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  • Cell Line  (44)
  • American Association for the Advancement of Science (AAAS)  (44)
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  • 1
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    Expression of interleukin-10 activity by Epstein-Barr virus protein BCRF1 (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1990-11-09
    Beschreibung: Cytokine synthesis inhibitory factor (CSIF; interleukin-10), a product of mouse TH2 T cell clones that inhibits synthesis of cytokines by mouse TH1 T cell clones, exhibits extensive sequence similarity to an uncharacterized open reading frame in the Epstein-Barr virus BCRF1. Recombinant BCRF1 protein mimics the activity of interleukin-10, suggesting that BCRF1 may have a role in the interaction of the virus with the host's immune system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hsu, D H -- de Waal Malefyt, R -- Fiorentino, D F -- Dang, M N -- Vieira, P -- de Vries, J -- Spits, H -- Mosmann, T R -- Moore, K W -- New York, N.Y. -- Science. 1990 Nov 9;250(4982):830-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, DNAX Research Institute, Palo Alto, CA 94304.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2173142" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Cell Line ; DNA, Viral/genetics ; Electrophoresis, Polyacrylamide Gel ; *Gene Expression Regulation, Viral ; Herpesvirus 4, Human/genetics/*immunology ; Humans ; Interleukin-10 ; Interleukins/*biosynthesis ; Killer Cells, Natural/immunology ; Mice ; Radioimmunoprecipitation Assay ; T-Lymphocytes/immunology ; Viral Proteins/genetics/*immunology
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 2
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    Mutations in FUS, an RNA processing protein, cause familial amyotrophic lateral sclerosis type 6 (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2009-03-03
    Beschreibung: Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease that is familial in 10% of cases. We have identified a missense mutation in the gene encoding fused in sarcoma (FUS) in a British kindred, linked to ALS6. In a survey of 197 familial ALS index cases, we identified two further missense mutations in eight families. Postmortem analysis of three cases with FUS mutations showed FUS-immunoreactive cytoplasmic inclusions and predominantly lower motor neuron degeneration. Cellular expression studies revealed aberrant localization of mutant FUS protein. FUS is involved in the regulation of transcription and RNA splicing and transport, and it has functional homology to another ALS gene, TARDBP, which suggests that a common mechanism may underlie motor neuron degeneration.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4516382/" 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/PMC4516382/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vance, Caroline -- Rogelj, Boris -- Hortobagyi, Tibor -- De Vos, Kurt J -- Nishimura, Agnes Lumi -- Sreedharan, Jemeen -- Hu, Xun -- Smith, Bradley -- Ruddy, Deborah -- Wright, Paul -- Ganesalingam, Jeban -- Williams, Kelly L -- Tripathi, Vineeta -- Al-Saraj, Safa -- Al-Chalabi, Ammar -- Leigh, P Nigel -- Blair, Ian P -- Nicholson, Garth -- de Belleroche, Jackie -- Gallo, Jean-Marc -- Miller, Christopher C -- Shaw, Christopher E -- 078662/Wellcome Trust/United Kingdom -- G0300329/Medical Research Council/United Kingdom -- G0500289/Medical Research Council/United Kingdom -- G0501573/Medical Research Council/United Kingdom -- G0600676/Medical Research Council/United Kingdom -- G0600974/Medical Research Council/United Kingdom -- G0900688/Medical Research Council/United Kingdom -- MC_G1000733/Medical Research Council/United Kingdom -- Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2009 Feb 27;323(5918):1208-11. doi: 10.1126/science.1165942.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Clinical Neuroscience, King's College London, Medical Research Council (MRC) Centre for Neurodegeneration Research, Institute of Psychiatry, London SE5 8AF, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19251628" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Age of Onset ; Amino Acid Sequence ; Amyotrophic Lateral Sclerosis/*genetics/metabolism/pathology ; Animals ; Brain/pathology ; Cell Line ; Cell Nucleus/metabolism ; Cytoplasm/metabolism ; DNA-Binding Proteins/analysis/genetics/metabolism ; Female ; Humans ; Inclusion Bodies/chemistry/ultrastructure ; Male ; Molecular Sequence Data ; Motor Neurons/metabolism ; *Mutation, Missense ; Pedigree ; RNA-Binding Protein FUS/analysis/*genetics/*metabolism ; Rats ; Spinal Cord/pathology ; Transfection
