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  • 1
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    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 1997-06-27
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Taubes, G -- New York, N.Y. -- Science. 1997 Jun 27;276(5321):1993.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9221506" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; DNA, Recombinant ; Diagnostic Imaging/*methods ; *Gene Expression Regulation ; Genetic Therapy ; HIV/physiology ; HIV Infections/virology ; Luciferases/*genetics ; Luminescence ; Mice ; Mice, Transgenic ; Salmonella Infections, Animal/drug therapy/microbiology ; Virus Replication
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 2
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    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 1997-03-07
    Beschreibung: The DED1 gene, which encodes a putative RNA helicase, has been implicated in nuclear pre-messenger RNA splicing in the yeast Saccharomyces cerevisiae. It is shown here by genetic and biochemical analysis that translation, rather than splicing, is severely impaired in two newly isolated ded1 conditional mutants. Preliminary evidence suggests that the protein Ded1p may be required for the initiation step of translation, as is the distinct DEAD-box protein, eukaryotic initiation factor 4A (eIF4A). The DED1 gene could be functionally replaced by a mouse homolog, PL10, which suggests that the function of Ded1p in translation is evolutionarily conserved.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chuang, R Y -- Weaver, P L -- Liu, Z -- Chang, T H -- GM48752/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1997 Mar 7;275(5305):1468-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular, Cellular, and Developmental Biology Program, Ohio State University, Columbus, OH 43210, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9045610" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Cytoplasm/metabolism ; DEAD-box RNA Helicases ; Eukaryotic Initiation Factor-4A ; Genes, Fungal ; Mice ; Mutation ; Peptide Initiation Factors/genetics/metabolism ; Phenotype ; *Protein Biosynthesis ; RNA Helicases ; RNA Nucleotidyltransferases/genetics/*metabolism ; RNA Splicing ; RNA, Fungal/*genetics ; RNA, Messenger/*genetics ; Recombinant Fusion Proteins/metabolism ; Saccharomyces cerevisiae/enzymology/*genetics ; *Saccharomyces cerevisiae Proteins
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 3
    Publikationsdatum: 1997-07-04
    Beschreibung: Angiogenesis is thought to depend on a precise balance of positive and negative regulation. Angiopoietin-1 (Ang1) is an angiogenic factor that signals through the endothelial cell-specific Tie2 receptor tyrosine kinase. Like vascular endothelial growth factor, Ang1 is essential for normal vascular development in the mouse. An Ang1 relative, termed angiopoietin-2 (Ang2), was identified by homology screening and shown to be a naturally occurring antagonist for Ang1 and Tie2. Transgenic overexpression of Ang2 disrupts blood vessel formation in the mouse embryo. In adult mice and humans, Ang2 is expressed only at sites of vascular remodeling. Natural antagonists for vertebrate receptor tyrosine kinases are atypical; thus, the discovery of a negative regulator acting on Tie2 emphasizes the need for exquisite regulation of this angiogenic receptor system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Maisonpierre, P C -- Suri, C -- Jones, P F -- Bartunkova, S -- Wiegand, S J -- Radziejewski, C -- Compton, D -- McClain, J -- Aldrich, T H -- Papadopoulos, N -- Daly, T J -- Davis, S -- Sato, T N -- Yancopoulos, G D -- New York, N.Y. -- Science. 1997 Jul 4;277(5322):55-60.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Regeneron Pharmaceuticals Inc., 777 Old Saw Mill River Road, Tarrytown, NY 10591, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9204896" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acid Sequence ; Angiopoietin-1 ; Angiopoietin-2 ; Animals ; Blood Vessels/embryology/*metabolism ; Cells, Cultured ; Cloning, Molecular ; Embryo, Mammalian/metabolism ; Endothelial Growth Factors/genetics/metabolism ; Endothelium, Vascular/*cytology/metabolism ; Female ; Humans ; Ligands ; Lymphokines/genetics/metabolism ; Membrane Glycoproteins/antagonists & inhibitors/metabolism ; Mice ; Mice, Transgenic ; Molecular Sequence Data ; *Neovascularization, Physiologic ; Phosphorylation ; Proteins/chemistry/*metabolism ; Rats ; Rats, Sprague-Dawley ; Receptor Protein-Tyrosine Kinases/*antagonists & inhibitors/metabolism ; Receptor, TIE-2 ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Vascular Endothelial Growth Factor A ; Vascular Endothelial Growth Factors
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 4
    Publikationsdatum: 1997-09-26
    Beschreibung: To determine which proteinases are responsible for the lung destruction characteristic of pulmonary emphysema, macrophage elastase-deficient (MME-/-) mice were subjected to cigarette smoke. In contrast to wild-type mice, MME-/- mice did not have increased numbers of macrophages in their lungs and did not develop emphysema in response to long-term exposure to cigarette smoke. Smoke-exposed MME-/- mice that received monthly intratracheal instillations of monocyte chemoattractant protein-1 showed accumulation of alveolar macrophages but did not develop air space enlargement. Thus, macrophage elastase is probably sufficient for the development of emphysema that results from chronic inhalation of cigarette smoke.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hautamaki, R D -- Kobayashi, D K -- Senior, R M -- Shapiro, S D -- New York, N.Y. -- Science. 1997 Sep 26;277(5334):2002-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Internal Medicine, Washington University School of Medicine at Barnes-Jewish Hospital, St. Louis, MO 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9302297" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Cell Count ; Chemokine CCL2/pharmacology ; Gene Targeting ; Lung/pathology ; Macrophages, Alveolar/*enzymology/physiology ; Matrix Metalloproteinase 12 ; Metalloendopeptidases/genetics/*metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Inbred Strains ; Neutrophils ; Plants, Toxic ; Pulmonary Alveoli/pathology ; Pulmonary Emphysema/enzymology/*etiology/pathology ; Smoke/adverse effects ; Smoking/*adverse effects ; Tobacco
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 5
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    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 1997-09-26
    Beschreibung: A selection strategy was devised to identify bacterial genes preferentially expressed when a bacterium associates with its host cell. Fourteen Salmonella typhimurium genes, which were under the control of at least four independent regulatory circuits, were identified to be selectively induced in host macrophages. Four genes encode virulence factors, including a component of a type III secretory apparatus. This selection methodology should be generally applicable to the identification of genes from pathogenic organisms that are induced upon association with host cells or tissues.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Valdivia, R H -- Falkow, S -- AI26195/AI/NIAID NIH HHS/ -- DK38707/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1997 Sep 26;277(5334):2007-11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA. valdivia@cmgm.stanford.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9302299" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Bacterial Proteins/genetics ; Cell Line ; Cloning, Molecular ; Female ; Flow Cytometry ; Fluorescence ; *Gene Expression Regulation, Bacterial ; Green Fluorescent Proteins ; HeLa Cells ; Humans ; Luminescent Proteins/genetics ; Macrophages/*microbiology ; Mice ; Mice, Inbred BALB C ; Microscopy, Fluorescence ; Molecular Sequence Data ; Open Reading Frames ; Promoter Regions, Genetic ; Recombinant Fusion Proteins ; Salmonella Infections, Animal/microbiology ; Salmonella typhimurium/*genetics/isolation & purification/*pathogenicity ; Spleen/microbiology ; Transcription Factors/genetics ; Virulence/genetics
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 6
    Publikationsdatum: 1997-01-17
    Beschreibung: Familial combined hyperlipidemia (FCHL) is a common inherited lipid disorder, affecting 1 to 2 percent of the population in Westernized societies. Individuals with FCHL have large quantities of very low density lipoprotein (VLDL) and low density lipoprotein (LDL) and develop premature coronary heart disease. A mouse model displaying some of the features of FCHL was created by crossing mice carrying the human apolipoprotein C-III (APOC3) transgene with mice deficient in the LDL receptor. A synergistic interaction between the apolipoprotein C-III and the LDL receptor defects produced large quantities of VLDL and LDL and enhanced the development of atherosclerosis. This mouse model may provide clues to the origin of human FCHL.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Masucci-Magoulas, L -- Goldberg, I J -- Bisgaier, C L -- Serajuddin, H -- Francone, O L -- Breslow, J L -- Tall, A R -- HL 21006/HL/NHLBI NIH HHS/ -- HL 54591/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1997 Jan 17;275(5298):391-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Columbia University, 630 West 168 Street, New York, NY 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8994037" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Apolipoprotein C-III ; Apolipoproteins B/blood ; Apolipoproteins C/*genetics ; Apolipoproteins E/blood ; Arteriosclerosis/etiology ; Carrier Proteins/genetics ; Cholesterol/blood ; Cholesterol Ester Transfer Proteins ; Cholesterol, HDL/blood ; Cholesterol, LDL/blood ; Cholesterol, VLDL/blood ; Diet ; *Disease Models, Animal ; Disease Susceptibility ; Female ; *Glycoproteins ; Humans ; *Hyperlipidemia, Familial Combined/blood/genetics ; Hyperlipoproteinemia Type IV/genetics ; Lipoproteins/blood ; Lipoproteins, VLDL/blood ; Male ; Mice ; Mice, Inbred C57BL ; *Mice, Transgenic ; Receptors, LDL/*genetics/metabolism ; Transgenes ; Triglycerides/blood
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 7
    Publikationsdatum: 1997-02-28
    Beschreibung: The small guanosine triphosphatase (GTPase) Rho is implicated in the formation of stress fibers and focal adhesions in fibroblasts stimulated by extracellular signals such as lysophosphatidic acid (LPA). Rho-kinase is activated by Rho and may mediate some biological effects of Rho. Microinjection of the catalytic domain of Rho-kinase into serum-starved Swiss 3T3 cells induced the formation of stress fibers and focal adhesions, whereas microinjection of the inactive catalytic domain, the Rho-binding domain, or the pleckstrin-homology domain inhibited the LPA-induced formation of stress fibers and focal adhesions. Thus, Rho-kinase appears to mediate signals from Rho and to induce the formation of stress fibers and focal adhesions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Amano, M -- Chihara, K -- Kimura, K -- Fukata, Y -- Nakamura, N -- Matsuura, Y -- Kaibuchi, K -- New York, N.Y. -- Science. 1997 Feb 28;275(5304):1308-11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Signal Transduction, Nara Institute of Science and Technology, Ikoma 630-01, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9036856" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): 3T3 Cells ; Actins/*metabolism ; Adenosine Triphosphate/metabolism ; Animals ; Binding Sites ; *Cell Adhesion ; Cell Line ; DNA, Complementary/genetics ; Enzyme Inhibitors/pharmacology ; GTP Phosphohydrolases/metabolism ; Intracellular Signaling Peptides and Proteins ; Lysophospholipids/pharmacology ; Mice ; Mutation ; Protein-Serine-Threonine Kinases/antagonists & inhibitors/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Staurosporine/pharmacology ; rho-Associated Kinases
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 8
    Publikationsdatum: 1997-02-14
    Beschreibung: For the past decade the immune system has been exploited as a rich source of de novo catalysts. Catalytic antibodies have been shown to have chemoselectivity, enantioselectivity, large rate accelerations, and even an ability to reroute chemical reactions. In many instances catalysts have been made for reactions for which there are no known natural or man-made enzymes. Yet, the full power of this combinatorial system can only be exploited if there was a system that allows for the direct selection of a particular function. A method that allows for the direct chemical selection for catalysis from antibody libraries was so devised, whereby the positive aspects of hybridoma technology were preserved and re-formatted in the filamentous phage system to allow direct selection of catalysis. This methodology is based on a purely chemical selection process, making it more general than biologically based selection systems because it is not limited to reaction products that perturb cellular machinery.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Janda, K D -- Lo, L C -- Lo, C H -- Sim, M M -- Wang, R -- Wong, C H -- Lerner, R A -- GM-43858/GM/NIGMS NIH HHS/ -- GM-44154/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1997 Feb 14;275(5302):945-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Scripps Research Institute, Department of Chemistry, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9020070" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; *Antibodies, Catalytic/genetics/metabolism ; Catalysis ; Cloning, Molecular ; Coliphages ; Dithiothreitol ; Enzyme-Linked Immunosorbent Assay ; Escherichia coli/genetics/metabolism ; Galactosides/metabolism ; Haptens ; Hybridomas ; Immunoglobulin Fab Fragments/genetics/metabolism ; Indoles/metabolism ; Isopropyl Thiogalactoside/metabolism ; Mice ; Nitrophenylgalactosides/metabolism ; *Peptide Library ; Polymerase Chain Reaction ; Serum Albumin, Bovine ; Transformation, Bacterial ; beta-Galactosidase/metabolism
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 9
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    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 1997-03-28
    Beschreibung: Neuroendocrine hormones of the hypothalamus-pituitary-thyroid axis can exert positive or negative immunoregulatory effects on intestinal lymphocytes. Small intestine epithelial cells were found to express receptors for thyrotropin-releasing hormone (TRH) and to be a primary source of intestine-derived thyroid-stimulating hormone (TSH). The gene for the TSH receptor (TSH-R) was expressed in intestinal T cells but not in epithelial cells, which suggested a hormone-mediated link between lymphoid and nonhematopoietic components of the intestine. Because mice with congenitally mutant TSH-R (hyt/hyt mice) have a selectively impaired intestinal T cell repertoire, TSH may be a key immunoregulatory mediator in the intestine.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, J -- Whetsell, M -- Klein, J R -- DK35566/DK/NIDDK NIH HHS/ -- R01 DK035566/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1997 Mar 28;275(5308):1937-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Science and Mervin Bovaird Center for Studies in Molecular Biology and Biotechnology, University of Tulsa, Tulsa, OK 74104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9072972" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Homeostasis ; *Immunity, Mucosal ; Intestinal Mucosa/cytology/*immunology/metabolism ; Intestine, Small/cytology/immunology/metabolism ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Nude ; Point Mutation ; Receptors, Thyrotropin/genetics/metabolism ; Receptors, Thyrotropin-Releasing Hormone/genetics/metabolism ; T-Lymphocyte Subsets/immunology/metabolism ; T-Lymphocytes/*immunology/metabolism ; Thyrotropin/genetics/*metabolism ; Thyrotropin-Releasing Hormone/*metabolism/pharmacology
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 10
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    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 1997-10-24
    Beschreibung: Genetically distinct populations are an important component of biodiversity. This work estimates the number of populations per area of a sample of species from literature on population differentiation and the average range area of a species from a sample of distribution maps. This yields an estimate of about 220 populations per species, or 1.1 to 6.6 billion populations globally. Assuming that population extinction is a linear function of habitat loss, approximately 1800 populations per hour (16 million annually) are being destroyed in tropical forests alone.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hughes, J B -- Daily, G C -- Ehrlich, P R -- New York, N.Y. -- Science. 1997 Oct 24;278(5338):689-92.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, Stanford University, Stanford, CA 94305-5020, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9381179" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; *Ecosystem ; *Genetics, Population ; Mathematics ; Plants ; Polymorphism, Restriction Fragment Length ; Population Density
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 11
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    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 1997-12-31
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Husten, L -- New York, N.Y. -- Science. 1997 Nov 14;278(5341):1228.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9411750" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adrenal Glands/metabolism ; Animals ; Antigens, CD36/genetics/*metabolism ; Arteriosclerosis/etiology/metabolism ; *Carrier Proteins ; Cholesterol/blood/metabolism ; Cloning, Molecular ; Humans ; Lipoproteins, HDL/blood/*metabolism ; Liver/metabolism ; *Membrane Proteins ; Mice ; Mice, Knockout ; *RNA-Binding Proteins ; *Receptors, Immunologic ; Receptors, Lipoprotein/genetics/*metabolism ; Receptors, Scavenger ; Scavenger Receptors, Class B
    Print ISSN: 0036-8075
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 12
    Publikationsdatum: 1997-12-31
    Beschreibung: A lymphocyte subpopulation, the Valpha14 natural killer T (NKT) cells, expresses both NK1.1 and a single invariant T cell receptor encoded by the Valpha14 and Jalpha281 gene segments. Mice with a deletion of the Jalpha281 gene segment were found to exclusively lack this subpopulation. The Valpha14 NKT cell-deficient mice could no longer mediate the interleukin-12 (IL-12)-induced rejection of tumors. Although the antitumor effect of IL-12 was thought to be mediated through natural killer cells and T cells, Valpha14 NKT cells were found to be an essential target of IL-12, and they mediated their cytotoxicity by an NK-like effector mechanism after activation with IL-12.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cui, J -- Shin, T -- Kawano, T -- Sato, H -- Kondo, E -- Toura, I -- Kaneko, Y -- Koseki, H -- Kanno, M -- Taniguchi, M -- New York, N.Y. -- Science. 1997 Nov 28;278(5343):1623-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Core Research for Evolutional Science and Technology (CREST) Project, Japan Science and Technology Corporation (JST), 1-8-1 Inohana, Chuo-ku, Chiba, Japan 260.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9374462" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Anti-Bacterial Agents/pharmacology ; *Cytotoxicity, Immunologic ; Gene Deletion ; Gene Targeting ; Genes, RAG-1 ; Genes, T-Cell Receptor alpha ; Interferon-gamma/immunology ; Interleukin-12/*immunology ; Killer Cells, Natural/*immunology ; *Macrolides ; Melanoma, Experimental/immunology ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Neoplasms, Experimental/*immunology ; Poly I-C/pharmacology ; Proton-Translocating ATPases/antagonists & inhibitors ; Receptors, Antigen, T-Cell, alpha-beta/genetics/*immunology ; T-Lymphocyte Subsets/*immunology
