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  • 1
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    Interactions between commensal fungi and the C-type lectin receptor Dectin-1 influence colitis (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-06-08
    Description: The intestinal microflora, typically equated with bacteria, influences diseases such as obesity and inflammatory bowel disease. Here, we show that the mammalian gut contains a rich fungal community that interacts with the immune system through the innate immune receptor Dectin-1. Mice lacking Dectin-1 exhibited increased susceptibility to chemically induced colitis, which was the result of altered responses to indigenous fungi. In humans, we identified a polymorphism in the gene for Dectin-1 (CLEC7A) that is strongly linked to a severe form of ulcerative colitis. Together, our findings reveal a eukaryotic fungal community in the gut (the "mycobiome") that coexists with bacteria and substantially expands the repertoire of organisms interacting with the intestinal immune system to influence health and disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3432565/" 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/PMC3432565/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Iliev, Iliyan D -- Funari, Vincent A -- Taylor, Kent D -- Nguyen, Quoclinh -- Reyes, Christopher N -- Strom, Samuel P -- Brown, Jordan -- Becker, Courtney A -- Fleshner, Phillip R -- Dubinsky, Marla -- Rotter, Jerome I -- Wang, Hanlin L -- McGovern, Dermot P B -- Brown, Gordon D -- Underhill, David M -- 086558/Wellcome Trust/United Kingdom -- AI071116/AI/NIAID NIH HHS/ -- P01-DK046763/DK/NIDDK NIH HHS/ -- R01 DK093426/DK/NIDDK NIH HHS/ -- UL1 RR033176/RR/NCRR NIH HHS/ -- UL1 TR000124/TR/NCATS NIH HHS/ -- UL1RR033176/RR/NCRR NIH HHS/ -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2012 Jun 8;336(6086):1314-7. doi: 10.1126/science.1221789. Epub 2012 Jun 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Inflammatory Bowel and Immunobiology Research Institute, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22674328" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Fungal/blood ; Candida tropicalis/immunology/isolation & purification/pathogenicity/physiology ; Colitis, Ulcerative/chemically induced/*immunology/*microbiology ; Colon/immunology/*microbiology ; Colony Count, Microbial ; Dextran Sulfate ; Disease Susceptibility ; Female ; Fungi/classification/*immunology/isolation & purification/*physiology ; Haplotypes ; Humans ; Immunity, Innate ; Immunity, Mucosal ; Intestinal Mucosa/immunology/*microbiology ; Intestines/immunology/microbiology ; Lectins, C-Type/deficiency/*genetics/*metabolism ; Metagenome ; Mice ; Mice, Inbred C57BL ; Polymorphism, Single Nucleotide
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
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    Comment on "Tumor response to radiotherapy regulated by endothelial cell apoptosis" (II) (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-12-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brown, Martin -- Bristow, Robert -- Glazer, Peter -- Hill, Richard -- McBride, William -- McKenna, Gillies -- Muschel, Ruth -- New York, N.Y. -- Science. 2003 Dec 12;302(5652):1894; author reply 1894.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Radiation Oncology, Stanford University, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14671275" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Disease Models, Animal ; Endothelium, Vascular/*pathology/radiation effects ; Melanoma, Experimental/blood supply/immunology/pathology/*radiotherapy ; Mice ; Radiation Tolerance ; Sphingomyelin Phosphodiesterase/genetics/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    More deafness genes (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-06-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Steel, K P -- Brown, S D -- New York, N.Y. -- Science. 1998 May 29;280(5368):1403.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council, Institute of Hearing Research, University Park, Nottingham NG7 2RD, UK. karen@ihr.mrc.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9634418" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/physiology ; Animals ; Cilia/physiology ; Deafness/*genetics ; Dyneins ; Extracellular Matrix Proteins/*genetics/physiology ; GPI-Linked Proteins ; Hair Cells, Auditory/physiology/ultrastructure ; Hearing ; Humans ; Membrane Glycoproteins/*genetics/physiology ; Mice ; Mice, Mutant Strains ; Mutation ; Myosin Heavy Chains/genetics/physiology ; Myosins/*genetics/physiology ; Tectorial Membrane/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    Lymphatic metastasis in the absence of functional intratumor lymphatics (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-04-27
