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  • 1
    Schriftenreihen ausleihbar
    Schriftenreihen ausleihbar
    Distribution of foraminifera in Chaleur Bay, Gulf of St. Lawrence (1978)
    Ottawa : Geological Survey of Canada
    Dazugehörige Bände
    Details Verfügbarkeit
    Signatur: SR 90.0008(77-30)
    In: Paper
    Materialart: Schriftenreihen ausleihbar
    Seiten: 55 S.
    ISBN: 0660015331
    Serie: Paper / Geological Survey of Canada 77-30
    Sprache: Englisch
    Standort: Kompaktmagazin unten
    Zweigbibliothek: GFZ Bibliothek
    Standort Signatur Erwartet Verfügbarkeit
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  • 2
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    Annotated bibliography of studies on the geology, geochemistry, mineral resources, and geophysical character of the early Mesozoic basins of the Eastern United States, 1880-1984 (1986)
    Washington, DC : United States Gov. Print. Off.
    Dazugehörige Bände
    Details Verfügbarkeit
    Signatur: SR 90.0001(1688)
    In: U.S. Geological Survey bulletin
    Materialart: Schriftenreihen ausleihbar
    Seiten: III, 492 S.
    Serie: U.S. Geological Survey bulletin 1688
    Sprache: Englisch
    Standort: Kompaktmagazin unten
    Zweigbibliothek: GFZ Bibliothek
    Standort Signatur Erwartet Verfügbarkeit
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  • 3
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    Composition of isolated synaptic boutons reveals the amounts of vesicle trafficking proteins (2014)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2014-05-31
    Beschreibung: Synaptic vesicle recycling has long served as a model for the general mechanisms of cellular trafficking. We used an integrative approach, combining quantitative immunoblotting and mass spectrometry to determine protein numbers; electron microscopy to measure organelle numbers, sizes, and positions; and super-resolution fluorescence microscopy to localize the proteins. Using these data, we generated a three-dimensional model of an "average" synapse, displaying 300,000 proteins in atomic detail. The copy numbers of proteins involved in the same step of synaptic vesicle recycling correlated closely. In contrast, copy numbers varied over more than three orders of magnitude between steps, from about 150 copies for the endosomal fusion proteins to more than 20,000 for the exocytotic ones.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wilhelm, Benjamin G -- Mandad, Sunit -- Truckenbrodt, Sven -- Krohnert, Katharina -- Schafer, Christina -- Rammner, Burkhard -- Koo, Seong Joo -- Classen, Gala A -- Krauss, Michael -- Haucke, Volker -- Urlaub, Henning -- Rizzoli, Silvio O -- New York, N.Y. -- Science. 2014 May 30;344(6187):1023-8. doi: 10.1126/science.1252884.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuro- and Sensory Physiology, University of Gottingen Medical Center, European Neuroscience Institute, Cluster of Excellence Nanoscale Microscopy and Molecular Physiology of the Brain, Gottingen, Germany. International Max Planck Research School Neurosciences, 37077 Gottingen, Germany. ; Bioanalytical Mass Spectrometry Group, Max-Planck-Institute for Biophysical Chemistry, 37077 Gottingen, Germany. ; Department of Neuro- and Sensory Physiology, University of Gottingen Medical Center, European Neuroscience Institute, Cluster of Excellence Nanoscale Microscopy and Molecular Physiology of the Brain, Gottingen, Germany. International Max Planck Research School Molecular Biology, 37077 Gottingen, Germany. ; Department of Neuro- and Sensory Physiology, University of Gottingen Medical Center, European Neuroscience Institute, Cluster of Excellence Nanoscale Microscopy and Molecular Physiology of the Brain, Gottingen, Germany. ; Leibniz Institut fur Molekulare Pharmakologie, Department of Molecular Pharmacology and Cell Biology, Robert-Rossle-Strasse 10, 13125 Berlin, Germany. ; Bioanalytical Mass Spectrometry Group, Max-Planck-Institute for Biophysical Chemistry, 37077 Gottingen, Germany. Bioanalytics, Department of Clinical Chemistry, University Medical Center Gottingen, 37075 Gottingen, Germany. ; Department of Neuro- and Sensory Physiology, University of Gottingen Medical Center, European Neuroscience Institute, Cluster of Excellence Nanoscale Microscopy and Molecular Physiology of the Brain, Gottingen, Germany. srizzol@gwdg.de.