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 3
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    Adenylate cyclases of Trypanosoma brucei inhibit the innate immune response of the host (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2012-06-16
    Beschreibung: The parasite Trypanosoma brucei possesses a large family of transmembrane receptor-like adenylate cyclases. Activation of these enzymes requires the dimerization of the catalytic domain and typically occurs under stress. Using a dominant-negative strategy, we found that reducing adenylate cyclase activity by about 50% allowed trypanosome growth but reduced the parasite's ability to control the early innate immune defense of the host. Specifically, activation of trypanosome adenylate cyclase resulting from parasite phagocytosis by liver myeloid cells inhibited the synthesis of the trypanosome-controlling cytokine tumor necrosis factor-alpha through activation of protein kinase A in these cells. Thus, adenylate cyclase activity of lyzed trypanosomes favors early host colonization by live parasites. The role of adenylate cyclases at the host-parasite interface could explain the expansion and polymorphism of this gene family.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Salmon, Didier -- Vanwalleghem, Gilles -- Morias, Yannick -- Denoeud, Julie -- Krumbholz, Carsten -- Lhomme, Frederic -- Bachmaier, Sabine -- Kador, Markus -- Gossmann, Jasmin -- Dias, Fernando Braga Stehling -- De Muylder, Geraldine -- Uzureau, Pierrick -- Magez, Stefan -- Moser, Muriel -- De Baetselier, Patrick -- Van Den Abbeele, Jan -- Beschin, Alain -- Boshart, Michael -- Pays, Etienne -- New York, N.Y. -- Science. 2012 Jul 27;337(6093):463-6. doi: 10.1126/science.1222753. Epub 2012 Jun 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Parasitology, Institute for Molecular Biology and Medicine, Universite Libre de Bruxelles, 12, rue des Professeurs Jeener et Brachet, B6041 Gosselies, Belgium. salmon@bioqmed.ufrj.br〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22700656" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adenylyl Cyclases/chemistry/genetics/*metabolism ; Animals ; Catalytic Domain ; Cell Line ; Cyclic AMP/metabolism ; Cyclic AMP-Dependent Protein Kinases/metabolism ; Enzyme Activation ; Host-Parasite Interactions ; *Immunity, Innate ; Liver/cytology ; Mice ; Mice, Inbred C57BL ; Mutagenesis, Site-Directed ; Myeloid Cells/immunology ; Parasitemia ; Phagocytosis ; Protozoan Proteins/chemistry/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Trypanosoma brucei brucei/*enzymology/growth & development/*immunology ; Trypanosomiasis, African/*immunology/metabolism/parasitology ; Tumor Necrosis Factor-alpha/biosynthesis/blood
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 4
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    Recognition of HLA-A2 by cytotoxic T lymphocytes after DNA transfer into human and murine cells (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1984-11-30
    Beschreibung: A gene coding for the major histocompatibility antigen HLA-A2 was transferred into human HLA-A2 negative M1 cells and murine L cells. Following transfection, these cells expressed molecules at the cell surface that are biochemically indistinguishable from HLA-A2 antigens on the human cell line JY from which the HLA-A2 gene was isolated. The M1A2 cells were recognized and lysed by a cytolytic T-cell clone specific for HLA-A2. The transfected L cells which express HLA-A2 in association with human beta 2-microglobulin were not lysed by this T-cell clone. The specific cytolysis of M1A2 cells could be inhibited by monoclonal antibodies to HLA-A2, and monoclonal antibodies to T3, T8, and LFA-1 on cytotoxic T lymphocytes. These results suggest that killing by allospecific T cells requires HLA-A2 antigens as well as other species-specific structures on the target cell surface.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉van de Rijn, M -- Bernabeu, C -- Royer-Pokora, B -- Weiss, J -- Seidman, J G -- de Vries, J -- Spits, H -- Terhorst, C -- AI 19148/AI/NIAID NIH HHS/ -- AI-15066/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1984 Nov 30;226(4678):1083-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6333726" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Cell Line ; Cytotoxicity, Immunologic ; *Genes ; HLA Antigens/*genetics ; HLA-A2 Antigen ; Humans ; L Cells (Cell Line)/immunology ; *Major Histocompatibility Complex ; Mice ; T-Lymphocytes, Cytotoxic/*immunology ; *Transfection