    Print ISSN: 0036-8075
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 13
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    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 1997-02-28
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dempster, W F -- New York, N.Y. -- Science. 1997 Feb 28;275(5304):1247-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9064774" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Arizona ; Atmosphere ; *Ecological Systems, Closed ; *Ecosystem ; Humans
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 14
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    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 1997-06-27
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vogel, G -- New York, N.Y. -- Science. 1997 Jun 27;276(5321):1973.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9221499" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Chromosome Mapping ; Chromosomes, Human, Pair 4 ; Genetic Markers ; Humans ; Lewy Bodies/chemistry ; Mice ; Mice, Transgenic ; Nerve Tissue Proteins/analysis/chemistry/*genetics ; Oxidative Stress ; Parkinson Disease/etiology/*genetics ; Point Mutation ; Protein Conformation ; Protein Folding ; Rats ; Synucleins
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 15
    Publikationsdatum: 1997-06-13
    Beschreibung: Two families of small peptides that bind to the human thrombopoietin receptor and compete with the binding of the natural ligand thrombopoietin (TPO) were identified from recombinant peptide libraries. The sequences of these peptides were not found in the primary sequence of TPO. Screening libraries of variants of one of these families under affinity-selective conditions yielded a 14-amino acid peptide (Ile-Glu-Gly-Pro-Thr-Leu-Arg-Gln-Trp-Leu-Ala-Ala-Arg-Ala) with high affinity (dissociation constant approximately 2 nanomolar) that stimulates the proliferation of a TPO-responsive Ba/F3 cell line with a median effective concentration (EC50) of 400 nanomolar. Dimerization of this peptide by a carboxyl-terminal linkage to a lysine branch produced a compound with an EC50 of 100 picomolar, which was equipotent to the 332-amino acid natural cytokine in cell-based assays. The peptide dimer also stimulated the in vitro proliferation and maturation of megakaryocytes from human bone marrow cells and promoted an increase in platelet count when administered to normal mice.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cwirla, S E -- Balasubramanian, P -- Duffin, D J -- Wagstrom, C R -- Gates, C M -- Singer, S C -- Davis, A M -- Tansik, R L -- Mattheakis, L C -- Boytos, C M -- Schatz, P J -- Baccanari, D P -- Wrighton, N C -- Barrett, R W -- Dower, W J -- New York, N.Y. -- Science. 1997 Jun 13;276(5319):1696-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Affymax Research Institute, 4001 Miranda Avenue, Palo Alto, CA 94304, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9180079" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acid Sequence ; Animals ; Binding, Competitive ; Blood Platelets/cytology ; Cell Division ; Cell Line ; Cells, Cultured ; Consensus Sequence ; Dimerization ; Erythropoietin/pharmacology ; Hematopoiesis/drug effects ; Humans ; Megakaryocytes/cytology ; Mice ; Molecular Sequence Data ; *Neoplasm Proteins ; Oligopeptides/*metabolism/*pharmacology ; Peptide Library ; Peptides/metabolism/pharmacology ; Platelet Count ; Proto-Oncogene Proteins/*agonists/metabolism ; *Receptors, Cytokine ; Receptors, Thrombopoietin ; Recombinant Proteins/metabolism/pharmacology ; Thrombopoietin/*metabolism/pharmacology ; Transfection
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  • 16
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    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 1997-12-31
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1997 Nov 21;278(5342):1404-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9411764" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Brain/metabolism ; Copper/*metabolism/toxicity ; Copper Sulfate/poisoning ; Mice ; Mice, Knockout ; Neurons/drug effects/physiology ; PrPC Proteins/genetics/*metabolism ; Prion Diseases/etiology
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 17
    Publikationsdatum: 1997-12-31
    Beschreibung: Natural killer T (NKT) lymphocytes express an invariant T cell antigen receptor (TCR) encoded by the Valpha14 and Jalpha281 gene segments. A glycosylceramide-containing alpha-anomeric sugar with a longer fatty acyl chain (C26) and sphingosine base (C18) was identified as a ligand for this TCR. Glycosylceramide-mediated proliferative responses of Valpha14 NKT cells were abrogated by treatment with chloroquine-concanamycin A or by monoclonal antibodies against CD1d/Vbeta8, CD40/CD40L, or B7/CTLA-4/CD28, but not by interference with the function of a transporter-associated protein. Thus, this lymphocyte shares distinct recognition systems with either T or NK cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kawano, T -- Cui, J -- Koezuka, Y -- Toura, I -- Kaneko, Y -- Motoki, K -- Ueno, H -- Nakagawa, R -- Sato, H -- Kondo, E -- Koseki, H -- Taniguchi, M -- New York, N.Y. -- Science. 1997 Nov 28;278(5343):1626-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉CREST (Core Research for Evolutional Science and Technology) Project, Japan Science and Technology Corporation (JST), 1-8-1 Inohana, Chuo, Chiba 260, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9374463" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Antigens, CD1/*immunology ; Carbohydrate Conformation ; Cells, Cultured ; Ceramides/chemistry/metabolism/*pharmacology ; Cerebrosides/chemistry/metabolism/*pharmacology ; Coculture Techniques ; Galactosylceramides/chemistry/metabolism/pharmacology ; Glucosylceramides/chemistry/metabolism/pharmacology ; Killer Cells, Natural/*immunology ; Ligands ; *Lymphocyte Activation ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Receptors, Antigen, T-Cell, alpha-beta/*immunology ; Structure-Activity Relationship ; T-Lymphocyte Subsets/*immunology
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 18
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    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 1997-05-16
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1997 May 16;276(5315):1030-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9173537" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acid Sequence ; Animals ; Biological Clocks/*genetics ; CLOCK Proteins ; Chromosome Mapping ; Circadian Rhythm/*genetics ; Cloning, Molecular ; Gene Expression Regulation ; Mice ; Mutation ; Trans-Activators/chemistry/*genetics/physiology
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 19
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    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 1997-08-22
    Beschreibung: Tuberculosis is the leading cause of death due to an infectious organism, killing an estimated 3 million people annually. Mycobacterium tuberculosis, the causative agent of tuberculosis, and other pathogenic mycobacteria require entry into host macrophages to initiate infection. An invasion mechanism was defined that was shared among pathogenic mycobacteria including M. tuberculosis, M. leprae, and M. avium but not by nonpathogenic mycobacteria or nonmycobacterial intramacrophage pathogens. This pathway required the association of the complement cleavage product C2a with mycobacteria resulting in the formation of a C3 convertase. The mycobacteria-associated C2a cleaved C3, resulting in C3b opsonization of the mycobacteria and recognition by macrophages.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schorey, J S -- Carroll, M C -- Brown, E J -- AI33348/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1997 Aug 22;277(5329):1091-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Internal Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9262476" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acid Sequence ; Animals ; Complement C2/*physiology ; Complement C2a ; Complement C3/metabolism ; Complement C3-C5 Convertases/metabolism ; Complement C3b/immunology ; Horses ; Humans ; In Vitro Techniques ; Isoflurophate/pharmacology ; Macrophages/immunology/*microbiology ; Mice ; Molecular Sequence Data ; Mycobacterium/*pathogenicity ; Mycobacterium avium Complex/immunology/*pathogenicity ; Mycobacterium bovis/immunology/pathogenicity ; Mycobacterium leprae/immunology/pathogenicity ; Mycobacterium tuberculosis/immunology/pathogenicity ; Opsonin Proteins ; Virulence
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 20
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    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 1997-01-17
    Beschreibung: The proto-oncogene-encoded transcription factor c-Jun activates genes in response to a number of inducers that act through mitogen-activated protein kinase (MAPK) signal transduction pathways. The activation of c-Jun after phosphorylation by MAPK is accompanied by a reduction in c-Jun ubiquitination and consequent stabilization of the protein. These results illustrate the relevance of regulated protein degradation in the signal-dependent control of gene expression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Musti, A M -- Treier, M -- Bohmann, D -- New York, N.Y. -- Science. 1997 Jan 17;275(5298):400-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉European Molecular Biology Laboratory, Meyerhofstr. 1, 69117 Heidelberg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8994040" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): 3T3 Cells ; Animals ; Calcium-Calmodulin-Dependent Protein Kinases/*metabolism ; Cell Cycle Proteins/metabolism ; GTP-Binding Proteins/metabolism ; Gene Expression Regulation ; JNK Mitogen-Activated Protein Kinases ; Mice ; *Mitogen-Activated Protein Kinases ; Phosphorylation ; Proto-Oncogene Proteins c-jun/*metabolism ; Signal Transduction ; Transfection ; Ubiquitins/*metabolism ; cdc42 GTP-Binding Protein, Saccharomyces cerevisiae
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 21
    Publikationsdatum: 1997-02-14
    Beschreibung: Mutations in the Caenorhabditis elegans gene clk-1 affect biological timing and extend longevity. The gene clk-1 was identified, and the cloned gene complemented the clk-1 phenotypes and restored normal longevity. The CLK-1 protein was found to be conserved among eukaryotes, including humans, and structurally similar to the yeast metabolic regulator Cat5p (also called Coq7p). These proteins contain a tandem duplication of a core 82-residue domain. clk-1 complemented the phenotype of cat5/coq7 null mutants, demonstrating that clk-1 and CAT5/COQ7 share biochemical function and that clk-1 acts at the level of cellular physiology.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ewbank, J J -- Barnes, T M -- Lakowski, B -- Lussier, M -- Bussey, H -- Hekimi, S -- New York, N.Y. -- Science. 1997 Feb 14;275(5302):980-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, McGill University, 1205 Avenue Docteur Penfield, Montreal, Quebec, Canada H3A 1B1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9020081" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acid Sequence ; Animals ; Caenorhabditis elegans/*genetics/metabolism/*physiology ; *Caenorhabditis elegans Proteins ; Cell Aging/*genetics ; Chromosome Mapping ; Conserved Sequence ; Exons ; Fungal Proteins/chemistry/genetics/physiology ; *Genes, Helminth ; Genetic Complementation Test ; Glycerol/metabolism ; Helminth Proteins/chemistry/*genetics/physiology ; Humans ; Longevity/genetics ; Mice ; Molecular Sequence Data ; Phenotype ; Protein Structure, Secondary ; Protein Structure, Tertiary ; RNA Splicing ; *Saccharomyces cerevisiae Proteins
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 22
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    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 1997-04-25
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Service, R F -- New York, N.Y. -- Science. 1997 Apr 25;276(5312):533.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9148412" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adhesins, Bacterial/*immunology ; *Adhesins, Escherichia coli ; Animals ; Antibodies, Bacterial/biosynthesis ; *Bacterial Vaccines/administration & dosage/immunology ; Clinical Trials as Topic ; Escherichia coli/*immunology ; Escherichia coli Infections/*prevention & control ; Female ; *Fimbriae Proteins ; Humans ; Immunoglobulin G/biosynthesis ; Mice ; Urinary Tract Infections/immunology/*prevention & control ; Vaccination ; Vaccines, Inactivated/administration & dosage/immunology ; *Vaccines, Synthetic/administration & dosage/immunology
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 23
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    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 1997-08-22
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉O'Gorman, S -- Wahl, G M -- New York, N.Y. -- Science. 1997 Aug 22;277(5329):1025.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9289845" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; DNA Nucleotidyltransferases/*metabolism ; *Genetic Engineering ; Integrases/metabolism ; Licensure ; Mice ; *Mice, Transgenic ; *Viral Proteins
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 24
    Publikationsdatum: 1997-05-30
    Beschreibung: Despite myriads of biological activities ascribed to uteroglobin (UG), a steroid-inducible secreted protein, its physiological functions are unknown. Mice in which the uteroglobin gene was disrupted had severe renal disease that was associated with massive glomerular deposition of predominantly multimeric fibronectin (Fn). The molecular mechanism that normally prevents Fn deposition appears to involve high-affinity binding of UG with Fn to form Fn-UG heteromers that counteract Fn self-aggregation, which is required for abnormal tissue deposition. Thus, UG is essential for maintaining normal renal function in mice, which raises the possibility that an analogous pathogenic mechanism may underlie genetic Fn-deposit human glomerular disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Z -- Kundu, G C -- Yuan, C J -- Ward, J M -- Lee, E J -- DeMayo, F -- Westphal, H -- Mukherjee, A B -- HL47620/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1997 May 30;276(5317):1408-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section on Developmental Genetics, Heritable Disorders Branch, National Institute of Child Health and Human Development (NICHD), National Insitutes of Health (NIH), Bethesda, MD 20892-1830, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9162006" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Cells, Cultured ; Crosses, Genetic ; Fibronectins/*metabolism ; Gene Targeting ; Humans ; Kidney Diseases/embryology/genetics/pathology ; *Kidney Glomerulus/embryology/metabolism/ultrastructure ; Mice ; Mice, Inbred C57BL ; Uteroglobin/deficiency/genetics/*physiology
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 25
    Publikationsdatum: 1997-10-06
    Beschreibung: Familial adenomatous polyposis coli (FAP) is a disease characterized by the development of multiple colorectal adenomas, and affected individuals carry germline mutations in the APC gene. With the use of a conditional gene targeting system, a mouse model of FAP was created that circumvents the embryonic lethality of Apc deficiency and directs Apc inactivation specifically to the colorectal epithelium. loxP sites were inserted into the introns around Apc exon 14, and the resultant mutant allele (Apc580S) was introduced into the mouse germline. Mice homozygous for Apc580S were normal; however, upon infection of the colorectal region with an adenovirus encoding the Cre recombinase, the mice developed adenomas within 4 weeks. The adenomas showed deletion of Apc exon 14, indicating that the loss of Apc function was caused by Cre-loxP-mediated recombination.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shibata, H -- Toyama, K -- Shioya, H -- Ito, M -- Hirota, M -- Hasegawa, S -- Matsumoto, H -- Takano, H -- Akiyama, T -- Toyoshima, K -- Kanamaru, R -- Kanegae, Y -- Saito, I -- Nakamura, Y -- Shiba, K -- Noda, T -- New York, N.Y. -- Science. 1997 Oct 3;278(5335):120-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Cancer Institute, Toshima-ku, Tokyo 170, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9311916" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adenomatous Polyposis Coli/*genetics ; Adenomatous Polyposis Coli Protein ; Adenoviridae/genetics ; Animals ; Colon/metabolism ; Cytoskeletal Proteins/biosynthesis ; Disease Models, Animal ; Exons ; Female ; Frameshift Mutation ; Gene Deletion ; *Gene Targeting ; *Genes, APC ; Genetic Vectors ; Germ-Line Mutation ; Homozygote ; Integrases/genetics/metabolism ; Introns ; Male ; Mice ; Mice, Inbred C57BL ; Recombination, Genetic ; *Viral Proteins
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 26
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    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 1997-07-11
    Beschreibung: BOB.1/OBF.1 is a transcriptional coactivator that is constitutively expressed in B cells and interacts with the Oct1 and Oct2 transcription factors. Upon activation of Jurkat T cells and primary murine thymocytes with phorbol esters and ionomycin, BOB.1/OBF.1 expression and transactivation function were induced. BOB.1/OBF.1 was phosphorylated at Ser184 both in vivo and in vitro, and this modification was required for inducible activation. Mutation of Ser184 also diminished transactivation function in B cells, suggesting that the activating phosphorylation that is inducible in T cells is constitutively present in B cells. Thus, BOB.1/OBF.1 is a transcriptional coactivator that is critically regulated by posttranslational modifications to mediate cell type-specific gene expression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zwilling, S -- Dieckmann, A -- Pfisterer, P -- Angel, P -- Wirth, T -- New York, N.Y. -- Science. 1997 Jul 11;277(5323):221-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉MSZ, Institut fur Medizinische Strahlenkunde und Zellforschung, Universitat Wurzburg, Versbacher Strasse 5, 97078 Wurzburg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9211847" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acid Sequence ; Animals ; B-Lymphocytes/metabolism ; Cells, Cultured ; *DNA-Binding Proteins ; *Gene Expression Regulation ; HeLa Cells ; Homeodomain Proteins/metabolism ; Host Cell Factor C1 ; Humans ; Immunosuppressive Agents/pharmacology ; Ionomycin/pharmacology ; Jurkat Cells ; *Lymphocyte Activation ; Mice ; Molecular Sequence Data ; Octamer Transcription Factor-1 ; Phosphorylation ; Phosphoserine/metabolism ; Recombinant Fusion Proteins/metabolism ; T-Lymphocytes/immunology/*metabolism ; Tetradecanoylphorbol Acetate/pharmacology ; Trans-Activators/genetics/*metabolism ; Transcription Factors/metabolism ; *Transcriptional Activation
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 27
    Publikationsdatum: 1997-09-05
