermal stem cells. These Axin2-expressing cells constitute the majority of the basal epidermal layer, compete neutrally, and require Wnt/beta-catenin signaling to proliferate. The same cells contribute robustly to wound healing, with no requirement for a quiescent stem cell subpopulation. By means of double-labeling RNA in situ hybridization in mice, we showed that the Axin2-expressing cells themselves produce Wnt signals as well as long-range secreted Wnt inhibitors, suggesting an autocrine mechanism of stem cell self-renewal.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4081860/" 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/PMC4081860/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lim, Xinhong -- Tan, Si Hui -- Koh, Winston Lian Chye -- Chau, Rosanna Man Wah -- Yan, Kelley S -- Kuo, Calvin J -- van Amerongen, Renee -- Klein, Allon Moshe -- Nusse, Roel -- 1R01DK085720/DK/NIDDK NIH HHS/ -- 1U01DK085527/DK/NIDDK NIH HHS/ -- 5K08DK096048/DK/NIDDK NIH HHS/ -- K08 DK096048/DK/NIDDK NIH HHS/ -- P30 DK026743/DK/NIDDK NIH HHS/ -- R01 DK085720/DK/NIDDK NIH HHS/ -- U01 DK085527/DK/NIDDK NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2013 Dec 6;342(6163):1226-30. doi: 10.1126/science.1239730.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Developmental Biology, Howard Hughes Medical Institute (HHMI), Institute for Stem Cell Biology and Regenerative Medicine, School of Medicine, Stanford University, Stanford, CA, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24311688" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Autocrine Communication ; Axin Protein/genetics/metabolism ; Cell Differentiation ; Cell Lineage ; Cell Proliferation ; Cells, Cultured ; Epidermis/*cytology/injuries/metabolism ; Epithelial Cells/cytology/metabolism ; Gene Expression ; Homeostasis ; Humans ; Intercellular Signaling Peptides and Proteins/metabolism ; Keratinocytes/cytology/metabolism ; Mice ; Regeneration ; Skin/injuries ; Stem Cell Niche ; Stem Cells/cytology/*physiology ; Wnt Proteins/metabolism ; *Wnt Signaling Pathway ; Wound Healing ; beta Catenin/genetics/metabolism
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  • 75
    Publication Date: 2013-05-21
    Description: The generation of high-affinity antibodies depends on the ability of B cells to extract antigens from the surfaces of antigen-presenting cells. B cells that express high-affinity B cell receptors (BCRs) acquire more antigen and obtain better T cell help. However, the mechanisms by which B cells extract antigen remain unclear. Using fluid and flexible membrane substrates to mimic antigen-presenting cells, we showed that B cells acquire antigen by dynamic myosin IIa-mediated contractions that pull out and invaginate the presenting membranes. The forces generated by myosin IIa contractions ruptured most individual BCR-antigen bonds and promoted internalization of only high-affinity, multivalent BCR microclusters. Thus, B cell contractility contributes to affinity discrimination by mechanically testing the strength of antigen binding.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3713314/" 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/PMC3713314/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Natkanski, Elizabeth -- Lee, Wing-Yiu -- Mistry, Bhakti -- Casal, Antonio -- Molloy, Justin E -- Tolar, Pavel -- MC_U117570592/Medical Research Council/United Kingdom -- MC_U117597138/Medical Research Council/United Kingdom -- U117570592/Medical Research Council/United Kingdom -- U117597138/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2013 Jun 28;340(6140):1587-90. doi: 10.1126/science.1237572. Epub 2013 May 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Immune Cell Biology, MRC National Institute for Medical Research, Mill Hill, London NW7 1AA, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23686338" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antibody Affinity ; *Antigen Presentation ; Antigens/*immunology ; B-Lymphocytes/*immunology ; Cells, Cultured ; Mechanical Processes ; Mice ; Mice, Inbred C57BL ; Microscopy, Atomic Force ; Nonmuscle Myosin Type IIA/*physiology ; Receptors, Antigen, B-Cell/immunology
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  • 76
    Publication Date: 2013-08-10
    Description: Numerous volatile organic compounds (VOCs) exist in Earth's atmosphere, most of which originate from biogenic emissions. Despite VOCs' critical role in tropospheric chemistry, studies for evaluating their atmosphere-ecosystem exchange (emission and deposition) have been limited to a few dominant compounds owing to a lack of appropriate measurement techniques. Using a high-mass resolution proton transfer reaction-time of flight-mass spectrometer and an absolute value eddy-covariance method, we directly measured 186 organic ions with net deposition, and 494 that have bidirectional flux. This observation of active atmosphere-ecosystem exchange of the vast majority of detected VOCs poses a challenge to current emission, air quality, and global climate models, which do not account for this extremely large range of compounds. This observation also provides new insight for understanding the atmospheric VOC budget.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Park, J-H -- Goldstein, A H -- Timkovsky, J -- Fares, S -- Weber, R -- Karlik, J -- Holzinger, R -- New York, N.Y. -- Science. 2013 Aug 9;341(6146):643-7. doi: 10.1126/science.1235053.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Environmental Science, Policy, and Management, University of California at Berkeley, Berkeley, CA 94720, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23929979" target="_blank"〉PubMed〈/a〉