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 5
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    Two-amino acid molecular switch in an epithelial morphogen that regulates binding to two distinct receptors (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2000-10-20
    Beschreibung: Ectodysplasin, a member of the tumor necrosis factor family, is encoded by the anhidrotic ectodermal dysplasia (EDA) gene. Mutations in EDA give rise to a clinical syndrome characterized by loss of hair, sweat glands, and teeth. EDA-A1 and EDA-A2 are two isoforms of ectodysplasin that differ only by an insertion of two amino acids. This insertion functions to determine receptor binding specificity, such that EDA-A1 binds only the receptor EDAR, whereas EDA-A2 binds only the related, but distinct, X-linked ectodysplasin-A2 receptor (XEDAR). In situ binding and organ culture studies indicate that EDA-A1 and EDA-A2 are differentially expressed and play a role in epidermal morphogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yan, M -- Wang, L C -- Hymowitz, S G -- Schilbach, S -- Lee, J -- Goddard, A -- de Vos, A M -- Gao, W Q -- Dixit, V M -- New York, N.Y. -- Science. 2000 Oct 20;290(5491):523-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Oncology, Genentech, 1 DNA Way, South San Francisco, CA 94080, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11039935" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acid Sequence ; Amino Acid Substitution ; Animals ; Binding Sites ; Cell Line ; DNA-Binding Proteins/metabolism ; Ectodermal Dysplasia/genetics ; Ectodysplasins ; Epidermis/embryology/*metabolism ; Humans ; *I-kappa B Proteins ; In Situ Hybridization ; Ligands ; Membrane Proteins/*chemistry/*metabolism ; Mice ; Models, Molecular ; Molecular Sequence Data ; Morphogenesis ; NF-kappa B/metabolism ; Phosphorylation ; Point Mutation ; Protein Conformation ; Proteins/metabolism ; Receptors, Cell Surface/chemistry/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; TNF Receptor-Associated Factor 6 ; Transfection
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 6
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    Senescence induced by altered telomere state, not telomere loss (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2002-03-30
    Beschreibung: Primary human cells in culture invariably stop dividing and enter a state of growth arrest called replicative senescence. This transition is induced by programmed telomere shortening, but the underlying mechanisms are unclear. Here, we report that overexpression of TRF2, a telomeric DNA binding protein, increased the rate of telomere shortening in primary cells without accelerating senescence. TRF2 reduced the senescence setpoint, defined as telomere length at senescence, from 7 to 4 kilobases. TRF2 protected critically short telomeres from fusion and repressed chromosome-end fusions in presenescent cultures, which explains the ability of TRF2 to delay senescence. Thus, replicative senescence is induced by a change in the protected status of shortened telomeres rather than by a complete loss of telomeric DNA.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Karlseder, Jan -- Smogorzewska, Agata -- de Lange, Titia -- AG16643/AG/NIA NIH HHS/ -- CA76027/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2002 Mar 29;295(5564):2446-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory for Cell Biology and Genetics, The Rockefeller University, 1230 York Avenue, New York, NY 10021, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11923537" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Antigens, Polyomavirus Transforming/genetics/metabolism ; *Cell Aging ; *Cell Division ; Cell Line ; Cells, Cultured ; DNA/*metabolism ; DNA-Binding Proteins/genetics/*metabolism ; Humans ; Oncogene Proteins, Viral/genetics/metabolism ; Papillomavirus E7 Proteins ; *Repressor Proteins ; Retinoblastoma Protein/metabolism ; Retroviridae/genetics ; Telomere/metabolism/*physiology ; Telomeric Repeat Binding Protein 2 ; Transformation, Genetic ; Tumor Suppressor Protein p53/metabolism