    Beschreibung: In response to DNA damage, mammalian cells prevent cell cycle progression through the control of critical cell cycle regulators. A human gene was identified that encodes the protein Chk1, a homolog of the Schizosaccharomyces pombe Chk1 protein kinase, which is required for the DNA damage checkpoint. Human Chk1 protein was modified in response to DNA damage. In vitro Chk1 bound to and phosphorylated the dual-specificity protein phosphatases Cdc25A, Cdc25B, and Cdc25C, which control cell cycle transitions by dephosphorylating cyclin-dependent kinases. Chk1 phosphorylates Cdc25C on serine-216. As shown in an accompanying paper by Peng et al. in this issue, serine-216 phosphorylation creates a binding site for 14-3-3 protein and inhibits function of the phosphatase. These results suggest a model whereby in response to DNA damage, Chk1 phosphorylates and inhibits Cdc25C, thus preventing activation of the Cdc2-cyclin B complex and mitotic entry.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sanchez, Y -- Wong, C -- Thoma, R S -- Richman, R -- Wu, Z -- Piwnica-Worms, H -- Elledge, S J -- GM17763/GM/NIGMS NIH HHS/ -- GM44664/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1997 Sep 5;277(5331):1497-501.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Verna and Marrs McLean Department of Biochemistry, Howard Hughes Medical Institute, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9278511" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): 14-3-3 Proteins ; Amino Acid Sequence ; Animals ; CDC2 Protein Kinase/*metabolism ; Cell Cycle Proteins/antagonists & inhibitors/*metabolism ; Chromosome Mapping ; Chromosomes, Human, Pair 11 ; Cytoskeletal Proteins ; *DNA Damage ; *F-Box Proteins ; G2 Phase ; HeLa Cells ; Humans ; Mice ; *Mitosis ; Molecular Sequence Data ; Phosphoprotein Phosphatases/metabolism ; Phosphorylation ; Phosphoserine/metabolism ; Protein Kinases/chemistry/genetics/*metabolism ; Protein Tyrosine Phosphatases/metabolism ; Proteins/metabolism ; Recombinant Fusion Proteins/metabolism ; Schizosaccharomyces pombe Proteins ; Signal Transduction ; Transfection ; *Tyrosine 3-Monooxygenase ; *Ubiquitin-Protein Ligases ; *cdc25 Phosphatases
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 28
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    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 1997-10-27
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Williams, N -- New York, N.Y. -- Science. 1997 Oct 3;278(5335):31.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9340753" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Brain/*pathology ; Brain Chemistry ; Cattle ; Creutzfeldt-Jakob Syndrome/pathology/*transmission ; Encephalopathy, Bovine Spongiform/pathology/*transmission ; Humans ; Mice ; Mice, Transgenic ; Prions/*chemistry
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 29
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 1997-01-17
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Frank, E -- New York, N.Y. -- Science. 1997 Jan 17;275(5298):324-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, University of Pittsburgh, Pittsburgh, PA 15261, USA. efrank+@pitt.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9005555" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Acetylcholine/metabolism ; Action Potentials ; Animals ; Axons/physiology ; Central Nervous System/physiology ; Mice ; Motor Neurons/*physiology ; Muscle Fibers, Skeletal/physiology ; Neuromuscular Junction/*physiology ; Receptors, Cholinergic/metabolism ; Synapses/*physiology ; *Synaptic Transmission
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 30
    Publikationsdatum: 1997-07-18
    Beschreibung: CD1 represents a third lineage of antigen-presenting molecules that are distantly related to major histocompatibility complex (MHC) molecules in the immune system. The crystal structure of mouse CD1d1, corresponding to human CD1d, at 2.8 resolution shows that CD1 adopts an MHC fold that is more closely related to that of MHC class I than to that of MHC class II. The binding groove, although significantly narrower, is substantially larger because of increased depth and it has only two major pockets that are almost completely hydrophobic. The extreme hydrophobicity and shape of the binding site are consistent with observations that human CD1b and CD1c can present mycobacterial cell wall antigens, such as mycolic acid and lipoarabinomannans. However, mouse CD1d1 can present very hydrophobic peptides, but must do so in a very different way from MHC class Ia and class II molecules.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zeng, Z -- Castano, A R -- Segelke, B W -- Stura, E A -- Peterson, P A -- Wilson, I A -- CA-58896/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1997 Jul 18;277(5324):339-45.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology and the Skaggs Institute for Chemical Biology at the Scripps Research Institute, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9219685" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; *Antigen Presentation ; Antigens, CD1/*chemistry/immunology/metabolism ; Binding Sites ; Crystallization ; Crystallography, X-Ray ; Glycolipids/chemistry/immunology/metabolism ; Histocompatibility Antigens Class I/chemistry ; Histocompatibility Antigens Class II/chemistry ; Humans ; Hydrogen Bonding ; Ligands ; Lipid Metabolism ; Lipids/chemistry/immunology ; Mice ; Models, Molecular ; *Protein Conformation ; *Protein Folding ; Protein Structure, Secondary ; Protein Structure, Tertiary ; T-Lymphocyte Subsets/immunology
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 31
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 1997-03-28
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shanahan, F -- New York, N.Y. -- Science. 1997 Mar 28;275(5308):1897-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, National University of Ireland, Cork, University Hospital, Cork, Ireland. fshanahan@iruccvax.ucc.ie〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9122691" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; CD8-Positive T-Lymphocytes/cytology/immunology/metabolism ; Cell Communication ; Cell Division ; *Immunity, Mucosal ; Intestinal Mucosa/cytology/*immunology/metabolism ; Lymphocyte Activation ; Mice ; Receptors, Thyrotropin-Releasing Hormone/metabolism ; T-Lymphocytes/cytology/*immunology/metabolism ; Thyrotropin/*metabolism/pharmacology ; Thyrotropin-Releasing Hormone/*metabolism/pharmacology
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 32
    Publikationsdatum: 1997-10-10
    Beschreibung: The caspase-3 (CPP32, apopain, YAMA) family of cysteinyl proteases has been implicated as key mediators of apoptosis in mammalian cells. Gelsolin was identified as a substrate for caspase-3 by screening the translation products of small complementary DNA pools for sensitivity to cleavage by caspase-3. Gelsolin was cleaved in vivo in a caspase-dependent manner in cells stimulated by Fas. Caspase-cleaved gelsolin severed actin filaments in vitro in a Ca2+-independent manner. Expression of the gelsolin cleavage product in multiple cell types caused the cells to round up, detach from the plate, and undergo nuclear fragmentation. Neutrophils isolated from mice lacking gelsolin had delayed onset of both blebbing and DNA fragmentation, following apoptosis induction, compared with wild-type neutrophils. Thus, cleaved gelsolin may be one physiological effector of morphologic change during apoptosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kothakota, S -- Azuma, T -- Reinhard, C -- Klippel, A -- Tang, J -- Chu, K -- McGarry, T J -- Kirschner, M W -- Koths, K -- Kwiatkowski, D J -- Williams, L T -- P01 HL48743/HL/NHLBI NIH HHS/ -- R01 HL54188/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1997 Oct 10;278(5336):294-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Chiron Corporation, Emeryville, CA 94608, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9323209" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Actins/metabolism ; Amino Acid Chloromethyl Ketones/pharmacology ; Animals ; Antigens, CD95/physiology ; *Apoptosis ; Caspase 3 ; *Caspases ; Cell Line ; *Cell Size ; Cycloheximide/pharmacology ; Cysteine Endopeptidases/*metabolism ; Cysteine Proteinase Inhibitors/pharmacology ; Cytoskeleton/metabolism ; DNA Fragmentation ; Gelsolin/*metabolism ; Humans ; Mice ; Neutrophils/cytology/metabolism ; Recombinant Proteins/metabolism ; Transfection ; Tumor Cells, Cultured ; Tumor Necrosis Factor-alpha/pharmacology
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 33
    Publikationsdatum: 1997-10-06
    Beschreibung: Expression of Agouti protein is normally limited to the skin where it affects pigmentation, but ubiquitous expression causes obesity. An expressed sequence tag was identified that encodes Agouti-related protein, whose RNA is normally expressed in the hypothalamus and whose levels were increased eightfold in ob/ob mice. Recombinant Agouti-related protein was a potent, selective antagonist of Mc3r and Mc4r, melanocortin receptor subtypes implicated in weight regulation. Ubiquitous expression of human AGRP complementary DNA in transgenic mice caused obesity without altering pigmentation. Thus, Agouti-related protein is a neuropeptide implicated in the normal control of body weight downstream of leptin signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ollmann, M M -- Wilson, B D -- Yang, Y K -- Kerns, J A -- Chen, Y -- Gantz, I -- Barsh, G S -- EY07106/EY/NEI NIH HHS/ -- GM07365/GM/NIGMS NIH HHS/ -- P30DK-34933/DK/NIDDK NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1997 Oct 3;278(5335):135-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatrics, Howard Hughes Medical Institute, Stanford University School of Medicine, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9311920" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adrenal Glands/metabolism ; Amino Acid Sequence ; Animals ; Female ; Humans ; Hypothalamus/metabolism ; Male ; Melanocyte-Stimulating Hormones/antagonists & inhibitors/pharmacology ; Melanophores/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Inbred CBA ; Mice, Obese ; Mice, Transgenic ; Molecular Sequence Data ; Obesity/etiology ; Organophosphorus Compounds/pharmacology ; Proteins/chemistry/genetics/pharmacology/*physiology ; RNA/genetics/metabolism ; Receptor, Melanocortin, Type 3 ; Receptor, Melanocortin, Type 4 ; Receptors, Corticotropin/*antagonists & inhibitors/metabolism ; Receptors, Peptide/*antagonists & inhibitors/metabolism ; Recombinant Proteins/metabolism ; Signal Transduction ; Xenopus
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 34
    Publikationsdatum: 1997-03-21
    Beschreibung: The adenomatous polyposis coli (APC) tumor suppressor protein binds to beta-catenin, a protein recently shown to interact with Tcf and Lef transcription factors. The gene encoding hTcf-4, a Tcf family member that is expressed in colonic epithelium, was cloned and characterized. hTcf-4 transactivates transcription only when associated with beta-catenin. Nuclei of APC-/- colon carcinoma cells were found to contain a stable beta-catenin-hTcf-4 complex that was constitutively active, as measured by transcription of a Tcf reporter gene. Reintroduction of APC removed beta-catenin from hTcf-4 and abrogated the transcriptional transactivation. Constitutive transcription of Tcf target genes, caused by loss of APC function, may be a crucial event in the early transformation of colonic epithelium.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Korinek, V -- Barker, N -- Morin, P J -- van Wichen, D -- de Weger, R -- Kinzler, K W -- Vogelstein, B -- Clevers, H -- CA57345/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1997 Mar 21;275(5307):1784-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, University Hospital, Post Office Box 85500, 3508 GA Utrecht, Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9065401" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adenomatous Polyposis Coli Protein ; Amino Acid Sequence ; Animals ; Cell Line ; Cell Transformation, Neoplastic ; Cloning, Molecular ; Colon/metabolism ; Colonic Neoplasms/*genetics/metabolism ; Cytoskeletal Proteins/genetics/*metabolism ; Gene Expression Regulation, Neoplastic ; *Genes, APC ; Genes, Reporter ; Humans ; Intestinal Mucosa/metabolism ; Mice ; Molecular Sequence Data ; Signal Transduction ; TCF Transcription Factors ; *Trans-Activators ; Transcription Factor 7-Like 2 Protein ; Transcription Factors/chemistry/genetics/*metabolism ; *Transcriptional Activation ; Transfection ; Tumor Cells, Cultured ; beta Catenin
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 35
    Publikationsdatum: 1997-10-10
    Beschreibung: The clonal selection theory states that B lymphocytes producing high-affinity immunoglobulins are selected from a pool of cells undergoing antibody gene mutation. Somatic hypermutation is a well-documented mechanism for achieving diversification of immune responses in mature B cells. Antibody genes were also found to be modified in such cells in germinal centers by recombination of the variable (V), diversity (D), and joining (J) segments. The ability to alter immunoglobulin expression by V(D)J recombination in the selective environment of the germinal center may be an additional mechanism for inactivation or diversification of immune responses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Papavasiliou, F -- Casellas, R -- Suh, H -- Qin, X F -- Besmer, E -- Pelanda, R -- Nemazee, D -- Rajewsky, K -- Nussenzweig, M C -- AI33890/AI/NIAID NIH HHS/ -- R01 AI033608/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1997 Oct 10;278(5336):298-301.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Immunology, Rockefeller University, New York, NY 10021, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9323210" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; *Antibody Diversity ; B-Lymphocytes/*immunology ; Cells, Cultured ; DNA Nucleotidyltransferases/genetics/metabolism ; DNA-Binding Proteins/genetics ; Gene Expression ; *Gene Rearrangement, B-Lymphocyte ; Genes, Immunoglobulin ; Genes, RAG-1 ; Germinal Center/cytology/immunology ; Immunoglobulin Joining Region/*genetics ; Immunoglobulin M/biosynthesis/genetics ; Immunoglobulin Variable Region/*genetics ; Lymphocyte Activation ; Mice ; *Recombination, Genetic ; VDJ Recombinases
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 36
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 1997-07-11
    Beschreibung: Platelet-derived growth factor (PDGF)-B-deficient mouse embryos were found to lack microvascular pericytes, which normally form part of the capillary wall, and they developed numerous capillary microaneurysms that ruptured at late gestation. Endothelial cells of the sprouting capillaries in the mutant mice appeared to be unable to attract PDGF-Rbeta-positive pericyte progenitor cells. Pericytes may contribute to the mechanical stability of the capillary wall. Comparisons made between PDGF null mouse phenotypes suggest a general role for PDGFs in the development of myofibroblasts.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lindahl, P -- Johansson, B R -- Leveen, P -- Betsholtz, C -- New York, N.Y. -- Science. 1997 Jul 11;277(5323):242-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Biochemistry, University of Goteborg, Medicinaregatan 9A, S-413 90 Goteborg, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9211853" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Aneurysm/*etiology ; Animals ; Brain/blood supply ; Capillaries/*cytology/embryology/metabolism ; Cell Movement ; Endothelium, Vascular/cytology/metabolism ; Hemorrhage/etiology ; Mice ; Mice, Inbred C57BL ; Mutation ; Neovascularization, Physiologic ; Platelet-Derived Growth Factor/deficiency/genetics/*physiology ; Proto-Oncogene Proteins/deficiency/genetics/*physiology ; Proto-Oncogene Proteins c-sis ; Receptor Protein-Tyrosine Kinases/metabolism ; Receptor, Platelet-Derived Growth Factor beta ; Receptor, TIE-2 ; Receptors, Platelet-Derived Growth Factor/metabolism ; Signal Transduction ; Stem Cells/cytology/metabolism ; Up-Regulation
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 37
    Publikationsdatum: 1997-06-13
    Beschreibung: Extracellular levels of the excitatory neurotransmitter glutamate in the nervous system are maintained by transporters that actively remove glutamate from the extracellular space. Homozygous mice deficient in GLT-1, a widely distributed astrocytic glutamate transporter, show lethal spontaneous seizures and increased susceptibility to acute cortical injury. These effects can be attributed to elevated levels of residual glutamate in the brains of these mice.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tanaka, K -- Watase, K -- Manabe, T -- Yamada, K -- Watanabe, M -- Takahashi, K -- Iwama, H -- Nishikawa, T -- Ichihara, N -- Kikuchi, T -- Okuyama, S -- Kawashima, N -- Hori, S -- Takimoto, M -- Wada, K -- New York, N.Y. -- Science. 1997 Jun 13;276(5319):1699-702.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Degenerative Neurological Diseases, National Institute of Neuroscience, Kodaira, Tokyo 187, Japan. tanaka@ncnaxp.ncap.go.jp〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9180080" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): ATP-Binding Cassette Transporters/genetics/*metabolism ; Amino Acid Transport System X-AG ; Animals ; Biological Transport ; Brain/*metabolism/pathology ; Brain Injuries/*metabolism/pathology ; Electroencephalography ; Epilepsy/*metabolism/pathology ; Gene Targeting ; Glutamic Acid/*metabolism ; Hippocampus/metabolism/pathology ; Mice ; Mice, Inbred C57BL ; Nerve Degeneration ; Pyramidal Cells/pathology/physiology ; Synapses/metabolism ; Synaptic Transmission
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 38
    Publikationsdatum: 1997-10-06
    Beschreibung: Immunotherapy of mice with preexisting cancers with heat shock protein preparations derived from autologous cancer resulted in retarded progression of the primary cancer, a reduced metastatic load, and prolongation of life-span. Treatment with heat shock protein preparations derived from cancers other than the autologous cancer did not provide significant protection. Spontaneous cancers (lung cancer and melanoma), chemically induced cancers (fibrosarcoma and colon carcinoma), and an ultraviolet radiation-induced spindle cell carcinoma were tested, and the results support the efficacy of autologous cancer-derived heat shock protein-peptide complexes in immunotherapy of cancers without the need to identify specific tumor antigenic epitopes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tamura, Y -- Peng, P -- Liu, K -- Daou, M -- Srivastava, P K -- CA44786/CA/NCI NIH HHS/ -- CA64394/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1997 Oct 3;278(5335):117-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Immunotherapy of Cancer and Infectious Diseases, MC1601, University of Connecticut School of Medicine, Farmington, CT 06030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9311915" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Antigens, Neoplasm/*immunology/therapeutic use ; Autoimmunity ; CD4-Positive T-Lymphocytes/immunology ; CD8-Positive T-Lymphocytes/immunology ; HSP70 Heat-Shock Proteins/immunology ; Heat-Shock Proteins/*immunology/therapeutic use ; Immunization ; *Immunotherapy ; Killer Cells, Natural/immunology ; Lung Neoplasms/immunology/pathology/secondary/therapy ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Neoplasm Metastasis ; Neoplasms/immunology/pathology/*therapy ; Neoplasms, Experimental/immunology/pathology/*therapy
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 39
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 1997-12-31
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kang, S M -- Hoffmann, A -- Le, D -- Springer, M L -- Stock, P G -- Blau, H M -- F32 HL08991/HL/NHLBI NIH HHS/ -- R01-CA59717/CA/NCI NIH HHS/ -- R01-HD18179/HD/NICHD NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1997 Nov 14;278(5341):1322-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9411754" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Antigens, CD95/biosynthesis ; Apoptosis ; Cell Differentiation ; Cell Transplantation ; Fas Ligand Protein ; *Graft Rejection ; Immune Tolerance ; Islets of Langerhans/cytology ; *Islets of Langerhans Transplantation ; Membrane Glycoproteins/genetics/*physiology ; Mice ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Muscle Fibers, Skeletal/*cytology/metabolism ; Muscle, Skeletal/*cytology/metabolism ; Neutrophils/*immunology ; Transfection