    Keywords: Atmosphere/*chemistry ; *Ecosystem ; Mass Spectrometry ; Ozone/analysis/chemistry ; Plants/chemistry ; Volatile Organic Compounds/analysis/*chemistry
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  • 77
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2013-10-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Aspinall, Richard -- Gregory, Peter -- New York, N.Y. -- Science. 2013 Oct 25;342(6157):421. doi: 10.1126/science.342.6157.421-a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉James Hutton Institute, Craigiebuckler, Aberdeen, AB15 8QH, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24159029" target="_blank"〉PubMed〈/a〉
    Keywords: *Agriculture ; Animals ; *Climate Change ; *Conservation of Natural Resources ; *Decision Support Techniques ; *Ecosystem ; *Models, Economic
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 78
    Publication Date: 2013-07-03
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pedaste, Margus -- de Jong, Ton -- Sarapuu, Tago -- Piksoot, Jaanika -- van Joolingen, Wouter R -- Giemza, Adam -- New York, N.Y. -- Science. 2013 Jun 28;340(6140):1537-8. doi: 10.1126/science.1229908.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of Tartu, 50103 Tartu, Estonia. margus.pedaste@ut.ee〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23812708" target="_blank"〉PubMed〈/a〉
    Keywords: Ecology/*education ; *Ecosystem ; Estonia ; Germany ; Netherlands ; Problem-Based Learning/*methods ; Research Design ; *Software
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  • 79
    Publication Date: 2013-04-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Austin, A T -- Bustamante, M M C -- Nardoto, G B -- Mitre, S K -- Perez, T -- Ometto, J P H B -- Ascarrunz, N L -- Forti, M C -- Longo, K -- Gavito, M E -- Enrich-Prast, A -- Martinelli, L A -- New York, N.Y. -- Science. 2013 Apr 12;340(6129):149. doi: 10.1126/science.1231679.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Universidad de Buenos Aires, IFEVA-CONICET, Buenos Aires, Argentina.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23580515" target="_blank"〉PubMed〈/a〉
    Keywords: Agriculture ; Biomass ; *Conservation of Natural Resources ; *Ecosystem ; *Environment ; Human Activities ; Humans ; Latin America ; Nitrogen ; *Nitrogen Cycle ; Politics ; Public Health ; Public Policy
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  • 80
    Publication Date: 2013-08-03
    Description: The future impacts of anthropogenic global change on marine ecosystems are highly uncertain, but insights can be gained from past intervals of high atmospheric carbon dioxide partial pressure. The long-term geological record reveals an early Cenozoic warm climate that supported smaller polar ecosystems, few coral-algal reefs, expanded shallow-water platforms, longer food chains with less energy for top predators, and a less oxygenated ocean than today. The closest analogs for our likely future are climate transients, 10,000 to 200,000 years in duration, that occurred during the long early Cenozoic interval of elevated warmth. Although the future ocean will begin to resemble the past greenhouse world, it will retain elements of the present "icehouse" world long into the future. Changing temperatures and ocean acidification, together with rising sea level and shifts in ocean productivity, will keep marine ecosystems in a state of continuous change for 100,000 years.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Norris, R D -- Turner, S Kirtland -- Hull, P M -- Ridgwell, A -- New York, N.Y. -- Science. 2013 Aug 2;341(6145):492-8. doi: 10.1126/science.1240543.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Scripps Institution of Oceanography, University of California, San Diego, La Jolla, CA 92093, USA. rnorris@ucsd.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23908226" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Evolution ; *Climate Change/history ; *Ecosystem ; Greenhouse Effect ; History, Ancient ; *Oceans and Seas ; *Seawater ; Temperature ; Tidal Waves ; Vertebrates
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  • 81
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2013-09-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fung, Inez -- New York, N.Y. -- Science. 2013 Sep 6;341(6150):1075-6. doi: 10.1126/science.1242004.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of California, Berkeley, Berkeley, CA 94720-4767, USA. ifung@berkeley.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24009383" target="_blank"〉PubMed〈/a〉
    Keywords: Atmosphere/*chemistry ; *Carbon Cycle ; Carbon Dioxide/*chemistry ; *Ecosystem ; *Trees
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  • 82