    Description: Lymphatic metastasis contributes to mortality from solid tumors. Whether metastasizing cancer cells reach lymph nodes via intratumor lymphatic vessels is unknown. Here, we examine functional lymphatics associated with mouse tumors expressing normal or elevated levels of vascular endothelial growth factor-C (VEGF-C), a molecule that stimulates lymphangiogenesis. Although VEGF-C overexpression increased lymphatic surface area in the tumor margin and lymphatic metastasis, these tumors contained no functional lymphatics, as assessed by four independent functional assays and immunohistochemical staining. These findings suggest that the functional lymphatics in the tumor margin alone are sufficient for lymphatic metastasis and should be targeted therapeutically.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Padera, Timothy P -- Kadambi, Ananth -- di Tomaso, Emmanuelle -- Carreira, Carla Mouta -- Brown, Edward B -- Boucher, Yves -- Choi, Noah C -- Mathisen, Douglas -- Wain, John -- Mark, Eugene J -- Munn, Lance L -- Jain, Rakesh K -- R24-CA85140/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2002 Jun 7;296(5574):1883-6. Epub 2002 Apr 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉E. L. Steele Laboratory, Department of Radiation Oncology, Massachusetts General Hospital, Harvard Medical School, 100 Blossom Street, Boston, MA 02114, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11976409" target="_blank"〉PubMed〈/a〉
    Keywords: Adenocarcinoma/chemistry/pathology ; Animals ; Antigens, Surface/analysis ; Endothelial Growth Factors/metabolism ; Extracellular Space/physiology ; Fibrosarcoma/metabolism/*pathology/physiopathology/secondary ; Glycoproteins/analysis ; Humans ; Immunohistochemistry ; Lung Neoplasms/chemistry/pathology/physiopathology/secondary ; *Lymphatic Metastasis ; Lymphatic System/chemistry/*pathology/physiology ; Lymphography ; Melanoma, Experimental/metabolism/*pathology/physiopathology/secondary ; Mice ; Mice, Inbred C3H ; Mice, Nude ; Microscopy/methods ; Neoplasm Transplantation ; Neoplasms/metabolism/*pathology/physiopathology ; Pressure ; Tumor Cells, Cultured ; Vascular Endothelial Growth Factor C ; Vesicular Transport Proteins
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    Response to RAG-mediated VDJ cleavage by NBS1 and gamma-H2AX (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-12-09
    Description: Genetic disorders affecting cellular responses to DNA damage are characterized by high rates of translocations involving antigen receptor loci and increased susceptibility to lymphoid malignancies. We report that the Nijmegen breakage syndrome protein (NBS1) and histone gamma-H2AX, which associate with irradiation-induced DNA double-strand breaks (DSBs), are also found at sites of VDJ (variable, diversity, joining) recombination-induced DSBs. In developing thymocytes, NBS1 and gamma-H2AX form nuclear foci that colocalize with the T cell receptor alpha locus in response to recombination activating gene (RAG) protein-mediated VDJ cleavage. Our results suggest that surveillance of T cell receptor recombination intermediates by NBS1 and gamma-H2AX may be important for preventing oncogenic translocations.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4721589/" 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/PMC4721589/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, H T -- Bhandoola, A -- Difilippantonio, M J -- Zhu, J -- Brown, M J -- Tai, X -- Rogakou, E P -- Brotz, T M -- Bonner, W M -- Ried, T -- Nussenzweig, A -- Z99 CA999999/Intramural NIH HHS/ -- New York, N.Y. -- Science. 2000 Dec 8;290(5498):1962-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Experimental Immunology Branch, National Cancer Institute, 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/11110662" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cell Nucleus/metabolism ; DNA Damage ; DNA-Binding Proteins/metabolism ; Fluorescent Antibody Technique ; *Gene Rearrangement, alpha-Chain T-Cell Antigen Receptor ; *Genes, T-Cell Receptor alpha ; Histones/*metabolism ; Homeodomain Proteins/metabolism ; Mice ; Mice, Transgenic ; Microscopy, Confocal ; Molecular Sequence Data ; Nuclear Proteins/*metabolism ; Phosphorylation ; *Recombination, Genetic ; T-Lymphocytes/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    Circadian rhythms. Chronobiology--reducing time (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-07-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schibler, U -- Ripperger, J A -- Brown, S A -- New York, N.Y. -- Science. 2001 Jul 20;293(5529):437-8. Epub 2001 Jul 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Sciences II, University of Geneva, CH-1211 Geneva 4, Switzerland. ueli.schibler@molbio.unige.ch〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11441150" target="_blank"〉PubMed〈/a〉