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 7
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    Perforin gene defects in familial hemophagocytic lymphohistiocytosis (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1999-12-03
    Beschreibung: Familial hemophagocytic lymphohistiocytosis (FHL) is a rare, rapidly fatal, autosomal recessive immune disorder characterized by uncontrolled activation of T cells and macrophages and overproduction of inflammatory cytokines. Linkage analyses indicate that FHL is genetically heterogeneous and linked to 9q21.3-22, 10q21-22, or another as yet undefined locus. Sequencing of the coding regions of the perforin gene of eight unrelated 10q21-22-linked FHL patients revealed homozygous nonsense mutations in four patients and missense mutations in the other four patients. Cultured lymphocytes from patients had defective cytotoxic activity, and immunostaining revealed little or no perforin in the granules. Thus, defects in perforin are responsible for 10q21-22-linked FHL. Perforin-based effector systems are, therefore, involved not only in the lysis of abnormal cells but also in the down-regulation of cellular immune activation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stepp, S E -- Dufourcq-Lagelouse, R -- Le Deist, F -- Bhawan, S -- Certain, S -- Mathew, P A -- Henter, J I -- Bennett, M -- Fischer, A -- de Saint Basile, G -- Kumar, V -- New York, N.Y. -- Science. 1999 Dec 3;286(5446):1957-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and the Graduate Program in Immunology, University of Texas Southwestern Medical School, Dallas, TX 75235, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10583959" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Antigen-Presenting Cells/immunology ; Cell Death ; Cell Line ; Cells, Cultured ; Chromosome Mapping ; Chromosomes, Human, Pair 10/*genetics ; Codon, Terminator ; Cytoplasmic Granules/chemistry ; Cytotoxicity, Immunologic ; Frameshift Mutation ; Genetic Linkage ; Granzymes ; Heterozygote ; Histiocytosis, Non-Langerhans-Cell/*genetics/immunology ; Humans ; Lymphocyte Activation ; Membrane Glycoproteins/analysis/*genetics/physiology ; Mutation, Missense ; Perforin ; Point Mutation ; Pore Forming Cytotoxic Proteins ; Serine Endopeptidases/analysis ; T-Lymphocytes, Cytotoxic/chemistry/immunology
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 8
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    Transcriptional regulation of cortical neuron migration by POU domain factors (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2002-02-23
    Beschreibung: The identification of pathways mediated by the kinase Cdk5 and the ligand reelin has provided a conceptual framework for exploring the molecular mechanisms underlying proper lamination of the developing mammalian cerebral cortex. In this report, we identify a component of the regulation of Cdk5-mediated cortical lamination by genetic analysis of the roles of the class III POU domain transcription factors, Brn-1 and Brn-2, expressed during the development of the forebrain and coexpressed in most layer II-V cortical neurons. Brn-1 and Brn-2 appear to critically control the initiation of radial migration, redundantly regulating the cell-autonomous expression of the p35 and p39 regulatory subunits of Cdk5 in migrating cortical neurons, with Brn-1(-/-)/Brn-2(-/-) mice exhibiting cortical inversion.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McEvilly, Robert J -- de Diaz, Marcela Ortiz -- Schonemann, Marcus D -- Hooshmand, Farideh -- Rosenfeld, Michael G -- New York, N.Y. -- Science. 2002 Feb 22;295(5559):1528-32.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department and School of Medicine, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92037-0648, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11859196" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Brain/cytology/embryology/metabolism ; Cell Adhesion Molecules, Neuronal/genetics/metabolism ; Cell Line ; Cell Movement ; Cerebral Cortex/cytology/embryology/*metabolism ; Cyclin-Dependent Kinase 5 ; Cyclin-Dependent Kinases/metabolism ; Extracellular Matrix Proteins/genetics/metabolism ; Female ; Gene Targeting ; Hippocampus/cytology/embryology/metabolism ; Homeodomain Proteins ; In Situ Hybridization ; Male ; Mice ; Mutation ; Nerve Tissue Proteins/genetics/metabolism ; Neurons/*physiology ; Neuropeptides/genetics/*physiology ; POU Domain Factors ; Serine Endopeptidases ; Trans-Activators/genetics/*physiology ; Transcription Factors/genetics/*physiology ; *Transcription, Genetic