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2013-10-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Obst, Carl -- Edens, Bram -- Hein, Lars -- New York, N.Y. -- Science. 2013 Oct 25;342(6157):420. doi: 10.1126/science.342.6157.420-a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Melbourne Sustainable Society Institute, University of Melbourne, Victoria, 3010 Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24159027" target="_blank"〉PubMed〈/a〉
    Keywords: *Agriculture ; Animals ; *Climate Change ; *Conservation of Natural Resources ; *Decision Support Techniques ; *Ecosystem ; *Models, Economic
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  • 83
    Publication Date: 2013-04-06
    Description: A number of human cancers harbor somatic point mutations in the genes encoding isocitrate dehydrogenases 1 and 2 (IDH1 and IDH2). These mutations alter residues in the enzyme active sites and confer a gain-of-function in cancer cells, resulting in the accumulation and secretion of the oncometabolite (R)-2-hydroxyglutarate (2HG). We developed a small molecule, AGI-6780, that potently and selectively inhibits the tumor-associated mutant IDH2/R140Q. A crystal structure of AGI-6780 complexed with IDH2/R140Q revealed that the inhibitor binds in an allosteric manner at the dimer interface. The results of steady-state enzymology analysis were consistent with allostery and slow-tight binding by AGI-6780. Treatment with AGI-6780 induced differentiation of TF-1 erythroleukemia and primary human acute myelogenous leukemia cells in vitro. These data provide proof-of-concept that inhibitors targeting mutant IDH2/R140Q could have potential applications as a differentiation therapy for cancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Fang -- Travins, Jeremy -- DeLaBarre, Byron -- Penard-Lacronique, Virginie -- Schalm, Stefanie -- Hansen, Erica -- Straley, Kimberly -- Kernytsky, Andrew -- Liu, Wei -- Gliser, Camelia -- Yang, Hua -- Gross, Stefan -- Artin, Erin -- Saada, Veronique -- Mylonas, Elena -- Quivoron, Cyril -- Popovici-Muller, Janeta -- Saunders, Jeffrey O -- Salituro, Francesco G -- Yan, Shunqi -- Murray, Stuart -- Wei, Wentao -- Gao, Yi -- Dang, Lenny -- Dorsch, Marion -- Agresta, Sam -- Schenkein, David P -- Biller, Scott A -- Su, Shinsan M -- de Botton, Stephane -- Yen, Katharine E -- New York, N.Y. -- Science. 2013 May 3;340(6132):622-6. doi: 10.1126/science.1234769. Epub 2013 Apr 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Agios Pharmaceuticals, Cambridge, MA 02139-4169, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23558173" target="_blank"〉PubMed〈/a〉
    Keywords: Allosteric Site ; Antineoplastic Agents/chemistry/metabolism/pharmacology ; Catalytic Domain ; Cell Line, Tumor ; Cell Proliferation ; Cells, Cultured ; Crystallography, X-Ray ; Enzyme Inhibitors/chemistry/metabolism/*pharmacology ; Erythropoiesis/drug effects ; Gene Expression Regulation, Leukemic ; Glutarates/metabolism ; Hematopoiesis/*drug effects ; Humans ; Isocitrate Dehydrogenase/*antagonists & inhibitors/chemistry/*genetics/metabolism ; Leukemia, Erythroblastic, Acute ; Leukemia, Myeloid, Acute/drug therapy/*enzymology/genetics/pathology ; Molecular Targeted Therapy ; Mutant Proteins/antagonists & inhibitors/chemistry/metabolism ; Phenylurea Compounds/chemistry/metabolism/*pharmacology ; Point Mutation ; Protein Multimerization ; Protein Structure, Secondary ; Small Molecule Libraries ; Sulfonamides/chemistry/metabolism/*pharmacology
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  • 84
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2013-01-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chown, S L -- New York, N.Y. -- Science. 2013 Jan 11;339(6116):141. doi: 10.1126/science.339.6116.141-a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23307721" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Conservation of Natural Resources ; *Ecosystem ; Humans
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  • 85
    Publication Date: 2013-12-18
    Description: Erythropoietin is a signaling glycoprotein that controls the fundamental process of erythropoiesis, orchestrating the production and maintenance of red blood cells. As administrated clinically, erythropoietin has a polypeptide backbone with complex dishomogeneity in its carbohydrate domains. Here we describe the total synthesis of homogeneous erythropoietin with consensus carbohydrate domains incorporated at all of the native glycosylation sites. The oligosaccharide sectors were built by total synthesis and attached stereospecifically to peptidyl fragments of the wild-type primary sequence, themselves obtained by solid-phase peptide synthesis. The glycopeptidyl constructs were joined by chemical ligation, followed by metal-free dethiylation, and subsequently folded. This homogeneous erythropoietin glycosylated at the three wild-type aspartates with N-linked high-mannose sialic acid-containing oligosaccharides and O-linked glycophorin exhibits Procrit-level in vivo activity in mice.