    Keywords: ARNTL Transcription Factors ; Animals ; Basic Helix-Loop-Helix Transcription Factors ; Biological Clocks/*physiology ; CLOCK Proteins ; Cell Cycle Proteins ; Circadian Rhythm/*physiology ; Cryptochromes ; DNA/metabolism ; Dimerization ; *Drosophila Proteins ; Electron Transport ; *Eye Proteins ; Feedback ; Flavoproteins/metabolism ; Mice ; NAD/*metabolism ; Nerve Tissue Proteins/genetics/*metabolism ; Nuclear Proteins/metabolism ; Oxidation-Reduction ; Period Circadian Proteins ; *Photoreceptor Cells, Invertebrate ; Prosencephalon/metabolism ; Receptors, G-Protein-Coupled ; Suprachiasmatic Nucleus/physiology ; Trans-Activators/*metabolism ; Transcription Factors/genetics/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
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  • 7
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    Down-regulation of the macrophage lineage through interaction with OX2 (CD200) (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-12-02
    Description: OX2 (CD200) is a broadly expressed membrane glycoprotein, shown here to be important for regulation of the macrophage lineage. In mice lacking CD200, macrophage lineage cells, including brain microglia, exhibited an activated phenotype and were more numerous. Upon facial nerve transection, damaged CD200-deficient neurons elicited an accelerated microglial response. Lack of CD200 resulted in a more rapid onset of experimental autoimmune encephalomyelitis (EAE). Outside the brain, disruption of CD200-CD200 receptor interaction precipitated susceptibility to collagen-induced arthritis (CIA) in mice normally resistant to this disease. Thus, in diverse tissues OX2 delivers an inhibitory signal for the macrophage lineage.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hoek, R M -- Ruuls, S R -- Murphy, C A -- Wright, G J -- Goddard, R -- Zurawski, S M -- Blom, B -- Homola, M E -- Streit, W J -- Brown, M H -- Barclay, A N -- Sedgwick, J D -- New York, N.Y. -- Science. 2000 Dec 1;290(5497):1768-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉DNAX Research Institute of Molecular and Cellular Biology, 901 California Avenue, Palo Alto, CA 94304, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11099416" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD ; Antigens, Surface/*metabolism ; Arthritis, Experimental/immunology/pathology ; Cell Lineage ; Central Nervous System/immunology/pathology ; Denervation ; *Down-Regulation ; Encephalomyelitis, Autoimmune, Experimental/immunology/pathology ; Facial Nerve ; Gene Targeting ; Joints/immunology/pathology ; Lymph Nodes/cytology ; Macrophage Activation ; Macrophages/cytology/metabolism/*physiology ; Mice ; Mice, Inbred C57BL ; Microglia/physiology ; Neurons/physiology ; Rats ; Receptors, Immunologic/metabolism ; Spleen/cytology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
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  • 8
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    Vital involvement of a natural killer cell activation receptor in resistance to viral infection (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-05-08
    Description: Natural killer (NK) cells are lymphocytes that can be distinguished from T and B cells through their involvement in innate immunity and their lack of rearranged antigen receptors. Although NK cells and their receptors were initially characterized in terms of tumor killing in vitro, we have determined that the NK cell activation receptor, Ly-49H, is critically involved in resistance to murine cytomegalovirus in vivo. Ly-49H requires an immunoreceptor tyrosine-based activation motif (ITAM)-containing transmembrane molecule for expression and signal transduction. Thus, NK cells use receptors functionally resembling ITAM-coupled T and B cell antigen receptors to provide vital innate host defense.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brown, M G -- Dokun, A O -- Heusel, J W -- Smith, H R -- Beckman, D L -- Blattenberger, E A -- Dubbelde, C E -- Stone, L R -- Scalzo, A A -- Yokoyama, W M -- New York, N.Y. -- Science. 2001 May 4;292(5518):934-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Rheumatology Division, 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/11340207" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/immunology ; *Antigens, Ly ; Crosses, Genetic ; Cytotoxicity, Immunologic ; Female ; Haplotypes ; Herpesviridae Infections/*immunology ; Histocompatibility Antigens Class I/immunology ; Humans ; *Immunity, Innate ; Killer Cells, Natural/*immunology ; Lectins, C-Type ; Ligands ; *Lymphocyte Activation ; Male ; Membrane Glycoproteins/genetics/*immunology ; Mice ; Mice, Inbred C57BL ; Mice, Inbred DBA ; Muromegalovirus/*immunology ; Phenotype ; Receptors, Immunologic/*immunology ; Receptors, NK Cell Lectin-Like ; Tumor Cells, Cultured