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24876496" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Brain/*metabolism/ultrastructure ; Exocytosis ; Imaging, Three-Dimensional ; Immunoblotting/methods ; Mass Spectrometry/methods ; Microscopy, Electron/methods ; Models, Neurological ; Presynaptic Terminals/chemistry/*metabolism/ultrastructure ; Protein Transport ; Rats ; Rats, Wistar ; Synaptic Vesicles/chemistry/*metabolism ; Synaptosomes/chemistry/*metabolism/ultrastructure ; Vesicular Transport Proteins/analysis/*metabolism
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
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  • 4
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    Patterns and rates of exonic de novo mutations in autism spectrum disorders (2012)
    Nature Publishing Group (NPG)
    Details
    Publikationsdatum: 2012-04-13
    Beschreibung: Autism spectrum disorders (ASD) are believed to have genetic and environmental origins, yet in only a modest fraction of individuals can specific causes be identified. To identify further genetic risk factors, here we assess the role of de novo mutations in ASD by sequencing the exomes of ASD cases and their parents (n = 175 trios). Fewer than half of the cases (46.3%) carry a missense or nonsense de novo variant, and the overall rate of mutation is only modestly higher than the expected rate. In contrast, the proteins encoded by genes that harboured de novo missense or nonsense mutations showed a higher degree of connectivity among themselves and to previous ASD genes as indexed by protein-protein interaction screens. The small increase in the rate of de novo events, when taken together with the protein interaction results, are consistent with an important but limited role for de novo point mutations in ASD, similar to that documented for de novo copy number variants. Genetic models incorporating these data indicate that most of the observed de novo events are unconnected to ASD; those that do confer risk are distributed across many genes and are incompletely penetrant (that is, not necessarily sufficient for disease). Our results support polygenic models in which spontaneous coding mutations in any of a large number of genes increases risk by 5- to 20-fold. Despite the challenge posed by such models, results from de novo events and a large parallel case-control study provide strong evidence in favour of CHD8 and KATNAL2 as genuine autism risk factors.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3613847/" 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/PMC3613847/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Neale, Benjamin M -- Kou, Yan -- Liu, Li -- Ma'ayan, Avi -- Samocha, Kaitlin E -- Sabo, Aniko -- Lin, Chiao-Feng -- Stevens, Christine -- Wang, Li-San -- Makarov, Vladimir -- Polak, Paz -- Yoon, Seungtai -- Maguire, Jared -- Crawford, Emily L -- Campbell, Nicholas G -- Geller, Evan T -- Valladares, Otto -- Schafer, Chad -- Liu, Han -- Zhao, Tuo -- Cai, Guiqing -- Lihm, Jayon -- Dannenfelser, Ruth -- Jabado, Omar -- Peralta, Zuleyma -- Nagaswamy, Uma -- Muzny, Donna -- Reid, Jeffrey G -- Newsham, Irene -- Wu, Yuanqing -- Lewis, Lora -- Han, Yi -- Voight, Benjamin F -- Lim, Elaine -- Rossin, Elizabeth -- Kirby, Andrew -- Flannick, Jason -- Fromer, Menachem -- Shakir, Khalid -- Fennell, Tim -- Garimella, Kiran -- Banks, Eric -- Poplin, Ryan -- Gabriel, Stacey -- DePristo, Mark -- Wimbish, Jack R -- Boone, Braden E -- Levy, Shawn E -- Betancur, Catalina -- Sunyaev, Shamil -- Boerwinkle, Eric -- Buxbaum, Joseph D -- Cook, Edwin H Jr -- Devlin, Bernie -- Gibbs, Richard A -- Roeder, Kathryn -- Schellenberg, Gerard D -- Sutcliffe, James S -- Daly, Mark J -- KL2 RR024977/RR/NCRR NIH HHS/ -- P30 HD015052/HD/NICHD NIH HHS/ -- P50 GM071558/GM/NIGMS NIH HHS/ -- P50 HD055751/HD/NICHD NIH HHS/ -- R01 MH057881/MH/NIMH NIH HHS/ -- R01 MH061009/MH/NIMH NIH HHS/ -- R01 MH089004/MH/NIMH NIH HHS/ -- R01 MH089025/MH/NIMH NIH HHS/ -- R01 MH089175/MH/NIMH NIH HHS/ -- R01 MH089208/MH/NIMH NIH HHS/ -- R01 MH089482/MH/NIMH NIH HHS/ -- R01MH084676/MH/NIMH NIH HHS/ -- R01MH089175/MH/NIMH NIH HHS/ -- R01MH089208/MH/NIMH NIH HHS/ -- T32 GM007753/GM/NIGMS NIH HHS/ -- TL1 RR024978/RR/NCRR NIH HHS/ -- U54 HG003067/HG/NHGRI NIH HHS/ -- U54 HG003273/HG/NHGRI NIH HHS/ -- UL1 RR024975/RR/NCRR NIH HHS/ -- England -- Nature. 2012 Apr 4;485(7397):242-5. doi: 10.1038/nature11011.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Analytic and Translational Genetics Unit, Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22495311" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Autistic Disorder/*genetics ; Case-Control Studies ; DNA-Binding Proteins/*genetics ; Exome/genetics ; Exons/*genetics ; Family Health ; Genetic Predisposition to Disease/*genetics ; Humans ; Models, Genetic ; Multifactorial Inheritance/genetics ; Mutation/*genetics ; Phenotype ; Poisson Distribution ; Protein Interaction Maps ; Transcription Factors/*genetics
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von Nature Publishing Group (NPG)
    Standort Signatur Erwartet Verfügbarkeit
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  • 5
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    Synaptic, transcriptional and chromatin genes disrupted in autism (2014)
    Nature Publishing Group (NPG)
    Details
    Publikationsdatum: 2014-11-05
    Beschreibung: The genetic architecture of autism spectrum disorder involves the interplay of common and rare variants and their impact on hundreds of genes. Using exome sequencing, here we show that analysis of rare coding variation in 3,871 autism cases and 9,937 ancestry-matched or parental controls implicates 22 autosomal genes at a false discovery rate (FDR) 〈 0.05, plus a set of 107 autosomal genes strongly enriched for those likely to affect risk (FDR 〈 0.30). These 107 genes, which show unusual evolutionary constraint against mutations, incur de novo loss-of-function mutations in over 5% of autistic subjects. Many of the genes implicated encode proteins for synaptic formation, transcriptional regulation and chromatin-remodelling pathways. These include voltage-gated ion channels regulating the propagation of action potentials, pacemaking and excitability-transcription coupling, as well as histone-modifying enzymes and chromatin remodellers-most prominently those that mediate post-translational lysine methylation/demethylation modifications of histones.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4402723/" 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/PMC4402723/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉De Rubeis, Silvia -- He, Xin -- Goldberg, Arthur P -- Poultney, Christopher S -- Samocha, Kaitlin -- Cicek, A Erucment -- Kou, Yan -- Liu, Li -- Fromer, Menachem -- Walker, Susan -- Singh, Tarinder -- Klei, Lambertus -- Kosmicki, Jack -- Shih-Chen, Fu -- Aleksic, Branko -- Biscaldi, Monica -- Bolton, Patrick F -- Brownfeld, Jessica M -- Cai, Jinlu -- Campbell, Nicholas G -- Carracedo, Angel -- Chahrour, Maria H -- Chiocchetti, Andreas G -- Coon, Hilary -- Crawford, Emily L -- Curran, Sarah R -- Dawson, Geraldine -- Duketis, Eftichia -- Fernandez, Bridget A -- Gallagher, Louise -- Geller, Evan -- Guter, Stephen J -- Hill, R Sean -- Ionita-Laza, Juliana -- Jimenz Gonzalez, Patricia -- Kilpinen, Helena -- Klauck, Sabine M -- Kolevzon, Alexander -- Lee, Irene -- Lei, Irene -- Lei, Jing -- Lehtimaki, Terho -- Lin, Chiao-Feng -- Ma'ayan, Avi -- Marshall, Christian R -- McInnes, Alison L -- Neale, Benjamin -- Owen, Michael J -- Ozaki, Noriio -- Parellada, Mara -- Parr, Jeremy R -- Purcell, Shaun -- Puura, Kaija -- Rajagopalan, Deepthi -- Rehnstrom, Karola -- Reichenberg, Abraham -- Sabo, Aniko -- Sachse, Michael -- Sanders, Stephan J -- Schafer, Chad -- Schulte-Ruther, Martin -- Skuse, David -- Stevens, Christine -- Szatmari, Peter -- Tammimies, Kristiina -- Valladares, Otto -- Voran, Annette -- Li-San, Wang -- Weiss, Lauren A -- Willsey, A Jeremy -- Yu, Timothy W -- Yuen, Ryan K C -- DDD Study -- Homozygosity Mapping Collaborative for Autism -- UK10K Consortium -- Cook, Edwin H -- Freitag, Christine M -- Gill, Michael -- Hultman, Christina M -- Lehner, Thomas -- Palotie, Aaarno -- Schellenberg, Gerard D -- Sklar, Pamela -- State, Matthew W -- Sutcliffe, James S -- Walsh, Christiopher A -- Scherer, Stephen W -- Zwick, Michael E -- Barett, Jeffrey C -- Cutler, David J -- Roeder, Kathryn -- Devlin, Bernie -- Daly, Mark J -- Buxbaum, Joseph D -- 5UL1 RR024975/RR/NCRR NIH HHS/ -- MH077139/MH/NIMH NIH HHS/ -- MH089482/MH/NIMH NIH HHS/ -- MH095034/MH/NIMH NIH HHS/ -- P30 HD15052/HD/NICHD NIH HHS/ -- P50 HD055751/HD/NICHD NIH HHS/ -- R01 MH061009/MH/NIMH NIH HHS/ -- R01 MH083565/MH/NIMH NIH HHS/ -- R01 MH089482/MH/NIMH NIH HHS/ -- R01 MH094400/MH/NIMH NIH HHS/ -- R01 MH095797/MH/NIMH NIH HHS/ -- R01 MH097849/MH/NIMH NIH HHS/ -- R01 MH100229/MH/NIMH NIH HHS/ -- R01 NS073601/NS/NINDS NIH HHS/ -- R01MH083565/MH/NIMH NIH HHS/ -- R01MH089208/MH/NIMH NIH HHS/ -- R37 MH057881/MH/NIMH NIH HHS/ -- RC2MH089952/MH/NIMH NIH HHS/ -- T32 HG002295/HG/NHGRI NIH HHS/ -- U01 MH100209/MH/NIMH NIH HHS/ -- U01 MH100229/MH/NIMH NIH HHS/ -- U01 MH100233/MH/NIMH NIH HHS/ -- U01 MH100239/MH/NIMH NIH HHS/ -- U01MH100209/MH/NIMH NIH HHS/ -- U01MH100229/MH/NIMH NIH HHS/ -- U01MH100233/MH/NIMH NIH HHS/ -- U01MH100239/MH/NIMH NIH HHS/ -- U54 HG003067/HG/NHGRI NIH HHS/ -- UL1TR000445/TR/NCATS NIH HHS/ -- WT091310/Wellcome Trust/United Kingdom -- WT098051/Wellcome Trust/United Kingdom -- Howard Hughes Medical Institute/ -- England -- Nature. 2014 Nov 13;515(7526):209-15. doi: 10.1038/nature13772. Epub 2014 Oct 29.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25363760" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acid Sequence ; Child Development Disorders, Pervasive/*genetics/pathology ; Chromatin/*genetics/metabolism ; Chromatin Assembly and Disassembly ; Exome/genetics ; Female ; Genetic Predisposition to Disease/*genetics ; Germ-Line Mutation/genetics ; Humans ; Male ; Molecular Sequence Data ; Mutation/*genetics ; Mutation, Missense/genetics ; Nerve Net/metabolism ; Odds Ratio ; Synapses/*metabolism ; Transcription, Genetic/*genetics
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von Nature Publishing Group (NPG)
    Standort Signatur Erwartet Verfügbarkeit
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  • 6
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    Nephron progenitor compartments [Developmental Biology] (2013)
    National Academy of Sciences
    Details
    Publikationsdatum: 2013-03-20
    Beschreibung: Embryonic nephron progenitor cells are segregated in molecularly distinct compartments of unknown function. Our study reveals an integral role for bone morphogenetic protein-SMAD in promoting transition of progenitors from the primitive Cbp/p300-interacting transactivator 1 expressing (CITED1+) compartment to the uniquely sine oculis-related homeobox 2 expressing (SIX2-only) compartment where they become...