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4080428/" 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/PMC4080428/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Ping -- Dong, Suwei -- Shieh, Jae-Hung -- Peguero, Elizabeth -- Hendrickson, Ronald -- Moore, Malcolm A S -- Danishefsky, Samuel J -- HL025848/HL/NHLBI NIH HHS/ -- P30 CA008748/CA/NCI NIH HHS/ -- R01 GM109760/GM/NIGMS NIH HHS/ -- R01 HL025848/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2013 Dec 13;342(6164):1357-60. doi: 10.1126/science.1245095.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory for Bioorganic Chemistry, Sloan-Kettering Institute for Cancer Research, 1275 York Avenue, New York, NY 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24337294" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Aspartic Acid/chemistry ; Cells, Cultured ; Consensus Sequence ; Dose-Response Relationship, Drug ; Erythrocyte Count ; Erythropoietin/*administration & dosage/*chemical synthesis/chemistry ; Glycophorin/chemistry ; Glycosylation ; Injections, Subcutaneous ; Mannose/chemistry ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; N-Acetylneuraminic Acid/chemistry ; Oligosaccharides/chemistry ; Reticulocytes/drug effects
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  • 86
    Publication Date: 2013-01-19
    Description: A paper by Wearn et al. (Reports, 13 July 2012, p. 228) yields new insights on extinction debt. However, it leaves out the area dependence of the relaxation process. We show that this is not warranted on theoretical or observational grounds and that it may lead to erroneous conservation recommendations.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Halley, John M -- Iwasa, Yoh -- Vokou, Despoina -- New York, N.Y. -- Science. 2013 Jan 18;339(6117):271. doi: 10.1126/science.1231438.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Applications and Technology, University of Ioannina, Ioannina, Greece. jhalley@cc.uoi.gr〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23329033" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Conservation of Natural Resources ; *Ecosystem ; *Extinction, Biological ; *Trees ; *Vertebrates
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  • 87
    Publication Date: 2013-10-12
    Description: Genome-wide association studies (GWASs) have ascertained numerous trait-associated common genetic variants, frequently localized to regulatory DNA. We found that common genetic variation at BCL11A associated with fetal hemoglobin (HbF) level lies in noncoding sequences decorated by an erythroid enhancer chromatin signature. Fine-mapping uncovers a motif-disrupting common variant associated with reduced transcription factor (TF) binding, modestly diminished BCL11A expression, and elevated HbF. The surrounding sequences function in vivo as a developmental stage-specific, lineage-restricted enhancer. Genome engineering reveals the enhancer is required in erythroid but not B-lymphoid cells for BCL11A expression. These findings illustrate how GWASs may expose functional variants of modest impact within causal elements essential for appropriate gene expression. We propose the GWAS-marked BCL11A enhancer represents an attractive target for therapeutic genome engineering for the beta-hemoglobinopathies.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4018826/" 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/PMC4018826/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bauer, Daniel E -- Kamran, Sophia C -- Lessard, Samuel -- Xu, Jian -- Fujiwara, Yuko -- Lin, Carrie -- Shao, Zhen -- Canver, Matthew C -- Smith, Elenoe C -- Pinello, Luca -- Sabo, Peter J -- Vierstra, Jeff -- Voit, Richard A -- Yuan, Guo-Cheng -- Porteus, Matthew H -- Stamatoyannopoulos, John A -- Lettre, Guillaume -- Orkin, Stuart H -- 123382/Canadian Institutes of Health Research/Canada -- K08 DK093705/DK/NIDDK NIH HHS/ -- K08DK093705/DK/NIDDK NIH HHS/ -- P01HL032262/HL/NHLBI NIH HHS/ -- P30 DK049216/DK/NIDDK NIH HHS/ -- P30DK049216/DK/NIDDK NIH HHS/ -- R01 HG005085/HG/NHGRI NIH HHS/ -- R01 HL032259/HL/NHLBI NIH HHS/ -- R01HL032259/HL/NHLBI NIH HHS/ -- U54HG004594/HG/NHGRI NIH HHS/ -- U54HG007010/HG/NHGRI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2013 Oct 11;342(6155):253-7. doi: 10.1126/science.1242088.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Hematology/Oncology, Boston Children's Hospital, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24115442" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carrier Proteins/*genetics ; Cell Line, Tumor ; Cells, Cultured ; Chromatin/genetics/metabolism ; Chromatin Immunoprecipitation ; Chromosome Mapping ; *Enhancer Elements, Genetic ; Erythroid Cells/*metabolism ; Fetal Hemoglobin/*biosynthesis/genetics ; *Gene Expression Regulation ; Gene Targeting ; Genetic Engineering ; Genetic Variation ; Genome-Wide Association Study ; Hemoglobinopathies/*genetics/therapy ; Humans ; Mice ; Nuclear Proteins/*genetics ; Precursor Cells, B-Lymphoid/metabolism ; Transcription Factors/genetics/metabolism
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  • 88