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 40
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 1997-10-24
    Beschreibung: Extinction episodes, such as the anthropogenic one currently under way, result in a pruned tree of life. But what fraction of the underlying evolutionary history survives when k of n species in a taxon are lost? This is relevant both to how species loss has translated into a loss of evolutionary history and to assigning conservation priorities. Here it is shown that approximately 80 percent of the underlying tree of life can survive even when approximately 95 percent of species are lost, and that algorithms that maximize the amount of evolutionary history preserved are not much better than choosing the survivors at random. Given the political, economic, and social realities constraining conservation biology, these findings may be helpful.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nee, S -- May, R M -- New York, N.Y. -- Science. 1997 Oct 24;278(5338):692-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Zoology, Oxford University, South Parks Road, Oxford, OX1 3PS, UK. sean.nee@zoo.ox.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9381180" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; *Biological Evolution ; *Ecosystem ; Mathematics ; Population Density
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 41
    Publikationsdatum: 1997-08-15
    Beschreibung: The epithelium that lines the gut is impermeable to macromolecules and microorganisms, except in Peyer's patches (PPs), where the lymphoid follicle-associated epithelium (FAE) contains M cells that transport antigens and microorganisms. A cultured system that reproduces the main characteristics of FAE and M cells was established by cultivation of PP lymphocytes with the differentiated human intestinal cell line Caco-2. Lymphocytes settled into the epithelial monolayer, inducing reorganization of the brush border and a temperature-dependent transport of particles and Vibrio cholerae. This model system could prove useful for intestinal physiology, vaccine research, and drug delivery studies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kerneis, S -- Bogdanova, A -- Kraehenbuhl, J P -- Pringault, E -- New York, N.Y. -- Science. 1997 Aug 15;277(5328):949-52.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Swiss Institute for Experimental Cancer Research, and Institute of Biochemistry, University of Lausanne, CH-1066 Epalinges-Lausanne, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9252325" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; B-Lymphocytes/immunology ; *Bacterial Translocation ; Caco-2 Cells ; Carrier Proteins/analysis ; Cell Polarity ; Coculture Techniques ; Fluorescein-5-isothiocyanate ; Humans ; *Immunity, Mucosal ; Intestinal Mucosa/*cytology/*immunology/microbiology ; Lymphocytes/*immunology ; Mice ; Mice, Inbred BALB C ; Microfilament Proteins/analysis ; Microspheres ; Microvilli/chemistry/ultrastructure ; Peyer's Patches/cytology/*immunology ; Sucrase-Isomaltase Complex/analysis ; T-Lymphocytes/immunology ; Temperature ; Vibrio cholerae/*metabolism
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 42
    Publikationsdatum: 1997-01-24
    Beschreibung: Lymphocyte-specific interferon regulatory factor (LSIRF) (now called IRF4) is a transcription factor expressed only in lymphocytes. Mice deficient in IRF4 showed normal distribution of B and T lymphocyes at 4 to 5 weeks of age but developed progressive generalized lymphadenopathy. IRF4-deficient mice exhibited a profound reduction in serum immunoglobulin concentrations and did not mount detectable antibody responses. T lymphocyte function was also impaired in vivo; these mice could not generate cytotoxic or antitumor responses. Thus, IRF4 is essential for the function and homeostasis of both mature B and mature T lymphocytes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mittrucker, H W -- Matsuyama, T -- Grossman, A -- Kundig, T M -- Potter, J -- Shahinian, A -- Wakeham, A -- Patterson, B -- Ohashi, P S -- Mak, T W -- New York, N.Y. -- Science. 1997 Jan 24;275(5299):540-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, University of Toronto, Toronto, Ontario, M5G 2C1, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8999800" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Antigen Presentation ; B-Lymphocytes/*immunology ; Bone Marrow Cells ; Cytotoxicity, Immunologic ; DNA-Binding Proteins/genetics/*physiology ; Female ; Gene Targeting ; Graft vs Host Reaction ; Immunization ; Immunoglobulins/blood ; Interferon Regulatory Factors ; Lymphatic Diseases/etiology ; Lymphocyte Activation ; Lymphocyte Subsets/cytology ; Lymphoid Tissue/cytology ; Male ; Mast-Cell Sarcoma/immunology ; Mice ; Mice, Inbred C57BL ; Mice, SCID ; Neoplasm Transplantation ; T-Lymphocytes/*immunology ; T-Lymphocytes, Cytotoxic/immunology ; Transcription Factors/genetics/*physiology
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 43
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    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 1997-02-28
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nelson, M -- New York, N.Y. -- Science. 1997 Feb 28;275(5304):1248-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9064775" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Arizona ; *Ecological Systems, Closed ; *Ecosystem ; Humans
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 44
    Publikationsdatum: 1997-03-28
    Beschreibung: Signal transmission by many cell surface receptors results in the activation of phosphoinositide (PI) 3-kinases that phosphorylate the 3' position of polyphosphoinositides. From a screen for mouse proteins that bind phosphoinositides, the protein GRP1was identified. GRP1 binds phosphatidylinositol-3,4,5-trisphosphate [PtdIns(3,4, 5)P3] through a pleckstrin homology (PH) domain and displays a region of high sequence similarity to the yeast Sec7 protein. The PH domain of the closely related protein cytohesin-1, which, through its Sec7 homology domain, regulates integrin beta2 and catalyzes guanine nucleotide exchange of the small guanine nucleotide-binding protein ARF1, was also found to specifically bind PtdIns(3,4,5)P3. GRP1 and cytohesin-1 appear to connect receptor-activated PI 3-kinase signaling pathways with proteins that mediate biological responses such as cell adhesion and membrane trafficking.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Klarlund, J K -- Guilherme, A -- Holik, J J -- Virbasius, J V -- Chawla, A -- Czech, M P -- DK30648/DK/NIDDK NIH HHS/ -- DK30898/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1997 Mar 28;275(5308):1927-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program in Molecular Medicine and Department of Biochemistry and Molecular Biology, University of Massachusetts Medical Center, 373 Plantation Street, Worcester, MA 01605, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9072969" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): ADP-Ribosylation Factor 1 ; ADP-Ribosylation Factors ; Adipocytes/chemistry ; Amino Acid Sequence ; Animals ; Antigens, CD18/metabolism ; Blood Proteins/*chemistry ; Brain Chemistry ; Cell Adhesion Molecules/chemistry/*metabolism ; Cell Membrane/metabolism ; Cells, Cultured ; Cloning, Molecular ; DNA, Complementary ; Fungal Proteins/*chemistry ; GTP-Binding Proteins/metabolism ; *Guanine Nucleotide Exchange Factors ; Humans ; Mice ; Molecular Sequence Data ; Phosphatidylinositol 3-Kinases ; Phosphatidylinositol Phosphates/*metabolism ; *Phosphoproteins ; Phosphorylation ; Phosphotransferases (Alcohol Group Acceptor)/*metabolism ; Receptors, Cytoplasmic and Nuclear/metabolism ; Recombinant Fusion Proteins/chemistry/metabolism ; Sequence Homology, Amino Acid ; *Signal Transduction
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 45
    Publikationsdatum: 1997-10-24
    Beschreibung: Animals vary in their sensitivity to ethanol, a trait at least partly determined by genetic factors. In order to identify possible responsible genes, mice lacking Fyn, a non-receptor type tyrosine kinase, were investigated. These mice were hypersensitive to the hypnotic effect of ethanol. The administration of ethanol enhanced tyrosine phosphorylation of the N-methyl-D-aspartate receptor (NMDAR) in the hippocampus of control mice but not in Fyn-deficient mice. An acute tolerance to ethanol inhibition of NMDAR-mediated excitatory postsynaptic potentials in hippocampal slices developed in control mice but not in Fyn-deficient mice. These results indicate that Fyn affects behavioral, biochemical, and physiological responses to ethanol.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miyakawa, T -- Yagi, T -- Kitazawa, H -- Yasuda, M -- Kawai, N -- Tsuboi, K -- Niki, H -- New York, N.Y. -- Science. 1997 Oct 24;278(5338):698-701.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory for Neurobiology of Emotion, Brain Science Institute, RIKEN, Hirosawa, Wako-shi, Saitama-ken 351-01, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9381182" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Central Nervous System Depressants/*pharmacology ; Ethanol/*pharmacology ; Excitatory Postsynaptic Potentials/drug effects ; Flurazepam/pharmacology ; Hippocampus/metabolism ; Hypnotics and Sedatives/pharmacology ; In Vitro Techniques ; Male ; Mice ; Mice, Knockout ; Motor Activity/*drug effects ; N-Methylaspartate/pharmacology ; Phosphorylation ; Phosphotyrosine/metabolism ; Protein-Tyrosine Kinases/deficiency/genetics/*metabolism ; Proto-Oncogene Proteins/deficiency/genetics/*metabolism ; Proto-Oncogene Proteins c-fyn ; Receptors, N-Methyl-D-Aspartate/*metabolism
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 46
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 1997-12-31
    Beschreibung: Lhx3 and Lhx4 (Gsh4), two closely related LIM homeobox genes, determine formation of the pituitary gland in mice. Rathke's pouch is formed in two steps-first as a rudiment and later as a definitive pouch. Lhx3 and Lhx4 have redundant control over formation of the definitive pouch. Lhx3 controls a subsequent step of pituitary fate commitment. Thereafter, Lhx3 and Lhx4 together regulate proliferation and differentiation of pituitary-specific cell lineages. Thus, Lhx3 and Lhx4 dictate pituitary organ identity by controlling developmental decisions at multiple stages of organogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sheng, H Z -- Moriyama, K -- Yamashita, T -- Li, H -- Potter, S S -- Mahon, K A -- Westphal, H -- New York, N.Y. -- Science. 1997 Dec 5;278(5344):1809-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Mammalian Genes and Development, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9388186" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Cell Differentiation ; Cell Division ; Cell Lineage ; Embryonic and Fetal Development/genetics ; Gene Expression Regulation, Developmental ; *Genes, Homeobox ; Homeodomain Proteins/*genetics/physiology ; LIM-Homeodomain Proteins ; Mice ; Mutation ; Pituitary Gland/chemistry/cytology/*embryology ; Pituitary Hormones/analysis/genetics ; Stem Cells/cytology ; *Transcription Factors
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 47
    Publikationsdatum: 1997-10-06
    Beschreibung: Apoptosis of mouse neocortical neurons induced by serum deprivation or by staurosporine was associated with an early enhancement of delayed rectifier (IK) current and loss of total intracellular K+. This IK augmentation was not seen in neurons undergoing excitotoxic necrosis or in older neurons resistant to staurosporine-induced apoptosis. Attenuating outward K+ current with tetraethylammonium or elevated extracellular K+, but not blockers of Ca2+, Cl-, or other K+ channels, reduced apoptosis, even if associated increases in intracellular Ca2+ concentration were prevented. Furthermore, exposure to the K+ ionophore valinomycin or the K+-channel opener cromakalim induced apoptosis. Enhanced K+ efflux may mediate certain forms of neuronal apoptosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yu, S P -- Yeh, C H -- Sensi, S L -- Gwag, B J -- Canzoniero, L M -- Farhangrazi, Z S -- Ying, H S -- Tian, M -- Dugan, L L -- Choi, D W -- 30337/PHS HHS/ -- New York, N.Y. -- Science. 1997 Oct 3;278(5335):114-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for the Study of Nervous System Injury and Department of Neurology, Washington University School of Medicine, St. Louis, MO 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9311914" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acid Chloromethyl Ketones/pharmacology ; Animals ; *Apoptosis/drug effects ; Benzopyrans/pharmacology ; Calcium/metabolism ; Cerebral Cortex/cytology ; Cromakalim ; Cycloheximide/pharmacology ; Cysteine Proteinase Inhibitors/pharmacology ; Gadolinium/pharmacology ; Mice ; N-Methylaspartate/pharmacology ; Neurons/*cytology/metabolism ; Neuroprotective Agents/pharmacology ; Nifedipine/pharmacology ; Patch-Clamp Techniques ; Potassium/*metabolism ; Potassium Channels/drug effects/*metabolism ; Pyrroles/pharmacology ; Staurosporine/pharmacology ; Tetraethylammonium ; Tetraethylammonium Compounds/pharmacology ; Veratridine/pharmacology
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 48
    Publikationsdatum: 1997-01-31
    Beschreibung: The regulation of the serine-threonine kinase Akt by lipid products of phosphoinositide 3-kinase (PI 3-kinase) was investigated. Akt activity was found to correlate with the amount of phosphatidylinositol-3,4-bisphosphate (PtdIns-3,4-P2) in vivo, and synthetic PtdIns-3,4-P2 activated Akt both in vitro and in vivo. Binding of PtdIns-3,4-P2 occurred within the Akt pleckstrin homology (PH) domain and facilitated dimerization of Akt. Akt mutated in the PH domain was not activated by PI 3-kinase in vivo or by PtdIns-3, 4-P2 in vitro, and it was impaired in binding to PtdIns-3,4-P2. Examination of the binding to other phosphoinositides revealed that they bound to the Akt PH domain with much lower affinity than did PtdIns-3,4-P2 and failed to increase Akt activity. Thus, Akt is apparently regulated by the direct interaction of PtdIns-3,4-P2 with the Akt PH domain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Franke, T F -- Kaplan, D R -- Cantley, L C -- Toker, A -- GM41890/GM/NIGMS NIH HHS/ -- N01-CO-74101/CO/NCI NIH HHS/ -- R01 GM041890/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1997 Jan 31;275(5300):665-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉ABL-Basic Research Program, National Cancer Institute-Frederick Cancer Research Facility and Development Center (NCI-FCRFDC), Frederick, MD 21702, USA. tfranke@bidmc.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9005852" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): 3T3 Cells ; Animals ; COS Cells ; Dimerization ; Enzyme Activation ; Mice ; Phosphatidylinositol 3-Kinases ; Phosphatidylinositol Phosphates/*metabolism/pharmacology ; Phosphorylation ; Phosphotransferases (Alcohol Group Acceptor)/metabolism ; Platelet-Derived Growth Factor/pharmacology ; Point Mutation ; Protein-Serine-Threonine Kinases/chemistry/genetics/*metabolism ; Proto-Oncogene Proteins/chemistry/genetics/*metabolism ; Proto-Oncogene Proteins c-akt ; Recombinant Fusion Proteins/chemistry/metabolism
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 49
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 1997-10-23
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Freitas, A A -- Rocha, B -- New York, N.Y. -- Science. 1997 Sep 26;277(5334):1950.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratoire des Dynamiques Lymphocytaires, Institut Pasteur CNRS URA 1961, 75015 Paris, France. afreitas@pasteur.fr〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9333949" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Apoptosis ; CD8-Positive T-Lymphocytes/cytology/immunology ; Cell Survival ; Histocompatibility Antigens Class I/physiology ; Histocompatibility Antigens Class II/physiology ; Immunologic Memory ; Kruppel-Like Transcription Factors ; Lymphocyte Activation ; Mice ; T-Lymphocytes/*cytology/*immunology/metabolism ; Trans-Activators/*physiology ; Zinc Fingers
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 50
    Publikationsdatum: 1997-04-25
    Beschreibung: ARIA (for acetylcholine receptor-inducing activity), a protein purified on the basis of its ability to stimulate acetylcholine receptor (AChR) synthesis in cultured myotubes, is a member of the neuregulin family and is present at motor endplates. This suggests an important role for neuregulins in mediating the nerve-dependent accumulation of AChRs in the postsynaptic membrane. Nerve-muscle synapses have now been analyzed in neuregulin-deficient animals. Mice that are heterozygous for the deletion of neuregulin isoforms containing an immunoglobulin-like domain are myasthenic. Postsynaptic AChR density is significantly reduced, as judged by the decrease in the mean amplitude of spontaneous miniature endplate potentials and bungarotoxin binding. On the other hand, the mean amplitude of evoked endplate potentials was not decreased, due to an increase in the number of quanta released per impulse, a compensation that has been observed in other myasthenic states. Thus, the density of AChRs in the postsynaptic membrane depends on immunoglobulin-containing neuregulin isoforms throughout the life of the animal.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sandrock, A W Jr -- Dryer, S E -- Rosen, K M -- Gozani, S N -- Kramer, R -- Theill, L E -- Fischbach, G D -- K08-NS01580/NS/NINDS NIH HHS/ -- R01-NS18458/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1997 Apr 25;276(5312):599-603.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9110980" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Acetylcholine/metabolism ; Animals ; Bungarotoxins/metabolism ; Glycoproteins/genetics/*physiology ; Heterozygote ; Immunoglobulins/analysis ; In Vitro Techniques ; Membrane Potentials ; Mice ; Motor Endplate/metabolism/physiology ; Muscle Weakness/etiology ; Nerve Tissue Proteins/genetics/*physiology ; Neuregulin-1 ; Neuregulins ; Neuromuscular Junction/*metabolism ; Receptors, Cholinergic/genetics/*metabolism ; Synaptic Transmission
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 51
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 1997-03-14
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gallagher, R -- New York, N.Y. -- Science. 1997 Mar 14;275(5306):1615.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9072827" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Humans ; Immunophenotyping ; Interferons/pharmacology ; Interleukin-12/pharmacology ; Mice ; Receptors, Interleukin/*analysis/biosynthesis ; Receptors, Interleukin-12 ; Th2 Cells/*immunology
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 52
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 1997-06-20
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gallagher, R B -- New York, N.Y. -- Science. 1997 Jun 20;276(5320):1817.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9206842" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; B-Lymphocytes/*cytology/immunology/physiology ; Gene Rearrangement ; Genes, Immunoglobulin ; Homeostasis ; Lymphocyte Count ; Mice ; Mice, Transgenic ; Receptors, Antigen, B-Cell/analysis
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 53
    Publikationsdatum: 1997-12-31