    Print ISSN: 0027-8424
    Digitale ISSN: 1091-6490
    Thema: Biologie , Medizin , Allgemeine Naturwissenschaft
    Publiziert von National Academy of Sciences
    Standort Signatur Erwartet Verfügbarkeit
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  • 7
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    Allelic Variation in the Toll-Like Receptor Adaptor Protein Ticam2 Contributes to SARS-Coronavirus Pathogenesis in Mice (2017)
    Genetics Society of America (GSA)
    Details
    Publikationsdatum: 2017-06-08
    Beschreibung: Host genetic variation is known to contribute to differential pathogenesis following infection. Mouse models allow direct assessment of host genetic factors responsible for susceptibility to Severe Acute Respiratory Syndrome coronavirus (SARS-CoV). Based on an assessment of early stage lines from the Collaborative Cross mouse multi-parent population, we identified two lines showing highly divergent susceptibilities to SARS-CoV: the resistant CC003/Unc and the susceptible CC053/Unc. We generated 264 F2 mice between these strains, and infected them with SARS-CoV. Weight loss, pulmonary hemorrhage, and viral load were all highly correlated disease phenotypes. We identified a quantitative trait locus of major effect on chromosome 18 (27.1–58.6 Mb) which affected weight loss, viral titer and hemorrhage. Additionally, each of these three phenotypes had distinct quantitative trait loci [Chr 9 (weight loss), Chrs 7 and 12 (virus titer), and Chr 15 (hemorrhage)]. We identified Ticam2 , an adaptor protein in the TLR signaling pathways, as a candidate driving differential disease at the Chr 18 locus. Ticam2 –/– mice were highly susceptible to SARS-CoV infection, exhibiting increased weight loss and more pulmonary hemorrhage than control mice. These results indicate a critical role for Ticam2 in SARS-CoV disease, and highlight the importance of host genetic variation in disease responses.
    Digitale ISSN: 2160-1836
    Thema: Biologie
    Publiziert von Genetics Society of America (GSA)
    Standort Signatur Erwartet Verfügbarkeit
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  • 8
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    Tin Clathrates with the Type II Structure (2013)
    American Chemical Society (ACS)
    Details
    Publikationsdatum: 2013-01-24
    Beschreibung: Journal of the American Chemical Society DOI: 10.1021/ja3112934
    Print ISSN: 0002-7863
    Digitale ISSN: 1520-5126
    Thema: Chemie und Pharmazie
    Publiziert von American Chemical Society (ACS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 9
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    Blood vessel generation from human iPS cells [Engineering] (2013)
    National Academy of Sciences
    Details
    Publikationsdatum: 2013-07-31
    Beschreibung: Efficient generation of competent vasculogenic cells is a critical challenge of human induced pluripotent stem (hiPS) cell-based regenerative medicine. Biologically relevant systems to assess functionality of the engineered vessels in vivo are equally important for such development. Here, we report a unique approach for the derivation of endothelial precursor cells...
    Print ISSN: 0027-8424
    Digitale ISSN: 1091-6490
    Thema: Biologie , Medizin , Allgemeine Naturwissenschaft
    Publiziert von National Academy of Sciences
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  • 10
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    Detergent-free isolation of KcsA in nanodiscs [Biophysics and Computational Biology] (2014)
    National Academy of Sciences
    Details
    Publikationsdatum: 2014-12-31
    Beschreibung: A major obstacle in the study of membrane proteins is their solubilization in a stable and active conformation when using detergents. Here, we explored a detergent-free approach to isolating the tetrameric potassium channel KcsA directly from the membrane of Escherichia coli, using a styrene-maleic acid copolymer. This polymer self-inserts into...
    Print ISSN: 0027-8424
    Digitale ISSN: 1091-6490
    Thema: Biologie , Medizin , Allgemeine Naturwissenschaft
    Publiziert von National Academy of Sciences
    Standort Signatur Erwartet Verfügbarkeit
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