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2013-12-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Belgrano, Andrea -- Fowler, Charles W -- New York, N.Y. -- Science. 2013 Dec 6;342(6163):1176-7. doi: 10.1126/science.1245490.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Swedish University of Agricultural Sciences, Department of Aquatic Resources, Institute of Marine Research, Turistgatan 5, SE-453 30 Lysekil, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24311669" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Body Size ; Conservation of Natural Resources ; *Ecosystem ; *Fisheries/methods ; Fishes/anatomy & histology/*genetics/growth & development ; Phenotype ; Population Dynamics
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  • 89
    Publication Date: 2013-10-05
    Description: Jet-lag symptoms arise from temporal misalignment between the internal circadian clock and external solar time. We found that circadian rhythms of behavior (locomotor activity), clock gene expression, and body temperature immediately reentrained to phase-shifted light-dark cycles in mice lacking vasopressin receptors V1a and V1b (V1a(-/-)V1b(-/-)). Nevertheless, the behavior of V1a(-/-)V1b(-/-) mice was still coupled to the internal clock, which oscillated normally under standard conditions. Experiments with suprachiasmatic nucleus (SCN) slices in culture suggested that interneuronal communication mediated by V1a and V1b confers on the SCN an intrinsic resistance to external perturbation. Pharmacological blockade of V1a and V1b in the SCN of wild-type mice resulted in accelerated recovery from jet lag, which highlights the potential of vasopressin signaling as a therapeutic target for management of circadian rhythm misalignment, such as jet lag and shift work.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yamaguchi, Yoshiaki -- Suzuki, Toru -- Mizoro, Yasutaka -- Kori, Hiroshi -- Okada, Kazuki -- Chen, Yulin -- Fustin, Jean-Michel -- Yamazaki, Fumiyoshi -- Mizuguchi, Naoki -- Zhang, Jing -- Dong, Xin -- Tsujimoto, Gozoh -- Okuno, Yasushi -- Doi, Masao -- Okamura, Hitoshi -- New York, N.Y. -- Science. 2013 Oct 4;342(6154):85-90. doi: 10.1126/science.1238599.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Systems Biology, Graduate School of Pharmaceutical Sciences, Kyoto University, Sakyo-ku, Kyoto 606-8501, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24092737" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antidiuretic Hormone Receptor Antagonists ; Body Temperature/genetics ; CLOCK Proteins/genetics ; Cell Communication/drug effects/genetics ; Cells, Cultured ; Circadian Rhythm/genetics ; Gene Expression Regulation ; Jet Lag Syndrome/*genetics/physiopathology ; Mice ; Mice, Knockout ; Motor Activity/genetics ; Receptors, Vasopressin/*genetics ; Suprachiasmatic Nucleus/physiopathology
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  • 90
    Publication Date: 2013-01-12
    Description: The choice between double-strand break (DSB) repair by either homology-directed repair (HDR) or nonhomologous end joining (NHEJ) is tightly regulated. Defects in this regulation can induce genome instability and cancer. 53BP1 is critical for the control of DSB repair, promoting NHEJ, and inhibiting the 5' end resection needed for HDR. Using dysfunctional telomeres and genome-wide DSBs, we identify Rif1 as the main factor used by 53BP1 to impair 5' end resection. Rif1 inhibits resection involving CtIP, BLM, and Exo1; limits accumulation of BRCA1/BARD1 complexes at sites of DNA damage; and defines one of the mechanisms by which 53BP1 causes chromosomal abnormalities in Brca1-deficient cells. These data establish Rif1 as an important contributor to the control of DSB repair by 53BP1.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3664841/" 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/PMC3664841/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zimmermann, Michal -- Lottersberger, Francisca -- Buonomo, Sara B -- Sfeir, Agnel -- de Lange, Titia -- R37 GM049046/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2013 Feb 8;339(6120):700-4. doi: 10.1126/science.1231573. Epub 2013 Jan 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory for Cell Biology and Genetics, Rockefeller University, New York, NY 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23306437" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; BRCA1 Protein/metabolism ; Cells, Cultured ; Chromosomal Proteins, Non-Histone/chemistry/genetics/*metabolism ; DNA/metabolism ; *DNA Breaks, Double-Stranded ; DNA End-Joining Repair ; *DNA Repair ; DNA-Binding Proteins/chemistry/genetics/*metabolism ; Mice ; Replication Protein A/metabolism ; Telomere/*metabolism ; Telomere-Binding Proteins/*metabolism ; Telomeric Repeat Binding Protein 2/genetics/metabolism
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  • 91
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 2013-12-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stokstad, Erik -- New York, N.Y. -- Science. 2013 Dec 6;342(6163):1166-7. doi: 10.1126/science.342.6163.1166.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24311659" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Behavior, Animal ; *Colubridae/physiology ; *Ecosystem ; Female ; Guam ; *Introduced Species ; Male ; Mice ; Pest Control ; Population Density
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  • 92
    Publication Date: 2013-01-12