    Beschreibung: The lethal yellow (AY/a) mouse has a defect in proopiomelanocortin (POMC) signaling in the brain that leads to obesity, and is resistant to the anorexigenic effects of the hormone leptin. It has been proposed that the weight-reducing effects of leptin are thus transmitted primarily by way of POMC neurons. However, the central effects of defective POMC signaling, and the absence of leptin, on weight gain in double-mutant lethal yellow (AY/a) leptin-deficient (lepob/lepob) mice were shown to be independent and additive. Furthermore, deletion of the leptin gene restored leptin sensitivity to AY/a mice. This result implies that in the AY/a mouse, obesity is independent of leptin action, and resistance to leptin results from desensitization of leptin signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Boston, B A -- Blaydon, K M -- Varnerin, J -- Cone, R D -- DK/AR517330/DK/NIDDK NIH HHS/ -- DK02404/DK/NIDDK NIH HHS/ -- HD33703/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1997 Nov 28;278(5343):1641-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatrics, Oregon Health Sciences University, Portland, OR 97201, USA. Laboratories, Rahway, NJ 07065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9374468" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adrenalectomy ; Agouti Signaling Protein ; Alleles ; Animals ; Arcuate Nucleus of Hypothalamus/*metabolism ; Blood Glucose/analysis ; Corticosterone/blood ; Crosses, Genetic ; Eating/drug effects ; Energy Metabolism ; Female ; Homeostasis ; Insulin/blood ; *Intercellular Signaling Peptides and Proteins ; Leptin ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Obese ; Neurons/metabolism ; Obesity/genetics/*metabolism ; Pro-Opiomelanocortin/*metabolism ; Proteins/genetics/*metabolism/pharmacology ; Signal Transduction ; Weight Gain
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 54
    Publikationsdatum: 2005-12-03
    Beschreibung: Macrophages and dendritic cells (DCs) are crucial for immune and inflammatory responses and belong to a network of cells that has been termed the mononuclear phagocyte system (MPS). However, the origin and lineage of these cells remain poorly understood. Here, we describe the isolation and clonal analysis of a mouse bone marrow progenitor that is specific for monocytes, several macrophage subsets, and resident spleen DCs in vivo. It was also possible to recapitulate this differentiation in vitro by using treatment with the cytokines macrophage colony-stimulating factor and granulocyte-macrophage colony-stimulating factor. Thus, macrophages and DCs appear to renew from a common progenitor, providing a cellular and molecular basis for the concept of the MPS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fogg, Darin K -- Sibon, Claire -- Miled, Chaouki -- Jung, Steffen -- Aucouturier, Pierre -- Littman, Dan R -- Cumano, Ana -- Geissmann, Frederic -- A133856/PHS HHS/ -- G0900867/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2006 Jan 6;311(5757):83-7. Epub 2005 Dec 1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉INSERM, Laboratory of Mononuclear Phagocyte Biology, Avenir Team, Necker Enfants Malades Institute, 75015 Paris, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16322423" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Cell Differentiation ; Cell Lineage ; Cell Separation ; Clone Cells ; Colony-Stimulating Factors/pharmacology ; Dendritic Cells/*cytology ; Flow Cytometry ; Granulocyte Colony-Stimulating Factor/pharmacology ; Hematopoietic Stem Cell Transplantation ; Macrophage Colony-Stimulating Factor/pharmacology ; Macrophages/*cytology ; Mice ; Mice, Inbred C57BL ; Myeloid Progenitor Cells/*cytology/immunology ; Proto-Oncogene Proteins c-kit/analysis ; Receptors, Cytokine/analysis ; Receptors, HIV/analysis ; Recombinant Proteins ; Spleen/cytology
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 55
    Publikationsdatum: 2011-07-19
    Beschreibung: Until recently, large apex consumers were ubiquitous across the globe and had been for millions of years. The loss of these animals may be humankind's most pervasive influence on nature. Although such losses are widely viewed as an ethical and aesthetic problem, recent research reveals extensive cascading effects of their disappearance in marine, terrestrial, and freshwater ecosystems worldwide. This empirical work supports long-standing theory about the role of top-down forcing in ecosystems but also highlights the unanticipated impacts of trophic cascades on processes as diverse as the dynamics of disease, wildfire, carbon sequestration, invasive species, and biogeochemical cycles. These findings emphasize the urgent need for interdisciplinary research to forecast the effects of trophic downgrading on process, function, and resilience in global ecosystems.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Estes, James A -- Terborgh, John -- Brashares, Justin S -- Power, Mary E -- Berger, Joel -- Bond, William J -- Carpenter, Stephen R -- Essington, Timothy E -- Holt, Robert D -- Jackson, Jeremy B C -- Marquis, Robert J -- Oksanen, Lauri -- Oksanen, Tarja -- Paine, Robert T -- Pikitch, Ellen K -- Ripple, William J -- Sandin, Stuart A -- Scheffer, Marten -- Schoener, Thomas W -- Shurin, Jonathan B -- Sinclair, Anthony R E -- Soule, Michael E -- Virtanen, Risto -- Wardle, David A -- New York, N.Y. -- Science. 2011 Jul 15;333(6040):301-6. doi: 10.1126/science.1205106.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Ecology and Evolutionary Biology, University of California, Santa Cruz, CA 95060, USA. jestes@ucsc.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21764740" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Biodiversity ; *Ecosystem ; *Extinction, Biological ; Feeding Behavior ; *Food Chain ; Humans ; Introduced Species ; Population Dynamics ; Predatory Behavior
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 56
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    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2011-02-05
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ebert, Dieter -- New York, N.Y. -- Science. 2011 Feb 4;331(6017):539-40. doi: 10.1126/science.1202092.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Universitat Basel, Zoological Institute, Vesalgasse 1, 4059 Basel, Switzerland. dieter.ebert@unibas.ch〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21292957" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adaptation, Physiological ; Animals ; *Biological Evolution ; Daphnia/*genetics/physiology ; *Ecosystem ; *Environment ; Evolution, Molecular ; *Gene Duplication ; *Genome ; Phenotype
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  • 57
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    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2011-09-03
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stone, Richard -- New York, N.Y. -- Science. 2011 Sep 2;333(6047):1210-1. doi: 10.1126/science.333.6047.1210.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21885748" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Angiosperms/growth & development ; China ; *Ecosystem ; Eutrophication ; *Fresh Water/chemistry/microbiology ; *Harmful Algal Bloom ; Microcystis/*growth & development ; Potamogetonaceae/growth & development ; Water Pollutants, Chemical/*toxicity ; Water Pollution/economics/*prevention & control ; Water Supply
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 58
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2011-09-03
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stone, Richard -- New York, N.Y. -- Science. 2011 Sep 2;333(6047):1209. doi: 10.1126/science.333.6047.1209.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21885747" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Actinobacteria/*isolation & purification ; *Archaea/isolation & purification/physiology ; Bacteroidetes/*isolation & purification ; China ; *Ecosystem ; Food Chain ; Hot Springs/*microbiology
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 59
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    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2011-08-13
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stone, Richard -- New York, N.Y. -- Science. 2011 Aug 12;333(6044):817. doi: 10.1126/science.333.6044.817.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21835994" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; China/epidemiology ; *Ecosystem ; *Energy-Generating Resources ; *Environment ; Humans ; *Rivers ; Schistosomiasis/epidemiology/transmission ; Snails ; Water Movements
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 60
    Publikationsdatum: 2011-11-05
    Beschreibung: Climate change challenges organisms to adapt or move to track changes in environments in space and time. We used two measures of thermal shifts from analyses of global temperatures over the past 50 years to describe the pace of climate change that species should track: the velocity of climate change (geographic shifts of isotherms over time) and the shift in seasonal timing of temperatures. Both measures are higher in the ocean than on land at some latitudes, despite slower ocean warming. These indices give a complex mosaic of predicted range shifts and phenology changes that deviate from simple poleward migration and earlier springs or later falls. They also emphasize potential conservation concerns, because areas of high marine biodiversity often have greater velocities of climate change and seasonal shifts.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Burrows, Michael T -- Schoeman, David S -- Buckley, Lauren B -- Moore, Pippa -- Poloczanska, Elvira S -- Brander, Keith M -- Brown, Chris -- Bruno, John F -- Duarte, Carlos M -- Halpern, Benjamin S -- Holding, Johnna -- Kappel, Carrie V -- Kiessling, Wolfgang -- O'Connor, Mary I -- Pandolfi, John M -- Parmesan, Camille -- Schwing, Franklin B -- Sydeman, William J -- Richardson, Anthony J -- New York, N.Y. -- Science. 2011 Nov 4;334(6056):652-5. doi: 10.1126/science.1210288.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Ecology, Scottish Association for Marine Science, Scottish Marine Institute, Oban, Argyll, PA37 1QA, Scotland, UK. michael.burrows@sams.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22053045" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Biodiversity ; *Climate Change ; *Ecosystem ; Oceans and Seas ; Seasons
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 61
    Publikationsdatum: 2011-05-21
    Beschreibung: The interrelationships between our diets and the structure and operations of our gut microbial communities are poorly understood. A model community of 10 sequenced human gut bacteria was introduced into gnotobiotic mice, and changes in species abundance and microbial gene expression were measured in response to randomized perturbations of four defined ingredients in the host diet. From the responses, we developed a statistical model that predicted over 60% of the variation in species abundance evoked by diet perturbations, and we were able to identify which factors in the diet best explained changes seen for each community member. The approach is generally applicable, as shown by a follow-up study involving diets containing various mixtures of pureed human baby foods.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3303606/" 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/PMC3303606/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Faith, Jeremiah J -- McNulty, Nathan P -- Rey, Federico E -- Gordon, Jeffrey I -- DK30292/DK/NIDDK NIH HHS/ -- DK70977/DK/NIDDK NIH HHS/ -- R01 DK070977/DK/NIDDK NIH HHS/ -- R01 DK070977-08/DK/NIDDK NIH HHS/ -- R37 DK030292/DK/NIDDK NIH HHS/ -- R37 DK030292-31/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2011 Jul 1;333(6038):101-4. doi: 10.1126/science.1206025. Epub 2011 May 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Genome Sciences and Systems Biology, Washington University School of Medicine, St. Louis, MO 63108, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21596954" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Bacteroides/genetics/physiology ; Biomass ; Caseins/administration & dosage ; Desulfovibrio/genetics/physiology ; *Diet ; Dietary Carbohydrates/administration & dosage ; Dietary Fats, Unsaturated/administration & dosage ; Dietary Proteins/administration & dosage ; Dietary Sucrose/administration & dosage ; Escherichia coli/genetics/physiology ; Feces/*microbiology ; Gastrointestinal Tract/*microbiology ; Gene Expression Profiling ; Gene Expression Regulation, Bacterial ; *Germ-Free Life ; Gram-Negative Bacteria/*physiology ; Gram-Positive Bacteria/genetics/*physiology ; Humans ; Infant ; Infant Food ; Linear Models ; Male ; *Metagenome ; Mice ; Mice, Inbred C57BL ; Models, Animal
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 62
    Publikationsdatum: 2011-11-15
    Beschreibung: Intestinal epithelial stem cell identity and location have been the subject of substantial research. Cells in the +4 niche are slow-cycling and label-retaining, whereas a different stem cell niche located at the crypt base is occupied by crypt base columnar (CBC) cells. CBCs are distinct from +4 cells, and the relationship between them is unknown, though both give rise to all intestinal epithelial lineages. We demonstrate that Hopx, an atypical homeobox protein, is a specific marker of +4 cells. Hopx-expressing cells give rise to CBCs and all mature intestinal epithelial lineages. Conversely, CBCs can give rise to +4 Hopx-positive cells. These findings demonstrate a bidirectional lineage relationship between active and quiescent stem cells in their niches.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3705713/" 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/PMC3705713/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Takeda, Norifumi -- Jain, Rajan -- LeBoeuf, Matthew R -- Wang, Qiaohong -- Lu, Min Min -- Epstein, Jonathan A -- R01 HL071546/HL/NHLBI NIH HHS/ -- U01 HL100405/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2011 Dec 9;334(6061):1420-4. doi: 10.1126/science.1213214. Epub 2011 Nov 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell and Developmental Biology, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22075725" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Cell Cycle ; Cell Differentiation ; Cell Lineage ; Cell Proliferation ; Cells, Cultured ; Epithelial Cells/*cytology ; Homeodomain Proteins/analysis/genetics ; Intestinal Mucosa/*cytology/drug effects ; Intestine, Small/*cytology/drug effects ; Mice ; Models, Biological ; Multipotent Stem Cells/*cytology/physiology ; Paneth Cells/cytology ; *Stem Cell Niche ; Tamoxifen/pharmacology
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 63
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2011-10-25
    Beschreibung: Spatial representation is an active process that requires complex multimodal integration from a large interacting network of cortical and subcortical structures. We sought to determine the role of cerebellar protein kinase C (PKC)-dependent plasticity in spatial navigation by recording the activity of hippocampal place cells in transgenic L7PKCI mice with selective disruption of PKC-dependent plasticity at parallel fiber-Purkinje cell synapses. Place cell properties were exclusively impaired when L7PKCI mice had to rely on self-motion cues. The behavioral consequence of such a deficit is evidenced here by selectively impaired navigation capabilities during a path integration task. Together, these results suggest that cerebellar PKC-dependent mechanisms are involved in processing self-motion signals essential to the shaping of hippocampal spatial representation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rochefort, Christelle -- Arabo, Arnaud -- Andre, Marion -- Poucet, Bruno -- Save, Etienne -- Rondi-Reig, Laure -- New York, N.Y. -- Science. 2011 Oct 21;334(6054):385-9. doi: 10.1126/science.1207403.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neurobiologie des Processus Adaptatifs (UMR 7102), Navigation, Memory, and Aging (ENMVI) Team, Universite Pierre et Marie Curie-Centre National de la Recherche Scientifique (CNRS), F-75005 Paris, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22021859" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; CA1 Region, Hippocampal/cytology/*physiology ; Cerebellum/enzymology/*physiology ; Cues ; Darkness ; *Long-Term Synaptic Depression ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; *Motor Activity ; *Orientation ; Protein Kinase C/antagonists & inhibitors/metabolism ; Purkinje Cells/physiology ; Pyramidal Cells/*physiology ; *Space Perception
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 64
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2011-09-03
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nabel, Christopher S -- Kohli, Rahul M -- New York, N.Y. -- Science. 2011 Sep 2;333(6047):1229-30. doi: 10.1126/science.1211917.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21885763" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): 5-Methylcytosine/*metabolism ; Animals ; Cytosine/*analogs & derivatives/metabolism ; DNA/*metabolism ; DNA Methylation ; DNA-Binding Proteins/genetics/*metabolism ; Embryonic Stem Cells/metabolism ; Mice ; Oxidation-Reduction ; Proto-Oncogene Proteins/genetics/*metabolism ; Thymine DNA Glycosylase/metabolism
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 65
    Publikationsdatum: 2011-02-12
    Beschreibung: The identities of the digits of the avian forelimb are disputed. Whereas paleontological findings support the position that the digits correspond to digits one, two, and three, embryological evidence points to digit two, three, and four identities. By using transplantation and cell-labeling experiments, we found that the posteriormost digit in the wing does not correspond to digit four in the hindlimb; its progenitor segregates early from the zone of polarizing activity, placing it in the domain of digit three specification. We suggest that an avian-specific shift uncouples the digit anlagen from the molecular mechanisms that pattern them, resulting in the imposition of digit one, two, and three identities on the second, third, and fourth anlagens.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tamura, Koji -- Nomura, Naoki -- Seki, Ryohei -- Yonei-Tamura, Sayuri -- Yokoyama, Hitoshi -- New York, N.Y. -- Science. 2011 Feb 11;331(6018):753-7. doi: 10.1126/science.1198229.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Developmental Biology and Neurosciences, Graduate School of Life Sciences, Tohoku University, Aobayama, Aoba-ku, Sendai 980-8578, Japan. tam@m.tohoku.ac.jp〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21311019" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Biological Evolution ; Chick Embryo/*embryology ; Coturnix/*embryology ; Forelimb/embryology/transplantation ; Hedgehog Proteins/metabolism ; Hindlimb/embryology/transplantation ; Limb Buds/embryology ; Mice ; Signal Transduction ; Toes/embryology ; Wings, Animal/*embryology
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 66
    Publikationsdatum: 2011-04-16