    Print ISSN: 0036-8075
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  • 9
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    Germline transmission and tissue-specific expression of transgenes delivered by lentiviral vectors (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-01-12
    Description: Single-cell mouse embryos were infected in vitro with recombinant lentiviral vectors to generate transgenic mice carrying the green fluorescent protein (GFP) gene driven by a ubiquitously expressing promoter. Eighty percent of founder mice carried at least one copy of the transgene, and 90% of these expressed GFP at high levels. Progeny inherited the transgene(s) and displayed green fluorescence. Mice generated using lentiviral vectors with muscle-specific and T lymphocyte-specific promoters expressed high levels of GFP only in the appropriate cell types. We have also generated transgenic rats that express GFP at high levels, suggesting that this technique can be used to produce other transgenic animal species.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lois, Carlos -- Hong, Elizabeth J -- Pease, Shirley -- Brown, Eric J -- Baltimore, David -- New York, N.Y. -- Science. 2002 Feb 1;295(5556):868-72. Epub 2002 Jan 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biology, California Institute of Technology, Pasadena, CA 91125, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11786607" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Animals, Genetically Modified ; Blotting, Southern ; Blotting, Western ; Cell Lineage ; Crosses, Genetic ; DNA, Recombinant ; Embryo Transfer ; Embryo, Mammalian/*metabolism/virology ; Female ; Gene Dosage ; *Gene Expression ; Gene Silencing ; Genes, Reporter ; *Genetic Vectors ; Green Fluorescent Proteins ; HIV-1/genetics ; Hepatitis B Virus, Woodchuck/genetics ; Lentivirus/*genetics ; Luminescent Proteins/biosynthesis/genetics ; Male ; Mice ; Mice, Transgenic ; Muscle, Skeletal/embryology/metabolism ; Organ Specificity ; Promoter Regions, Genetic ; Proviruses/genetics ; Rats ; *Transgenes ; Virus Integration
    Print ISSN: 0036-8075
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  • 10
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    Resetting of circadian time in peripheral tissues by glucocorticoid signaling (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-09-29
    Description: In mammals, circadian oscillators reside not only in the suprachiasmatic nucleus of the brain, which harbors the central pacemaker, but also in most peripheral tissues. Here, we show that the glucocorticoid hormone analog dexamethasone induces circadian gene expression in cultured rat-1 fibroblasts and transiently changes the phase of circadian gene expression in liver, kidney, and heart. However, dexamethasone does not affect cyclic gene expression in neurons of the suprachiasmatic nucleus. This enabled us to establish an apparent phase-shift response curve specifically for peripheral clocks in intact animals. In contrast to the central clock, circadian oscillators in peripheral tissues appear to remain responsive to phase resetting throughout the day.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Balsalobre, A -- Brown, S A -- Marcacci, L -- Tronche, F -- Kellendonk, C -- Reichardt, H M -- Schutz, G -- Schibler, U -- New York, N.Y. -- Science. 2000 Sep 29;289(5488):2344-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departement de Biologie Moleculaire, Sciences II, Universite de Geneve, 30 Quai Ernest Ansermet, CH-1211 Geneve, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11009419" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Clocks/*physiology ; Cell Cycle Proteins ; Cell Line ; Circadian Rhythm/*physiology ; *DNA-Binding Proteins ; Dexamethasone/analogs & derivatives/*pharmacology ; Female ; *Gene Expression Regulation/drug effects ; Kidney/metabolism ; Liver/metabolism ; Male ; Mice ; Mice, Inbred Strains ; Mutation ; Myocardium/metabolism ; Neurons/metabolism ; Nuclear Proteins/genetics/metabolism ; Period Circadian Proteins ; Rats ; Receptors, Glucocorticoid/genetics/metabolism ; *Signal Transduction ; Suprachiasmatic Nucleus/metabolism ; Transcription Factors/genetics/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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