    Description: DNA double-strand breaks (DSBs) represent a threat to the genome because they can lead to the loss of genetic information and chromosome rearrangements. The DNA repair protein p53 binding protein 1 (53BP1) protects the genome by limiting nucleolytic processing of DSBs by a mechanism that requires its phosphorylation, but whether 53BP1 does so directly is not known. Here, we identify Rap1-interacting factor 1 (Rif1) as an ATM (ataxia-telangiectasia mutated) phosphorylation-dependent interactor of 53BP1 and show that absence of Rif1 results in 5'-3' DNA-end resection in mice. Consistent with enhanced DNA resection, Rif1 deficiency impairs DNA repair in the G(1) and S phases of the cell cycle, interferes with class switch recombination in B lymphocytes, and leads to accumulation of chromosome DSBs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3815530/" 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/PMC3815530/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Di Virgilio, Michela -- Callen, Elsa -- Yamane, Arito -- Zhang, Wenzhu -- Jankovic, Mila -- Gitlin, Alexander D -- Feldhahn, Niklas -- Resch, Wolfgang -- Oliveira, Thiago Y -- Chait, Brian T -- Nussenzweig, Andre -- Casellas, Rafael -- Robbiani, Davide F -- Nussenzweig, Michel C -- AI037526/AI/NIAID NIH HHS/ -- GM007739/GM/NIGMS NIH HHS/ -- GM103314/GM/NIGMS NIH HHS/ -- R01 AI037526/AI/NIAID NIH HHS/ -- RR00862/RR/NCRR NIH HHS/ -- RR022220/RR/NCRR NIH HHS/ -- Howard Hughes Medical Institute/ -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2013 Feb 8;339(6120):711-5. doi: 10.1126/science.1230624. Epub 2013 Jan 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Immunology, The Rockefeller University, New York, NY 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23306439" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Ataxia Telangiectasia Mutated Proteins ; B-Lymphocytes/immunology/metabolism ; Cell Cycle Proteins/antagonists & inhibitors/metabolism ; Cells, Cultured ; Chromosomal Proteins, Non-Histone/*metabolism ; DNA/*metabolism ; *DNA Breaks, Double-Stranded ; DNA Repair ; DNA-Binding Proteins/antagonists & inhibitors/*metabolism ; G1 Phase ; G2 Phase ; Genomic Instability ; *Immunoglobulin Class Switching ; Mice ; Phosphorylation ; Protein-Serine-Threonine Kinases/antagonists & inhibitors/metabolism ; S Phase ; Telomere-Binding Proteins/*metabolism ; Tumor Suppressor Proteins/antagonists & inhibitors/metabolism
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  • 93
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 2013-02-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stokstad, Erik -- New York, N.Y. -- Science. 2013 Feb 8;339(6120):636-7. doi: 10.1126/science.339.6120.636.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23393236" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Ecosystem ; Extraction and Processing Industry/economics ; Gulf of Mexico ; Organizations, Nonprofit/economics ; Petroleum ; *Petroleum Pollution/adverse effects/analysis/economics ; Research ; *Research Support as Topic
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  • 94
    Publication Date: 2013-08-21
    Description: During the past 50 years, the human population has more than doubled and global agricultural production has similarly risen. However, the productive arable area has increased by just 10%; thus the increased use of pesticides has been a consequence of the demands of human population growth, and its impact has reached global significance. Although we often know a pesticide's mode of action in the target species, we still largely do not understand the full impact of unintended side effects on wildlife, particularly at higher levels of biological organization: populations, communities, and ecosystems. In these times of regional and global species declines, we are challenged with the task of causally linking knowledge about the molecular actions of pesticides to their possible interference with biological processes, in order to develop reliable predictions about the consequences of pesticide use, and misuse, in a rapidly changing world.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kohler, Heinz-R -- Triebskorn, Rita -- New York, N.Y. -- Science. 2013 Aug 16;341(6147):759-65. doi: 10.1126/science.1237591.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Animal Physiological Ecology, Institute of Evolution and Ecology, University of Tubingen, Tubingen, Germany. heinz-r.koehler@uni-tuebingen.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23950533" target="_blank"〉PubMed〈/a〉
    Keywords: Agriculture ; Animals ; *Animals, Wild ; Aquatic Organisms ; Biological Evolution ; *Ecosystem ; Ecotoxicology/methods/trends ; Food Chain ; Humans ; Pesticides/*toxicity ; Population Dynamics ; Research
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  • 95
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 2013-03-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hsieh, Jenny -- Schneider, Jay W -- New York, N.Y. -- Science. 2013 Mar 29;339(6127):1534-5. doi: 10.1126/science.1237576.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. jenny.hsieh@utsouthwestern.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23539589" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*cytology/*physiology ; Calcium Channels/physiology ; Cells, Cultured ; Humans ; Neural Stem Cells/*physiology ; *Neurogenesis ; Receptors, N-Methyl-D-Aspartate/physiology ; *Synaptic Transmission ; gamma-Aminobutyric Acid/physiology