    Beschreibung: Transforming growth factor-beta (TGFbeta) signaling drives aneurysm progression in multiple disorders, including Marfan syndrome (MFS), and therapies that inhibit this signaling cascade are in clinical trials. TGFbeta can stimulate multiple intracellular signaling pathways, but it is unclear which of these pathways drives aortic disease and, when inhibited, which result in disease amelioration. Here we show that extracellular signal-regulated kinase (ERK) 1 and 2 and Smad2 are activated in a mouse model of MFS, and both are inhibited by therapies directed against TGFbeta. Whereas selective inhibition of ERK1/2 activation ameliorated aortic growth, Smad4 deficiency exacerbated aortic disease and caused premature death in MFS mice. Smad4-deficient MFS mice uniquely showed activation of Jun N-terminal kinase-1 (JNK1), and a JNK antagonist ameliorated aortic growth in MFS mice that lacked or retained full Smad4 expression. Thus, noncanonical (Smad-independent) TGFbeta signaling is a prominent driver of aortic disease in MFS mice, and inhibition of the ERK1/2 or JNK1 pathways is a potential therapeutic strategy for the disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3111087/" 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/PMC3111087/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Holm, Tammy M -- Habashi, Jennifer P -- Doyle, Jefferson J -- Bedja, Djahida -- Chen, YiChun -- van Erp, Christel -- Lindsay, Mark E -- Kim, David -- Schoenhoff, Florian -- Cohn, Ronald D -- Loeys, Bart L -- Thomas, Craig J -- Patnaik, Samarjit -- Marugan, Juan J -- Judge, Daniel P -- Dietz, Harry C -- P01 AR049698/AR/NIAMS NIH HHS/ -- P01 AR049698-07/AR/NIAMS NIH HHS/ -- R01 AR041135/AR/NIAMS NIH HHS/ -- R01 AR041135-12/AR/NIAMS NIH HHS/ -- R01 AR041135-17/AR/NIAMS NIH HHS/ -- Howard Hughes Medical Institute/ -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2011 Apr 15;332(6027):358-61. doi: 10.1126/science.1192149.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21493862" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Anthracenes/pharmacology/therapeutic use ; Aorta/pathology ; Aortic Aneurysm/*metabolism/pathology/physiopathology/prevention & control ; Diphenylamine/analogs & derivatives/pharmacology/therapeutic use ; Disease Models, Animal ; Disease Progression ; Enzyme Activation ; Losartan/pharmacology/therapeutic use ; *MAP Kinase Signaling System ; Marfan Syndrome/drug therapy/*metabolism/pathology ; Mice ; Mitogen-Activated Protein Kinase 1/antagonists & inhibitors/*metabolism ; Mitogen-Activated Protein Kinase 3/antagonists & inhibitors/*metabolism ; Mitogen-Activated Protein Kinase 8/antagonists & inhibitors/metabolism ; Protein Kinase Inhibitors/pharmacology/therapeutic use ; Smad2 Protein/metabolism ; Smad4 Protein/deficiency/genetics ; Sulfonamides/pharmacology/therapeutic use ; Transforming Growth Factor beta/antagonists & inhibitors/immunology/*metabolism
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 67
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2011-04-23
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nair, Gautham -- Raj, Arjun -- New York, N.Y. -- Science. 2011 Apr 22;332(6028):431-2. doi: 10.1126/science.1205995.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Bioengineering, University of Pennsylvania, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21512026" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; DNA-Directed RNA Polymerases/metabolism ; Fibroblasts ; *Gene Expression ; *Gene Silencing ; Genes, Fungal ; Kinetics ; Mice ; Models, Genetic ; RNA, Messenger/*genetics/metabolism ; Signal Processing, Computer-Assisted ; Stochastic Processes ; *Transcription, Genetic ; *Transcriptional Activation ; Yeasts/genetics
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 68
    Publikationsdatum: 2011-03-12
    Beschreibung: The growth factor progranulin (PGRN) has been implicated in embryonic development, tissue repair, tumorigenesis, and inflammation, but its receptors remain unidentified. We report that PGRN bound directly to tumor necrosis factor receptors (TNFRs) and disturbed the TNFalpha-TNFR interaction. PGRN-deficient mice were susceptible to collagen-induced arthritis, and administration of PGRN reversed inflammatory arthritis. Atsttrin, an engineered protein composed of three PGRN fragments, exhibited selective TNFR binding. PGRN and Atsttrin prevented inflammation in multiple arthritis mouse models and inhibited TNFalpha-activated intracellular signaling. Collectively, these findings demonstrate that PGRN is a ligand of TNFR, an antagonist of TNFalpha signaling, and plays a critical role in the pathogenesis of inflammatory arthritis in mice. They also suggest new potential therapeutic interventions for various TNFalpha-mediated pathologies and conditions, including rheumatoid arthritis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3104397/" 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/PMC3104397/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tang, Wei -- Lu, Yi -- Tian, Qing-Yun -- Zhang, Yan -- Guo, Feng-Jin -- Liu, Guang-Yi -- Syed, Nabeel Muzaffar -- Lai, Yongjie -- Lin, Edward Alan -- Kong, Li -- Su, Jeffrey -- Yin, Fangfang -- Ding, Ai-Hao -- Zanin-Zhorov, Alexandra -- Dustin, Michael L -- Tao, Jian -- Craft, Joseph -- Yin, Zhinan -- Feng, Jian Q -- Abramson, Steven B -- Yu, Xiu-Ping -- Liu, Chuan-ju -- AI43542/AI/NIAID NIH HHS/ -- AR040072/AR/NIAMS NIH HHS/ -- AR050620/AR/NIAMS NIH HHS/ -- AR053210/AR/NIAMS NIH HHS/ -- GM061710/GM/NIGMS NIH HHS/ -- R01 AI030165/AI/NIAID NIH HHS/ -- R01 AI030165-20/AI/NIAID NIH HHS/ -- R01 GM061710/GM/NIGMS NIH HHS/ -- R01 GM061710-08/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2011 Apr 22;332(6028):478-84. doi: 10.1126/science.1199214. Epub 2011 Mar 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Orthopaedic Surgery, New York University School of Medicine and NYU Hospital for Joint Diseases, New York, NY 10003, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21393509" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adolescent ; Adult ; Aged ; Animals ; Anti-Inflammatory Agents, Non-Steroidal/metabolism/pharmacology/therapeutic use ; Arthritis, Experimental/*drug therapy/*immunology/pathology/physiopathology ; Cartilage, Articular/metabolism/pathology ; Female ; Humans ; Intercellular Signaling Peptides and ; Proteins/chemistry/genetics/*metabolism/therapeutic use ; Ligands ; Male ; Mice ; Mice, Inbred Strains ; Mice, Knockout ; Mice, Transgenic ; Middle Aged ; Protein Interaction Domains and Motifs ; Receptors, Tumor Necrosis Factor, Type I/genetics/*metabolism ; Receptors, Tumor Necrosis Factor, Type II/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism/pharmacology/therapeutic use ; Recombinant Proteins/therapeutic use ; Signal Transduction ; T-Lymphocytes, Regulatory/immunology/physiology ; Tumor Necrosis Factor-alpha/*metabolism ; Young Adult
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  • 69
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2011-04-16
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Reardon, Sara -- New York, N.Y. -- Science. 2011 Apr 15;332(6027):292. doi: 10.1126/science.332.6027.292.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21493831" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Aquatic Organisms/*metabolism/*radiation effects ; *Ecosystem ; Food Chain ; Japan ; Pacific Ocean ; Phytoplankton/metabolism/radiation effects ; Radiation Dosage ; *Radioisotopes/pharmacokinetics/toxicity ; Seaweed/metabolism/radiation effects ; *Water Pollutants, Radioactive/pharmacokinetics/toxicity
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 70
    Publikationsdatum: 2011-03-12
    Beschreibung: Disruption of the circadian clock exacerbates metabolic diseases, including obesity and diabetes. We show that histone deacetylase 3 (HDAC3) recruitment to the genome displays a circadian rhythm in mouse liver. Histone acetylation is inversely related to HDAC3 binding, and this rhythm is lost when HDAC3 is absent. Although amounts of HDAC3 are constant, its genomic recruitment in liver corresponds to the expression pattern of the circadian nuclear receptor Rev-erbalpha. Rev-erbalpha colocalizes with HDAC3 near genes regulating lipid metabolism, and deletion of HDAC3 or Rev-erbalpha in mouse liver causes hepatic steatosis. Thus, genomic recruitment of HDAC3 by Rev-erbalpha directs a circadian rhythm of histone acetylation and gene expression required for normal hepatic lipid homeostasis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3389392/" 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/PMC3389392/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Feng, Dan -- Liu, Tao -- Sun, Zheng -- Bugge, Anne -- Mullican, Shannon E -- Alenghat, Theresa -- Liu, X Shirley -- Lazar, Mitchell A -- DK19525/DK/NIDDK NIH HHS/ -- DK43806/DK/NIDDK NIH HHS/ -- DK45586/DK/NIDDK NIH HHS/ -- DK49210/DK/NIDDK NIH HHS/ -- HG4069/HG/NHGRI NIH HHS/ -- P30 DK019525/DK/NIDDK NIH HHS/ -- R01 DK045586/DK/NIDDK NIH HHS/ -- R37 DK043806/DK/NIDDK NIH HHS/ -- R37 DK043806-20/DK/NIDDK NIH HHS/ -- RC1 DK086239/DK/NIDDK NIH HHS/ -- RC1DK08623/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2011 Mar 11;331(6022):1315-9. doi: 10.1126/science.1198125.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21393543" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Binding Sites ; Chromatin Immunoprecipitation ; Chronobiology Disorders/genetics/metabolism ; *Circadian Clocks ; *Circadian Rhythm ; DNA/metabolism ; Epigenesis, Genetic ; Fatty Liver/*metabolism ; Gene Expression Regulation ; *Genome ; Histone Deacetylases/*metabolism ; Histones/metabolism ; Homeostasis ; *Lipid Metabolism ; Lipogenesis/genetics ; Liver/*metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Molecular Sequence Data ; Nuclear Receptor Co-Repressor 1/metabolism ; Nuclear Receptor Subfamily 1, Group D, Member 1/genetics/metabolism ; RNA Polymerase II/metabolism ; Up-Regulation
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 71
    Publikationsdatum: 2011-09-17
    Beschreibung: Neural circuits regulate cytokine production to prevent potentially damaging inflammation. A prototypical vagus nerve circuit, the inflammatory reflex, inhibits tumor necrosis factor-alpha production in spleen by a mechanism requiring acetylcholine signaling through the alpha7 nicotinic acetylcholine receptor expressed on cytokine-producing macrophages. Nerve fibers in spleen lack the enzymatic machinery necessary for acetylcholine production; therefore, how does this neural circuit terminate in cholinergic signaling? We identified an acetylcholine-producing, memory phenotype T cell population in mice that is integral to the inflammatory reflex. These acetylcholine-producing T cells are required for inhibition of cytokine production by vagus nerve stimulation. Thus, action potentials originating in the vagus nerve regulate T cells, which in turn produce the neurotransmitter, acetylcholine, required to control innate immune responses.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4548937/" 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/PMC4548937/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rosas-Ballina, Mauricio -- Olofsson, Peder S -- Ochani, Mahendar -- Valdes-Ferrer, Sergio I -- Levine, Yaakov A -- Reardon, Colin -- Tusche, Michael W -- Pavlov, Valentin A -- Andersson, Ulf -- Chavan, Sangeeta -- Mak, Tak W -- Tracey, Kevin J -- R01 GM057226/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2011 Oct 7;334(6052):98-101. doi: 10.1126/science.1209985. Epub 2011 Sep 15.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Biomedical Science, The Feinstein Institute for Medical Research, 350 Community Drive, Manhasset, New York 11030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21921156" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Acetylcholine/*biosynthesis ; Action Potentials ; Animals ; CD4-Positive T-Lymphocytes/*immunology/*metabolism ; Choline O-Acetyltransferase/metabolism ; Cholinergic Agents/metabolism ; Female ; *Immunity, Innate ; Immunologic Memory ; Inflammation ; Lymphocyte Activation ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; *Neuroimmunomodulation ; Norepinephrine/pharmacology ; Receptors, Nicotinic/metabolism ; Signal Transduction ; Spleen/immunology/innervation/metabolism ; T-Lymphocyte Subsets/immunology/metabolism ; Tumor Necrosis Factor-alpha/blood ; Vagus Nerve/*physiology ; Vagus Nerve Stimulation ; alpha7 Nicotinic Acetylcholine Receptor
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 72
    Publikationsdatum: 2011-04-23
    Beschreibung: Protein synthesis and autophagic degradation are regulated in an opposite manner by mammalian target of rapamycin (mTOR), whereas under certain conditions it would be beneficial if they occurred in unison to handle rapid protein turnover. We observed a distinct cellular compartment at the trans side of the Golgi apparatus, the TOR-autophagy spatial coupling compartment (TASCC), where (auto)lysosomes and mTOR accumulated during Ras-induced senescence. mTOR recruitment to the TASCC was amino acid- and Rag guanosine triphosphatase-dependent, and disruption of mTOR localization to the TASCC suppressed interleukin-6/8 synthesis. TASCC formation was observed during macrophage differentiation and in glomerular podocytes; both displayed increased protein secretion. The spatial coupling of cells' catabolic and anabolic machinery could augment their respective functions and facilitate the mass synthesis of secretory proteins.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3426290/" 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/PMC3426290/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Narita, Masako -- Young, Andrew R J -- Arakawa, Satoko -- Samarajiwa, Shamith A -- Nakashima, Takayuki -- Yoshida, Sei -- Hong, Sungki -- Berry, Lorraine S -- Reichelt, Stefanie -- Ferreira, Manuela -- Tavare, Simon -- Inoki, Ken -- Shimizu, Shigeomi -- Narita, Masashi -- DK083491/DK/NIDDK NIH HHS/ -- R01 DK083491/DK/NIDDK NIH HHS/ -- R01 DK083491-03/DK/NIDDK NIH HHS/ -- Cancer Research UK/United Kingdom -- New York, N.Y. -- Science. 2011 May 20;332(6032):966-70. doi: 10.1126/science.1205407. Epub 2011 Apr 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Research UK Cambridge Research Institute (CRI), Li Ka Shing Centre, Robinson Way, Cambridge CB2 0RE, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21512002" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acids/metabolism ; Animals ; *Autophagy ; *Cell Aging ; Cell Line ; Cytoplasm/metabolism ; Cytoplasmic Vesicles/*metabolism/ultrastructure ; Endoplasmic Reticulum, Rough/ultrastructure ; Genes, ras ; Golgi Apparatus/ultrastructure ; HL-60 Cells ; Humans ; Interleukin-6/metabolism ; Interleukin-8/metabolism ; Lysosomes/metabolism/ultrastructure ; Mice ; Monomeric GTP-Binding Proteins/genetics/metabolism ; Nocodazole/pharmacology ; Phagosomes/metabolism/ultrastructure ; Phenotype ; Podocytes/metabolism/ultrastructure ; Protein Biosynthesis ; Proteins/*secretion ; TOR Serine-Threonine Kinases/*metabolism ; Vacuoles/ultrastructure ; trans-Golgi Network/metabolism/ultrastructure
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 73
    Publikationsdatum: 2011-07-23
    Beschreibung: 5-methylcytosine (5mC) in DNA plays an important role in gene expression, genomic imprinting, and suppression of transposable elements. 5mC can be converted to 5-hydroxymethylcytosine (5hmC) by the Tet (ten eleven translocation) proteins. Here, we show that, in addition to 5hmC, the Tet proteins can generate 5-formylcytosine (5fC) and 5-carboxylcytosine (5caC) from 5mC in an enzymatic activity-dependent manner. Furthermore, we reveal the presence of 5fC and 5caC in genomic DNA of mouse embryonic stem cells and mouse organs. The genomic content of 5hmC, 5fC, and 5caC can be increased or reduced through overexpression or depletion of Tet proteins. Thus, we identify two previously unknown cytosine derivatives in genomic DNA as the products of Tet proteins. Our study raises the possibility that DNA demethylation may occur through Tet-catalyzed oxidation followed by decarboxylation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3495246/" 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/PMC3495246/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ito, Shinsuke -- Shen, Li -- Dai, Qing -- Wu, Susan C -- Collins, Leonard B -- Swenberg, James A -- He, Chuan -- Zhang, Yi -- GM071440/GM/NIGMS NIH HHS/ -- GM68804/GM/NIGMS NIH HHS/ -- P30 ES010126/ES/NIEHS NIH HHS/ -- P30 ES010126-11/ES/NIEHS NIH HHS/ -- P30ES10126/ES/NIEHS NIH HHS/ -- P42 ES005948/ES/NIEHS NIH HHS/ -- P42 ES005948-17/ES/NIEHS NIH HHS/ -- P42ES5948/ES/NIEHS NIH HHS/ -- R01 GM068804/GM/NIGMS NIH HHS/ -- U01 DK089565/DK/NIDDK NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2011 Sep 2;333(6047):1300-3. doi: 10.1126/science.1210597. Epub 2011 Jul 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Biochemistry and Biophysics, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599-7295, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21778364" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): 5-Methylcytosine/*metabolism ; Animals ; Cell Line ; Cytosine/*analogs & derivatives/metabolism ; DNA/*metabolism ; DNA Methylation ; DNA-Binding Proteins/genetics/*metabolism ; Embryonic Stem Cells/metabolism ; Humans ; Mice ; Oxidation-Reduction ; Proto-Oncogene Proteins/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 74
    Publikationsdatum: 2011-02-12
    Beschreibung: Mucocutaneous leishmaniasis is caused by infections with intracellular parasites of the Leishmania Viannia subgenus, including Leishmania guyanensis. The pathology develops after parasite dissemination to nasopharyngeal tissues, where destructive metastatic lesions form with chronic inflammation. Currently, the mechanisms involved in lesion development are poorly understood. Here we show that metastasizing parasites have a high Leishmania RNA virus-1 (LRV1) burden that is recognized by the host Toll-like receptor 3 (TLR3) to induce proinflammatory cytokines and chemokines. Paradoxically, these TLR3-mediated immune responses rendered mice more susceptible to infection, and the animals developed an increased footpad swelling and parasitemia. Thus, LRV1 in the metastasizing parasites subverted the host immune response to Leishmania and promoted parasite persistence.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3253482/" 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/PMC3253482/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ives, Annette -- Ronet, Catherine -- Prevel, Florence -- Ruzzante, Giulia -- Fuertes-Marraco, Silvia -- Schutz, Frederic -- Zangger, Haroun -- Revaz-Breton, Melanie -- Lye, Lon-Fye -- Hickerson, Suzanne M -- Beverley, Stephen M -- Acha-Orbea, Hans -- Launois, Pascal -- Fasel, Nicolas -- Masina, Slavica -- A129646/PHS HHS/ -- R01 AI029646/AI/NIAID NIH HHS/ -- R01 AI029646-23/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2011 Feb 11;331(6018):775-8. doi: 10.1126/science.1199326.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, University of Lausanne, 1066 Epalinges, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21311023" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Chemokines/*metabolism ; Cytokines/*metabolism ; Inflammation Mediators/metabolism ; Leishmania guyanensis/*pathogenicity/*virology ; Leishmaniasis, Mucocutaneous/*immunology/parasitology ; Leishmaniavirus/*immunology/physiology ; Macrophages/immunology/parasitology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Parasitemia ; Phagosomes/parasitology ; RNA, Double-Stranded/immunology ; RNA, Viral/immunology ; Toll-Like Receptor 3/*immunology ; Toll-Like Receptors/immunology
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 75
    Publikationsdatum: 2011-12-07