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 9
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    p53- and ATM-dependent apoptosis induced by telomeres lacking TRF2 (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1999-02-26
    Beschreibung: Although broken chromosomes can induce apoptosis, natural chromosome ends (telomeres) do not trigger this response. It is shown that this suppression of apoptosis involves the telomeric-repeat binding factor 2 (TRF2). Inhibition of TRF2 resulted in apoptosis in a subset of mammalian cell types. The response was mediated by p53 and the ATM (ataxia telangiectasia mutated) kinase, consistent with activation of a DNA damage checkpoint. Apoptosis was not due to rupture of dicentric chromosomes formed by end-to-end fusion, indicating that telomeres lacking TRF2 directly signal apoptosis, possibly because they resemble damaged DNA. Thus, in some cells, telomere shortening may signal cell death rather than senescence.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Karlseder, J -- Broccoli, D -- Dai, Y -- Hardy, S -- de Lange, T -- GM49046/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1999 Feb 26;283(5406):1321-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory for Cell Biology and Genetics, The Rockefeller University, New York, NY 10021, USA. Cell Genesys, Foster City, CA 94405, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10037601" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adenoviridae/genetics/physiology ; Animals ; *Apoptosis ; Ataxia Telangiectasia/pathology ; Ataxia Telangiectasia Mutated Proteins ; B-Lymphocytes/cytology ; Cell Cycle Proteins ; Cell Line ; Cells, Cultured ; Cloning, Molecular ; DNA Damage ; DNA-Binding Proteins/chemistry/genetics/*physiology ; Genetic Vectors ; Humans ; In Situ Nick-End Labeling ; Mice ; Mitosis ; Phosphorylation ; *Protein-Serine-Threonine Kinases ; Proteins/metabolism ; T-Lymphocytes/cytology ; Telomere/*physiology ; Telomeric Repeat Binding Protein 2 ; Tumor Cells, Cultured ; Tumor Suppressor Protein p53/*metabolism ; Tumor Suppressor Proteins
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 10
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    Docosahexaenoic acid, a ligand for the retinoid X receptor in mouse brain (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2000-12-16
    Beschreibung: The retinoid X receptor (RXR) is a nuclear receptor that functions as a ligand-activated transcription factor. Little is known about the ligands that activate RXR in vivo. Here, we identified a factor in brain tissue from adult mice that activates RXR in cell-based assays. Purification and analysis of the factor by mass spectrometry revealed that it is docosahexaenoic acid (DHA), a long-chain polyunsaturated fatty acid that is highly enriched in the adult mammalian brain. Previous work has shown that DHA is essential for brain maturation, and deficiency of DHA in both rodents and humans leads to impaired spatial learning and other abnormalities. These data suggest that DHA may influence neural function through activation of an RXR signaling pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉de Urquiza, A M -- Liu, S -- Sjoberg, M -- Zetterstrom, R H -- Griffiths, W -- Sjovall, J -- Perlmann, T -- New York, N.Y. -- Science. 2000 Dec 15;290(5499):2140-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Ludwig Institute for Cancer Research, Stockholm Branch, Box 240, S-171 77 Stockholm, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11118147" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Biological Assay ; Brain/growth & development/metabolism ; *Brain Chemistry ; Cell Line ; Chromatography, High Pressure Liquid ; Culture Media, Conditioned ; Dimerization ; Docosahexaenoic Acids/*isolation & purification/*metabolism/pharmacology ; Fatty Acids, Unsaturated/pharmacology ; Histone Acetyltransferases ; Humans ; Ligands ; Male ; Mice ; Nuclear Receptor Coactivator 1 ; Receptors, Retinoic Acid/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Retinoid X Receptors ; Signal Transduction ; Spectrometry, Mass, Electrospray Ionization ; Transcription Factors/genetics/*metabolism ; Transfection ; Tumor Cells, Cultured
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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