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  • 96
    Publication Date: 2013-03-09
    Description: A molecule that treats multiple age-related diseases would have a major impact on global health and economics. The SIRT1 deacetylase has drawn attention in this regard as a target for drug design. Yet controversy exists around the mechanism of sirtuin-activating compounds (STACs). We found that specific hydrophobic motifs found in SIRT1 substrates such as PGC-1alpha and FOXO3a facilitate SIRT1 activation by STACs. A single amino acid in SIRT1, Glu(230), located in a structured N-terminal domain, was critical for activation by all previously reported STAC scaffolds and a new class of chemically distinct activators. In primary cells reconstituted with activation-defective SIRT1, the metabolic effects of STACs were blocked. Thus, SIRT1 can be directly activated through an allosteric mechanism common to chemically diverse STACs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3799917/" 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/PMC3799917/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hubbard, Basil P -- Gomes, Ana P -- Dai, Han -- Li, Jun -- Case, April W -- Considine, Thomas -- Riera, Thomas V -- Lee, Jessica E -- E, Sook Yen -- Lamming, Dudley W -- Pentelute, Bradley L -- Schuman, Eli R -- Stevens, Linda A -- Ling, Alvin J Y -- Armour, Sean M -- Michan, Shaday -- Zhao, Huizhen -- Jiang, Yong -- Sweitzer, Sharon M -- Blum, Charles A -- Disch, Jeremy S -- Ng, Pui Yee -- Howitz, Konrad T -- Rolo, Anabela P -- Hamuro, Yoshitomo -- Moss, Joel -- Perni, Robert B -- Ellis, James L -- Vlasuk, George P -- Sinclair, David A -- P01 AG027916/AG/NIA NIH HHS/ -- R01 AG019719/AG/NIA NIH HHS/ -- R01 AG028730/AG/NIA NIH HHS/ -- R37 AG028730/AG/NIA NIH HHS/ -- ZIA HL000659-20/Intramural NIH HHS/ -- New York, N.Y. -- Science. 2013 Mar 8;339(6124):1216-9. doi: 10.1126/science.1231097.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23471411" target="_blank"〉PubMed〈/a〉
    Keywords: Allosteric Regulation ; Amino Acid Motifs ; Amino Acid Sequence ; Amino Acid Substitution ; Animals ; Cells, Cultured ; Enzyme Activation ; Forkhead Transcription Factors/chemistry/genetics ; Glutamic Acid/chemistry/genetics ; Heterocyclic Compounds with 4 or More Rings/chemistry/pharmacology ; Humans ; Hydrophobic and Hydrophilic Interactions ; Mice ; Molecular Sequence Data ; Myoblasts/drug effects/enzymology ; Protein Structure, Tertiary ; Sirtuin 1/*chemistry/genetics/*metabolism ; Stilbenes/chemistry/*pharmacology ; Substrate Specificity
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  • 97
    Publication Date: 2013-02-09
    Description: Mass extinctions manifest in Earth's geologic record were turning points in biotic evolution. We present (40)Ar/(39)Ar data that establish synchrony between the Cretaceous-Paleogene boundary and associated mass extinctions with the Chicxulub bolide impact to within 32,000 years. Perturbation of the atmospheric carbon cycle at the boundary likely lasted less than 5000 years, exhibiting a recovery time scale two to three orders of magnitude shorter than that of the major ocean basins. Low-diversity mammalian fauna in the western Williston Basin persisted for as little as 20,000 years after the impact. The Chicxulub impact likely triggered a state shift of ecosystems already under near-critical stress.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Renne, Paul R -- Deino, Alan L -- Hilgen, Frederik J -- Kuiper, Klaudia F -- Mark, Darren F -- Mitchell, William S 3rd -- Morgan, Leah E -- Mundil, Roland -- Smit, Jan -- New York, N.Y. -- Science. 2013 Feb 8;339(6120):684-7. doi: 10.1126/science.1230492.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Berkeley Geochronology Center, 2455 Ridge Road, Berkeley, CA 94709, USA. prenne@bgc.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23393261" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Argon ; Chronology as Topic ; *Ecosystem ; *Extinction, Biological ; Geologic Sediments ; Mammals ; Mexico ; *Minor Planets ; Radioisotopes ; Radiometric Dating
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 98
    Publication Date: 2013-11-16