    Beschreibung: Epithelial cells respond to physicochemical damage with up-regulation of major histocompatibility complex-like ligands that can activate the cytolytic potential of neighboring intraepithelial T cells by binding the activating receptor, NKG2D. The systemic implications of this lymphoid stress-surveillance response, however, are unknown. We found that antigens encountered at the same time as cutaneous epithelial stress induced strong primary and secondary systemic, T helper 2 (T(H)2)-associated atopic responses in mice. These responses required NKG2D-dependent communication between dysregulated epithelial cells and tissue-associated lymphoid cells. These data are germane to uncertainty over the afferent induction of T(H)2 responses and provide a molecular framework for considering atopy as an important component of the response to tissue damage and carcinogenesis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3842529/" 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/PMC3842529/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Strid, Jessica -- Sobolev, Olga -- Zafirova, Biljana -- Polic, Bojan -- Hayday, Adrian -- 085780/Wellcome Trust/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2011 Dec 2;334(6060):1293-7. doi: 10.1126/science.1211250.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉London Research Institute, Cancer Research UK, London WC2A 3LY, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22144628" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Epidermis/*immunology ; Hypersensitivity, Immediate/*immunology ; Ligands ; Lymphoid Tissue/*immunology ; Membrane Proteins/immunology/metabolism ; Mice ; Mice, Transgenic ; NK Cell Lectin-Like Receptor Subfamily K/immunology/*metabolism ; Receptors, Antigen, T-Cell, gamma-delta/immunology ; Stress, Physiological ; T-Lymphocyte Subsets/*immunology ; Th2 Cells/*immunology ; Up-Regulation
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 76
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2011-02-19
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Leslie, Mitch -- New York, N.Y. -- Science. 2011 Feb 18;331(6019):837. doi: 10.1126/science.331.6019.837.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21330503" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Diabetes Mellitus, Type 2/*genetics/prevention & control ; Genetic Predisposition to Disease ; Human Growth Hormone/metabolism ; Humans ; Immunity, Innate/genetics ; Insulin-Like Growth Factor I/metabolism ; Laron Syndrome/*genetics ; Mice ; Neoplasms/*genetics/prevention & control ; *Point Mutation ; Receptors, Somatotropin/*genetics
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 77
    Publikationsdatum: 2011-09-03
    Beschreibung: The taste system is one of our fundamental senses, responsible for detecting and responding to sweet, bitter, umami, salty, and sour stimuli. In the tongue, the five basic tastes are mediated by separate classes of taste receptor cells each finely tuned to a single taste quality. We explored the logic of taste coding in the brain by examining how sweet, bitter, umami, and salty qualities are represented in the primary taste cortex of mice. We used in vivo two-photon calcium imaging to demonstrate topographic segregation in the functional architecture of the gustatory cortex. Each taste quality is represented in its own separate cortical field, revealing the existence of a gustotopic map in the brain. These results expose the basic logic for the central representation of taste.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3523322/" 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/PMC3523322/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Xiaoke -- Gabitto, Mariano -- Peng, Yueqing -- Ryba, Nicholas J P -- Zuker, Charles S -- Z01 DE000561-15/Intramural NIH HHS/ -- Z01 DE000561-16/Intramural NIH HHS/ -- ZIA DE000561-17/Intramural NIH HHS/ -- ZIA DE000561-18/Intramural NIH HHS/ -- ZIA DE000561-19/Intramural NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2011 Sep 2;333(6047):1262-6. doi: 10.1126/science.1204076.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Biochemistry and Molecular Biophysics, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21885776" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Afferent Pathways ; Animals ; *Brain Mapping ; Cerebral Cortex/cytology/*physiology ; Cycloheximide ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Molecular Imaging ; Neurons/*physiology ; Sodium Chloride ; Sodium Glutamate ; Sweetening Agents ; Taste/*physiology ; Taste Buds/physiology
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 78
    Publikationsdatum: 2011-06-18
    Beschreibung: The bacterial pathogen Legionella pneumophila exploits host cell vesicle transport by transiently manipulating the activity of the small guanosine triphosphatase (GTPase) Rab1. The effector protein SidM recruits Rab1 to the Legionella-containing vacuole (LCV), where it activates Rab1 and then AMPylates it by covalently adding adenosine monophosphate (AMP). L. pneumophila GTPase-activating protein LepB inactivates Rab1 before its removal from LCVs. Because LepB cannot bind AMPylated Rab1, the molecular events leading to Rab1 inactivation are unknown. We found that the effector protein SidD from L. pneumophila catalyzed AMP release from Rab1, generating de-AMPylated Rab1 accessible for inactivation by LepB. L. pneumophila mutants lacking SidD were defective for Rab1 removal from LCVs, identifying SidD as the missing link connecting the processes of early Rab1 accumulation and subsequent Rab1 removal during infection.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3209958/" 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/PMC3209958/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Neunuebel, M Ramona -- Chen, Yang -- Gaspar, Andrew H -- Backlund, Peter S Jr -- Yergey, Alfred -- Machner, Matthias P -- ZIA HD008893-01/Intramural NIH HHS/ -- New York, N.Y. -- Science. 2011 Jul 22;333(6041):453-6. doi: 10.1126/science.1207193. Epub 2011 Jun 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cell Biology and Metabolism Program, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21680813" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adenosine Monophosphate/*metabolism ; Animals ; Bacterial Proteins/genetics/*metabolism ; COS Cells ; Cercopithecus aethiops ; Golgi Apparatus/metabolism ; Guanine Nucleotide Exchange Factors/metabolism ; Guanosine Monophosphate/metabolism ; Guanosine Triphosphate/metabolism ; Humans ; Legionella pneumophila/*metabolism/pathogenicity ; Ligands ; Macrophages/metabolism/microbiology ; Mice ; Mice, Inbred A ; Models, Biological ; Mutant Proteins/metabolism ; U937 Cells ; Vacuoles/metabolism/*microbiology ; rab1 GTP-Binding Proteins/*metabolism
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 79
    Publikationsdatum: 2011-11-05
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fischer, Joern -- Batary, Peter -- Bawa, Kamaljit S -- Brussaard, Lijbert -- Chappell, M Jahi -- Clough, Yann -- Daily, Gretchen C -- Dorrough, Josh -- Hartel, Tibor -- Jackson, Louise E -- Klein, Alexandra M -- Kremen, Claire -- Kuemmerle, Tobias -- Lindenmayer, David B -- Mooney, Harold A -- Perfecto, Ivette -- Philpott, Stacy M -- Tscharntke, Teja -- Vandermeer, John -- Wanger, Thomas Cherico -- Von Wehrden, Henrik -- New York, N.Y. -- Science. 2011 Nov 4;334(6056):593; author reply 594-5. doi: 10.1126/science.334.6056.593-a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22053026" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): *Agriculture ; Animals ; *Biodiversity ; *Conservation of Natural Resources ; Crops, Agricultural/*growth & development ; *Ecosystem ; *Food
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 80
    Publikationsdatum: 2011-08-13
    Beschreibung: Estimates suggest that only one-tenth of the true fungal diversity has been described. Among numerous fungal lineages known only from environmental DNA sequences, Soil Clone Group 1 is the most ubiquitous. These globally distributed fungi may dominate below-ground fungal communities, but their placement in the fungal tree of life has been uncertain. Here, we report cultures of this group and describe the class, Archaeorhizomycetes, phylogenetically placed within subphylum Taphrinomycotina in the Ascomycota. Archaeorhizomycetes comprises hundreds of cryptically reproducing filamentous species that do not form recognizable mycorrhizal structures and have saprotrophic potential, yet are omnipresent in roots and rhizosphere soil and show ecosystem and host root habitat specificity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rosling, Anna -- Cox, Filipa -- Cruz-Martinez, Karelyn -- Ihrmark, Katarina -- Grelet, Gwen-Aelle -- Lindahl, Bjorn D -- Menkis, Audrius -- James, Timothy Y -- New York, N.Y. -- Science. 2011 Aug 12;333(6044):876-9. doi: 10.1126/science.1206958.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Forest Mycology and Pathology, Uppsala BioCentre, SLU, Box 7026, 750 07 Uppsala, Sweden. anna.rosling@slu.se〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21836015" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): *Ascomycota/classification/genetics/growth & development/isolation & purification ; Coniferophyta/microbiology ; *Ecosystem ; Genes, Fungal ; Genes, rRNA ; Meristem/*microbiology ; Molecular Sequence Data ; *Mycorrhizae/classification/genetics ; Phylogeny ; Rhizosphere ; *Soil Microbiology
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 81
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2011-07-19
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fisher, Brendan -- Naidoo, Robin -- New York, N.Y. -- Science. 2011 Jul 15;333(6040):287; author reply 287-8. doi: 10.1126/science.333.6040.287-a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21764731" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Agriculture/*economics ; Animals ; *Chiroptera ; Crops, Agricultural/*economics ; *Ecosystem ; Pest Control, Biological/*economics ; Population Dynamics ; United States
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 82
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2011-08-20
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Moore, Christopher -- New York, N.Y. -- Science. 2011 Aug 19;333(6045):936. doi: 10.1126/science.333.6045.936-b.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21852471" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Biodiversity ; *Conservation of Natural Resources ; *Ecosystem ; *Introduced Species
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 83
    Publikationsdatum: 2011-04-30
    Beschreibung: Catastrophic ecological regime shifts may be announced in advance by statistical early warning signals such as slowing return rates from perturbation and rising variance. The theoretical background for these indicators is rich, but real-world tests are rare, especially for whole ecosystems. We tested the hypothesis that these statistics would be early warning signals for an experimentally induced regime shift in an aquatic food web. We gradually added top predators to a lake over 3 years to destabilize its food web. An adjacent lake was monitored simultaneously as a reference ecosystem. Warning signals of a regime shift were evident in the manipulated lake during reorganization of the food web more than a year before the food web transition was complete, corroborating theory for leading indicators of ecological regime shifts.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Carpenter, S R -- Cole, J J -- Pace, M L -- Batt, R -- Brock, W A -- Cline, T -- Coloso, J -- Hodgson, J R -- Kitchell, J F -- Seekell, D A -- Smith, L -- Weidel, B -- New York, N.Y. -- Science. 2011 May 27;332(6033):1079-82. doi: 10.1126/science.1203672. Epub 2011 Apr 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Limnology, University of Wisconsin, Madison, WI 53706, USA. srcarpen@wisc.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21527677" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Bass ; Biomass ; Chlorophyll/analysis ; *Ecosystem ; *Fishes ; *Food Chain ; *Fresh Water/chemistry ; Models, Biological ; Nonlinear Dynamics ; *Phytoplankton ; Population Dynamics ; *Zooplankton
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 84
    Publikationsdatum: 2011-04-23
    Beschreibung: Mucosal surfaces constantly encounter microbes. Toll-like receptors (TLRs) mediate recognition of microbial patterns to eliminate pathogens. By contrast, we demonstrate that the prominent gut commensal Bacteroides fragilis activates the TLR pathway to establish host-microbial symbiosis. TLR2 on CD4(+) T cells is required for B. fragilis colonization of a unique mucosal niche in mice during homeostasis. A symbiosis factor (PSA, polysaccharide A) of B. fragilis signals through TLR2 directly on Foxp3(+) regulatory T cells to promote immunologic tolerance. B. fragilis lacking PSA is unable to restrain T helper 17 cell responses and is defective in niche-specific mucosal colonization. Therefore, commensal bacteria exploit the TLR pathway to actively suppress immunity. We propose that the immune system can discriminate between pathogens and the microbiota through recognition of symbiotic bacterial molecules in a process that engenders commensal colonization.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3164325/" 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/PMC3164325/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Round, June L -- Lee, S Melanie -- Li, Jennifer -- Tran, Gloria -- Jabri, Bana -- Chatila, Talal A -- Mazmanian, Sarkis K -- AI 080002/AI/NIAID NIH HHS/ -- AI 088626/AI/NIAID NIH HHS/ -- DK 078938/DK/NIDDK NIH HHS/ -- DK 083633/DK/NIDDK NIH HHS/ -- R01 AI085090/AI/NIAID NIH HHS/ -- R01 AI085090-01/AI/NIAID NIH HHS/ -- R01 AI085090-01S1/AI/NIAID NIH HHS/ -- R01 AI085090-02/AI/NIAID NIH HHS/ -- R01 AI085090-03/AI/NIAID NIH HHS/ -- R01 DK078938/DK/NIDDK NIH HHS/ -- R01 DK078938-01A2/DK/NIDDK NIH HHS/ -- R01 DK078938-02/DK/NIDDK NIH HHS/ -- R01 DK078938-03/DK/NIDDK NIH HHS/ -- R01 DK078938-04/DK/NIDDK NIH HHS/ -- R21 AI080002/AI/NIAID NIH HHS/ -- R21 AI080002-01/AI/NIAID NIH HHS/ -- R21 AI080002-02/AI/NIAID NIH HHS/ -- R21 AI088626/AI/NIAID NIH HHS/ -- R21 AI088626-01/AI/NIAID NIH HHS/ -- R21 AI088626-02/AI/NIAID NIH HHS/ -- R21 DK083633/DK/NIDDK NIH HHS/ -- R21 DK083633-01A1/DK/NIDDK NIH HHS/ -- R21 DK083633-02/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2011 May 20;332(6032):974-7. doi: 10.1126/science.1206095. Epub 2011 Apr 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biology, California Institute of Technology, Pasadena, CA 91125, USA. jround@caltech.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21512004" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Bacteroides fragilis/*growth & development/*immunology ; Colon/immunology/microbiology ; Germ-Free Life ; Homeostasis ; Humans ; *Immune Tolerance ; Immunity, Mucosal ; Interleukin-10/metabolism ; Intestinal Mucosa/*immunology/*microbiology ; Metagenome ; Mice ; Mice, Inbred C57BL ; Models, Biological ; Polysaccharides, Bacterial/immunology/*metabolism ; Signal Transduction ; Specific Pathogen-Free Organisms ; Symbiosis ; T-Lymphocytes, Regulatory/immunology ; Th17 Cells/immunology ; Toll-Like Receptor 2/immunology/*metabolism
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 85
    Publikationsdatum: 2011-08-06
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hulme, Mike -- Mahony, Martin -- Beck, Silke -- Gorg, Christoph -- Hansjurgens, Bernd -- Hauck, Jennifer -- Nesshover, Carsten -- Paulsch, Axel -- Vandewalle, Marie -- Wittmer, Heidi -- Boschen, Stefan -- Bridgewater, Peter -- Diaw, Mariteuw Chimere -- Fabre, Pierre -- Figueroa, Aurelia -- Heong, Kong Luen -- Korn, Horst -- Leemans, Rik -- Lovbrand, Eva -- Hamid, Mohd Norowi -- Monfreda, Chad -- Pielke, Roger Jr -- Settele, Josef -- Winter, Marten -- Vadrot, Alice B M -- van den Hove, Sybille -- van der Sluijs, Jeroen P -- New York, N.Y. -- Science. 2011 Aug 5;333(6043):697-8. doi: 10.1126/science.333.6043.697.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21817033" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): *Biodiversity ; *Ecosystem ; *Policy ; Policy Making
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 86
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2011-08-27
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Flueck, Werner T -- New York, N.Y. -- Science. 2011 Aug 26;333(6046):1092-3. doi: 10.1126/science.333.6046.1092-b.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21868651" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; *Ecosystem ; Entropy ; *Food Chain ; Photosynthesis ; Predatory Behavior ; Temperature
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 87
    Publikationsdatum: 2011-01-15
    Beschreibung: Satellite repeats in heterochromatin are transcribed into noncoding RNAs that have been linked to gene silencing and maintenance of chromosomal integrity. Using digital gene expression analysis, we showed that these transcripts are greatly overexpressed in mouse and human epithelial cancers. In 8 of 10 mouse pancreatic ductal adenocarcinomas (PDACs), pericentromeric satellites accounted for a mean 12% (range 1 to 50%) of all cellular transcripts, a mean 40-fold increase over that in normal tissue. In 15 of 15 human PDACs, alpha satellite transcripts were most abundant and HSATII transcripts were highly specific for cancer. Similar patterns were observed in cancers of the lung, kidney, ovary, colon, and prostate. Derepression of satellite transcripts correlated with overexpression of the long interspersed nuclear element 1 (LINE-1) retrotransposon and with aberrant expression of neuroendocrine-associated genes proximal to LINE-1 insertions. The overexpression of satellite transcripts in cancer may reflect global alterations in heterochromatin silencing and could potentially be useful as a biomarker for cancer detection.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3701432/" 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/PMC3701432/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ting, David T -- Lipson, Doron -- Paul, Suchismita -- Brannigan, Brian W -- Akhavanfard, Sara -- Coffman, Erik J -- Contino, Gianmarco -- Deshpande, Vikram -- Iafrate, A John -- Letovsky, Stan -- Rivera, Miguel N -- Bardeesy, Nabeel -- Maheswaran, Shyamala -- Haber, Daniel A -- CA129933/CA/NCI NIH HHS/ -- L30 CA142210/CA/NCI NIH HHS/ -- P01 CA117969/CA/NCI NIH HHS/ -- R01 CA129933/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2011 Feb 4;331(6017):593-6. doi: 10.1126/science.1200801. Epub 2011 Jan 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Massachusetts General Hospital Cancer Center and Department of Medicine, Harvard Medical School, Boston, MA 02114, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21233348" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Carcinoma in Situ/genetics/pathology ; Carcinoma, Pancreatic Ductal/genetics/pathology ; Colonic Neoplasms/genetics/pathology ; DNA Methylation ; DNA, Neoplasm/genetics ; DNA, Satellite/*genetics ; Female ; Gene Expression ; Gene Expression Profiling ; Heterochromatin/chemistry/genetics ; Humans ; Long Interspersed Nucleotide Elements ; Lung Neoplasms/genetics/pathology ; Male ; Mice ; Mice, Nude ; Neoplasms/*genetics/pathology ; Neurosecretory Systems/metabolism ; Ovarian Neoplasms/genetics/pathology ; Pancreatic Neoplasms/*genetics/pathology ; Prostatic Neoplasms/genetics/pathology ; RNA, Neoplasm/*genetics/metabolism ; RNA, Untranslated/*genetics/metabolism ; Transcription, Genetic
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 88
    Publikationsdatum: 2011-07-30