    Description: Bacterial invasion of host tissues triggers polymorphonuclear leukocytes to release DNA [neutrophil extracellular traps (NETs)], thereby immobilizing microbes for subsequent clearance by innate defenses including macrophage phagocytosis. We report here that Staphylococcus aureus escapes these defenses by converting NETs to deoxyadenosine, which triggers the caspase-3-mediated death of immune cells. Conversion of NETs to deoxyadenosine requires two enzymes, nuclease and adenosine synthase, that are secreted by S. aureus and are necessary for the exclusion of macrophages from staphylococcal abscesses. Thus, the pathogenesis of S. aureus infections has evolved to anticipate host defenses and to repurpose them for the destruction of the immune system.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4026193/" 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/PMC4026193/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thammavongsa, Vilasack -- Missiakas, Dominique M -- Schneewind, Olaf -- AI038897/AI/NIAID NIH HHS/ -- AI052474/AI/NIAID NIH HHS/ -- AI057153/AI/NIAID NIH HHS/ -- R01 AI038897/AI/NIAID NIH HHS/ -- R01 AI052474/AI/NIAID NIH HHS/ -- T32 AI007090/AI/NIAID NIH HHS/ -- U54 AI057153/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2013 Nov 15;342(6160):863-6. doi: 10.1126/science.1242255.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, University of Chicago, 920 East 58th Street, Chicago, IL 60637, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24233725" target="_blank"〉PubMed〈/a〉
    Keywords: Abscess/immunology/microbiology ; Animals ; Apoptosis/*immunology ; Cells, Cultured ; Cytotoxicity, Immunologic ; Deoxyadenosines/*metabolism ; Deoxyribonucleases/metabolism ; Host-Pathogen Interactions/*immunology ; Humans ; Macrophages/immunology/microbiology ; Mice, Inbred BALB C ; Neutrophils/*immunology/*microbiology ; Staphylococcal Infections/*immunology ; Staphylococcus aureus/enzymology/*pathogenicity
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    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 99
    Publication Date: 2013-07-23
    Description: Regulatory gene circuits with positive-feedback loops control stem cell differentiation, but several mechanisms can contribute to positive feedback. Here, we dissect feedback mechanisms through which the transcription factor PU.1 controls lymphoid and myeloid differentiation. Quantitative live-cell imaging revealed that developing B cells decrease PU.1 levels by reducing PU.1 transcription, whereas developing macrophages increase PU.1 levels by lengthening their cell cycles, which causes stable PU.1 accumulation. Exogenous PU.1 expression in progenitors increases endogenous PU.1 levels by inducing cell cycle lengthening, implying positive feedback between a regulatory factor and the cell cycle. Mathematical modeling showed that this cell cycle-coupled feedback architecture effectively stabilizes a slow-dividing differentiated state. These results show that cell cycle duration functions as an integral part of a positive autoregulatory circuit to control cell fate.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3913367/" 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/PMC3913367/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kueh, Hao Yuan -- Champhekar, Ameya -- Nutt, Stephen L -- Elowitz, Michael B -- Rothenberg, Ellen V -- R01 AI083514/AI/NIAID NIH HHS/ -- R01 CA090233/CA/NCI NIH HHS/ -- R01 CA90233/CA/NCI NIH HHS/ -- R33 HL089123/HL/NHLBI NIH HHS/ -- RC2 CA148278/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2013 Aug 9;341(6146):670-3. doi: 10.1126/science.1240831. Epub 2013 Jul 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biology, California Institute of Technology, Pasadena, CA, USA. kueh@caltech.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23868921" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Cycle/*genetics ; Cell Differentiation/*genetics ; Cells, Cultured ; Feedback, Physiological ; *Gene Expression Regulation ; *Gene Regulatory Networks ; Macrophages/cytology ; Mice ; Mice, Inbred Strains ; Myeloid Cells/*cytology ; Precursor Cells, B-Lymphoid/*cytology ; Proto-Oncogene Proteins/genetics/*physiology ; Trans-Activators/genetics/*physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 100
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2013-02-23
    Description: Shallow groundwater affects terrestrial ecosystems by sustaining river base-flow and root-zone soil water in the absence of rain, but little is known about the global patterns of water table depth and where it provides vital support for land ecosystems. We present global observations of water table depth compiled from government archives and literature, and fill in data gaps and infer patterns and processes using a groundwater model forced by modern climate, terrain, and sea level. Patterns in water table depth explain patterns in wetlands at the global scale and vegetation gradients at regional and local scales. Overall, shallow groundwater influences 22 to 32% of global land area, including ~15% as groundwater-fed surface water features and 7 to 17% with the water table or its capillary fringe within plant rooting depths.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fan, Y -- Li, H -- Miguez-Macho, G -- New York, N.Y. -- Science. 2013 Feb 22;339(6122):940-3. doi: 10.1126/science.1229881.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Earth and Planetary Sciences, Rutgers University, New Brunswick, NJ 08854, USA. yingfan@rci.rutgers.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23430651" target="_blank"〉PubMed〈/a〉
    Keywords: Climate ; *Ecosystem ; Geography ; *Groundwater ; Models, Theoretical ; Plants ; Rain ; Rivers ; Wetlands
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    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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