    Beschreibung: In the auditory epithelium of the cochlea, the sensory hair cells and supporting cells are arranged in a checkerboard-like fashion, but the mechanism underlying this cellular patterning is unclear. We found that mouse hair cells and supporting cells express the immunoglobulin-like adhesion molecules nectin-1 and -3, respectively, and that their interaction mediates the heterotypic adhesion between these two cell types. Genetic removal of nectin-1 or -3 disrupted the checkerboard-like pattern, inducing aberrant attachment between hair cells. When cells expressing either nectin-1 or -3 were cocultured, they arranged themselves into a mosaic pattern. Thus, nectin-1 and -3 promote the formation of the checkerboard-like pattern of the auditory epithelia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Togashi, Hideru -- Kominami, Kanoko -- Waseda, Masazumi -- Komura, Hitomi -- Miyoshi, Jun -- Takeichi, Masatoshi -- Takai, Yoshimi -- New York, N.Y. -- Science. 2011 Aug 26;333(6046):1144-7. doi: 10.1126/science.1208467. Epub 2011 Jul 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Molecular and Cellular Biology, Department of Biochemistry and Molecular Biology, Kobe University Graduate School of Medicine, Kobe 650-0017, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21798896" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adherens Junctions/metabolism ; Animals ; *Cell Adhesion ; Cell Adhesion Molecules/genetics/*metabolism ; Cell Differentiation ; Cell Line ; Coculture Techniques ; HEK293 Cells ; Hair Cells, Auditory/*cytology/*metabolism ; Humans ; Mice ; Mice, Knockout ; Organ of Corti/*cytology/*metabolism ; Phenotype ; Protein Binding ; RNA, Messenger/genetics/metabolism
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 89
    Publikationsdatum: 2011-03-19
    Beschreibung: In prokaryotes and eukaryotes, most genes appear to be transcribed during short periods called transcriptional bursts, interspersed by silent intervals. We describe how such bursts generate gene-specific temporal patterns of messenger RNA (mRNA) synthesis in mammalian cells. To monitor transcription at high temporal resolution, we established various gene trap cell lines and transgenic cell lines expressing a short-lived luciferase protein from an unstable mRNA, and recorded bioluminescence in real time in single cells. Mathematical modeling identified gene-specific on- and off-switching rates in transcriptional activity and mean numbers of mRNAs produced during the bursts. Transcriptional kinetics were markedly altered by cis-regulatory DNA elements. Our analysis demonstrated that bursting kinetics are highly gene-specific, reflecting refractory periods during which genes stay inactive for a certain time before switching on again.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Suter, David M -- Molina, Nacho -- Gatfield, David -- Schneider, Kim -- Schibler, Ueli -- Naef, Felix -- New York, N.Y. -- Science. 2011 Apr 22;332(6028):472-4. doi: 10.1126/science.1198817. Epub 2011 Mar 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Sciences III, University of Geneva, 30 Quai Ernest Ansermet, 1211 Geneva, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21415320" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Acetylation ; Animals ; Cells, Cultured ; Chromatin/physiology ; Circadian Rhythm/genetics ; Down-Regulation ; *Gene Expression ; Histones/metabolism ; Kinetics ; Luminescent Measurements ; Mice ; Models, Genetic ; NIH 3T3 Cells ; Promoter Regions, Genetic ; Protein Biosynthesis ; RNA, Messenger/genetics/metabolism ; Stochastic Processes ; *Transcription, Genetic ; Transcriptional Activation ; Transgenes ; Up-Regulation
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 90
    Publikationsdatum: 2011-12-14
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jepson, Paul -- Jennings, Steve -- Jones, Kate E -- Hodgetts, Timothy -- New York, N.Y. -- Science. 2011 Dec 9;334(6061):1351-2. doi: 10.1126/science.1213189.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Geography and the Environment, University of Oxford, Oxford, OX1 3QY, UK. paul.jepson@ouce.ox.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22158806" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Conservation of Natural Resources/*economics ; *Ecosystem ; *Environment ; International Cooperation ; Motion Pictures as Topic/*economics ; Organizations, Nonprofit ; Policy ; Television/*economics
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  • 91
    Publikationsdatum: 2011-10-15
    Beschreibung: The spatial and temporal control of Hox gene transcription is essential for patterning the vertebrate body axis. Although this process involves changes in histone posttranslational modifications, the existence of particular three-dimensional (3D) architectures remained to be assessed in vivo. Using high-resolution chromatin conformation capture methodology, we examined the spatial configuration of Hox clusters in embryonic mouse tissues where different Hox genes are active. When the cluster is transcriptionally inactive, Hox genes associate into a single 3D structure delimited from flanking regions. Once transcription starts, Hox clusters switch to a bimodal 3D organization where newly activated genes progressively cluster into a transcriptionally active compartment. This transition in spatial configurations coincides with the dynamics of chromatin marks, which label the progression of the gene clusters from a negative to a positive transcription status. This spatial compartmentalization may be key to process the colinear activation of these compact gene clusters.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Noordermeer, Daan -- Leleu, Marion -- Splinter, Erik -- Rougemont, Jacques -- De Laat, Wouter -- Duboule, Denis -- New York, N.Y. -- Science. 2011 Oct 14;334(6053):222-5. doi: 10.1126/science.1207194.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Research Centre Frontiers in Genetics, School of Life Sciences, Ecole Polytechnique Federale (EPFL), Lausanne, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21998387" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Chromatin/metabolism/ultrastructure ; Embryo, Mammalian/cytology/*metabolism ; Gene Expression Regulation, Developmental ; *Genes, Homeobox ; Histones/metabolism ; Mice ; Models, Genetic ; *Multigene Family ; Transcription, Genetic ; *Transcriptional Activation
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  • 92
    Publikationsdatum: 2011-10-25
    Beschreibung: Phospholipase A(2)(PLA(2)) enzymes are considered the primary source of arachidonic acid for cyclooxygenase (COX)-mediated biosynthesis of prostaglandins. Here, we show that a distinct pathway exists in brain, where monoacylglycerol lipase (MAGL) hydrolyzes the endocannabinoid 2-arachidonoylglycerol to generate a major arachidonate precursor pool for neuroinflammatory prostaglandins. MAGL-disrupted animals show neuroprotection in a parkinsonian mouse model. These animals are spared the hemorrhaging caused by COX inhibitors in the gut, where prostaglandins are instead regulated by cytosolic PLA(2). These findings identify MAGL as a distinct metabolic node that couples endocannabinoid to prostaglandin signaling networks in the nervous system and suggest that inhibition of this enzyme may be a new and potentially safer way to suppress the proinflammatory cascades that underlie neurodegenerative disorders.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3249428/" 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/PMC3249428/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nomura, Daniel K -- Morrison, Bradley E -- Blankman, Jacqueline L -- Long, Jonathan Z -- Kinsey, Steven G -- Marcondes, Maria Cecilia G -- Ward, Anna M -- Hahn, Yun Kyung -- Lichtman, Aron H -- Conti, Bruno -- Cravatt, Benjamin F -- 5P01DA009789/DA/NIDA NIH HHS/ -- AG028040/AG/NIA NIH HHS/ -- DA017259/DA/NIDA NIH HHS/ -- DA026261/DA/NIDA NIH HHS/ -- F31 DA026261-03/DA/NIDA NIH HHS/ -- K99 DA030908/DA/NIDA NIH HHS/ -- K99 DA030908-01/DA/NIDA NIH HHS/ -- K99DA030908/DA/NIDA NIH HHS/ -- P01 DA009789/DA/NIDA NIH HHS/ -- P01 DA009789-14/DA/NIDA NIH HHS/ -- P01 DA017259/DA/NIDA NIH HHS/ -- P01 DA017259-08/DA/NIDA NIH HHS/ -- P01DA01725/DA/NIDA NIH HHS/ -- R00 DA030908/DA/NIDA NIH HHS/ -- R00 DA030908-02/DA/NIDA NIH HHS/ -- R00DA030908/DA/NIDA NIH HHS/ -- R01 AG028040/AG/NIA NIH HHS/ -- R01 AG028040-04/AG/NIA NIH HHS/ -- R03 DA027936/DA/NIDA NIH HHS/ -- R03 DA027936-02/DA/NIDA NIH HHS/ -- R03DA027936/DA/NIDA NIH HHS/ -- T32 DA007027/DA/NIDA NIH HHS/ -- T32 DA007027-33/DA/NIDA NIH HHS/ -- T32DA007027/DA/NIDA NIH HHS/ -- New York, N.Y. -- Science. 2011 Nov 11;334(6057):809-13. doi: 10.1126/science.1209200. Epub 2011 Oct 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Skaggs Institute for Chemical Biology and Department of Chemical Physiology, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA. dnomura@berkeley.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22021672" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Arachidonic Acid/metabolism ; Arachidonic Acids/*metabolism ; Benzodioxoles/pharmacology ; Brain/drug effects/*metabolism/pathology ; Cannabinoid Receptor Modulators/*metabolism ; Cyclooxygenase 1/metabolism ; Cytokines/metabolism ; Eicosanoids/metabolism ; *Endocannabinoids ; Enzyme Inhibitors/pharmacology ; Glycerides/*metabolism ; Hydrolysis ; Inflammation/*metabolism/pathology ; Inflammation Mediators/pharmacology ; Lipopolysaccharides/pharmacology ; Liver/metabolism ; Lung/metabolism ; Metabolomics ; Mice ; Mice, Inbred C57BL ; Monoacylglycerol Lipases/antagonists & inhibitors/genetics/*metabolism ; Neuroprotective Agents/pharmacology ; Parkinsonian Disorders/metabolism/pathology ; Phospholipases A2/genetics/metabolism ; Piperidines/pharmacology ; Prostaglandins/biosynthesis/*metabolism ; Signal Transduction
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  • 93
    Publikationsdatum: 2011-08-27
    Beschreibung: Zhao and Running (Reports, 20 August 2010, p. 940) reported a reduction in global terrestrial net primary production (NPP) from 2000 through 2009. We argue that the small trends, regional patterns, and interannual variations that they describe are artifacts of their NPP model. Satellite observations of vegetation activity show no statistically significant changes in more than 85% of the vegetated lands south of 70 degrees N during the same 2000 to 2009 period.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Samanta, Arindam -- Costa, Marcos H -- Nunes, Edson L -- Vieira, Simone A -- Xu, Liang -- Myneni, Ranga B -- New York, N.Y. -- Science. 2011 Aug 26;333(6046):1093; author reply 1093. doi: 10.1126/science.1199048.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Geography and Environment, Boston University, Boston, MA 02215, USA. arindam.sam@gmail.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21868655" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Atmosphere ; Biomass ; *Carbon Cycle ; Carbon Dioxide ; *Droughts ; *Ecosystem ; Photosynthesis ; Plants/*metabolism ; South America
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  • 94
    Publikationsdatum: 2011-03-26
    Beschreibung: Axon-dendrite polarization is crucial for neural network wiring and information processing in the brain. Polarization begins with the transformation of a single neurite into an axon and its subsequent rapid extension, which requires coordination of cellular energy status to allow for transport of building materials to support axon growth. We found that activation of the energy-sensing adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK) pathway suppressed axon initiation and neuronal polarization. Phosphorylation of the kinesin light chain of the Kif5 motor protein by AMPK disrupted the association of the motor with phosphatidylinositol 3-kinase (PI3K), preventing PI3K targeting to the axonal tip and inhibiting polarization and axon growth.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3325765/" 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/PMC3325765/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Amato, Stephen -- Liu, Xiuxin -- Zheng, Bin -- Cantley, Lewis -- Rakic, Pasko -- Man, Heng-Ye -- GM41890/GM/NIGMS NIH HHS/ -- GM56203/GM/NIGMS NIH HHS/ -- K99CA133245/CA/NCI NIH HHS/ -- MH07907/MH/NIMH NIH HHS/ -- R00 CA133245/CA/NCI NIH HHS/ -- R01 GM056203/GM/NIGMS NIH HHS/ -- R01 NS014841/NS/NINDS NIH HHS/ -- R01 NS014841-32/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2011 Apr 8;332(6026):247-51. doi: 10.1126/science.1201678. Epub 2011 Mar 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Boston University, 5 Cummington Street, Boston, MA 02215, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21436401" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): AMP-Activated Protein Kinases/*metabolism ; Aminoimidazole Carboxamide/analogs & derivatives/pharmacology ; Animals ; Axons/enzymology/*physiology/ultrastructure ; *Cell Polarity/drug effects ; Cells, Cultured ; Hippocampus/cytology/embryology ; Metformin/pharmacology ; Mice ; Microtubule-Associated Proteins/metabolism ; Neurons/cytology/drug effects/enzymology/*physiology ; Phosphatidylinositol 3-Kinase/*metabolism ; Phosphorylation ; Proto-Oncogene Proteins c-akt/metabolism ; Rats ; Recombinant Fusion Proteins/metabolism ; Ribonucleotides/pharmacology ; Signal Transduction ; Tissue Culture Techniques
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  • 95
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2011-03-12
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, Jon -- New York, N.Y. -- Science. 2011 Mar 11;331(6022):1253-4. doi: 10.1126/science.331.6022.1253.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21393520" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Cell Line, Tumor ; Fatigue Syndrome, Chronic/*virology ; Humans ; Male ; Mice ; Neoplasm Transplantation ; Prostatic Neoplasms/*virology ; *Recombination, Genetic ; Transplantation, Heterologous ; *Xenotropic murine leukemia virus-related virus/genetics/physiology
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  • 96
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2011-10-25
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pala, Christopher -- New York, N.Y. -- Science. 2011 Oct 21;334(6054):303. doi: 10.1126/science.334.6054.303.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22021832" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Biomass ; *Ecosystem ; *Fisheries ; *Fishes ; *Fresh Water ; Kazakhstan ; Oceans and Seas ; Salinity
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  • 97
    Publikationsdatum: 2011-07-23
    Beschreibung: Many physiological responses in present-day coral reefs to climate change are interpreted as consistent with the imminent disappearance of modern reefs globally because of annual mass bleaching events, carbonate dissolution, and insufficient time for substantial evolutionary responses. Emerging evidence for variability in the coral calcification response to acidification, geographical variation in bleaching susceptibility and recovery, responses to past climate change, and potential rates of adaptation to rapid warming supports an alternative scenario in which reef degradation occurs with greater temporal and spatial heterogeneity than current projections suggest. Reducing uncertainty in projecting coral reef futures requires improved understanding of past responses to rapid climate change; physiological responses to interacting factors, such as temperature, acidification, and nutrients; and the costs and constraints imposed by acclimation and adaptation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pandolfi, John M -- Connolly, Sean R -- Marshall, Dustin J -- Cohen, Anne L -- New York, N.Y. -- Science. 2011 Jul 22;333(6041):418-22. doi: 10.1126/science.1204794.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Australian Research Council (ARC) Centre of Excellence for Coral Reef Studies, St. Lucia, Queensland 4072, Australia. j.pandolfi@uq.edu.au〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21778392" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; *Anthozoa/physiology ; Biodiversity ; Biological Evolution ; Calcification, Physiologic ; Carbon Dioxide/analysis ; Conservation of Natural Resources ; *Ecosystem ; Forecasting ; *Global Warming ; Hydrogen-Ion Concentration ; Oceans and Seas ; Seawater/*chemistry ; Symbiosis
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 98
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2011-09-03
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Godfray, H Charles J -- New York, N.Y. -- Science. 2011 Sep 2;333(6047):1231-2. doi: 10.1126/science.1211815.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Zoology and Oxford Martin School Institute of Biodiversity, University of Oxford, Oxford OX1 3PS, UK. charles.godfray@zoo.ox.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21885765" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): *Agriculture ; Animals ; *Biodiversity ; Birds ; *Conservation of Natural Resources ; Crops, Agricultural/*growth & development ; *Ecosystem ; *Food ; Ghana ; India ; Population Density ; Trees
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  • 99
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2011-02-26
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Godley, Lucy A -- Mondragon, Alfonso -- New York, N.Y. -- Science. 2011 Feb 25;331(6020):1017-8. doi: 10.1126/science.1202090.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Hematology/Oncology, Department of Medicine, The University of Chicago, Chicago, IL 60637, USA. lgodley@medicine.bsd.uchicago.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21350155" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Catalytic Domain ; Crystallography, X-Ray ; Cysteine/chemistry ; DNA/*chemistry/metabolism ; DNA (Cytosine-5-)-Methyltransferase/*chemistry/*metabolism ; *DNA Methylation ; Dinucleoside Phosphates/chemistry/metabolism ; Humans ; Mice ; Models, Molecular ; Protein Structure, Tertiary ; Substrate Specificity
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 100
    Publikationsdatum: 2011-02-12
    Beschreibung: Memory B cells formed in response to microbial antigens provide immunity to later infections; however, the inability to detect rare endogenous antigen-specific cells limits current understanding of this process. Using an antigen-based technique to enrich these cells, we found that immunization with a model protein generated B memory cells that expressed isotype-switched immunoglobulins (swIg) or retained IgM. The more numerous IgM(+) cells were longer lived than the swIg(+) cells. However, swIg(+) memory cells dominated the secondary response because of the capacity to become activated in the presence of neutralizing serum immunoglobulin. Thus, we propose that memory relies on swIg(+) cells until they disappear and serum immunoglobulin falls to a low level, in which case memory resides with durable IgM(+) reserves.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3993090/" 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/PMC3993090/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pape, Kathryn A -- Taylor, Justin J -- Maul, Robert W -- Gearhart, Patricia J -- Jenkins, Marc K -- F32 AI091033/AI/NIAID NIH HHS/ -- R01 AI036914/AI/NIAID NIH HHS/ -- R01 AI039614/AI/NIAID NIH HHS/ -- R37 AI027998/AI/NIAID NIH HHS/ -- T32 CA009138/CA/NCI NIH HHS/ -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2011 Mar 4;331(6021):1203-7. doi: 10.1126/science.1201730. Epub 2011 Feb 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, Center for Immunology, University of Minnesota Medical School, Minneapolis, MN 55455, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21310965" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Antigens/immunology ; Antigens, CD38/analysis ; B-Lymphocyte Subsets/*immunology ; Cell Survival ; Female ; Germinal Center/cytology/immunology ; Immunization ; *Immunoglobulin Class Switching ; Immunoglobulin M/genetics/*immunology ; *Immunologic Memory ; Lymph Nodes/cytology/immunology ; Lymphocyte Activation ; Male ; Mice ; Mice, Inbred C57BL ; Mutation ; Phycocyanin/immunology ; Phycoerythrin/immunology ; Spleen/cytology/immunology
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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