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  • United States  (1,085)
  • Cell Line  (506)
  • American Association for the Advancement of Science (AAAS)  (1,584)
  • American Association of Petroleum Geologists (AAPG)
  • Bonn: Institute of Labor Economics (IZA)
  • The International Collective in Support of Fishworkers (ICSF)
  • 1995-1999  (1,049)
  • 1980-1984  (535)
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  • American Association for the Advancement of Science (AAAS)  (1,584)
  • American Association of Petroleum Geologists (AAPG)
  • Bonn: Institute of Labor Economics (IZA)
  • The International Collective in Support of Fishworkers (ICSF)
  • Springer  (14)
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Year
  • 1
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-01-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Goldman, L R -- New York, N.Y. -- Science. 1998 Dec 4;282(5395):1825-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9874633" target="_blank"〉PubMed〈/a〉
    Keywords: Child ; Environmental Exposure ; Environmental Pollutants/adverse effects ; Government Agencies ; Humans ; Lead/adverse effects ; Lead Poisoning/*prevention & control ; United States ; United States Environmental Protection Agency
    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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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-01-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gough, M -- New York, N.Y. -- Science. 1998 Dec 4;282(5395):1823.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9874631" target="_blank"〉PubMed〈/a〉
    Keywords: 2,4,5-Trichlorophenoxyacetic Acid/adverse effects ; 2,4-Dichlorophenoxyacetic Acid/adverse effects ; Confidentiality/*legislation & jurisprudence ; Defoliants, Chemical ; Financing, Government ; Humans ; *Public Policy ; Research/*legislation & jurisprudence ; *Research Support as Topic ; Tetrachlorodibenzodioxin/adverse effects ; United States
    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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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-09-08
    Description: Postdoctoral appointments can have different functions and meanings, depending on the field and whether the postdoc is a man or a woman. The Ph.D.'s-Ten Years Later study confirmed that in biochemistry, the postdoc, not the Ph.D., has become the general proving ground for excellence both in academia and industry. Because they spent a longer time in these "mandatory" postdocs, biochemists had the largest proportion of untenured faculty 10 to 13 years after the Ph. D. In mathematics, where substantially fewer postdoctoral positions are available, Ph.D.'s taking postdocs are more likely to obtain faculty positions, but this is true only for men. University administrators should be accountable for monitoring the total time spent in these positions and should provide administrative assistance for skills training, career growth, and the job search. In addition, creative solutions concerning the dual-career couple phenomenon are necessary.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nerad, M -- Cerny, J -- New York, N.Y. -- Science. 1999 Sep 3;285(5433):1533-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Graduate Division, University of California, Berkeley, 424 Sproul Hall, Berkeley, CA 94720-5900, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10477510" target="_blank"〉PubMed〈/a〉
    Keywords: *Biochemistry/education ; *Career Mobility ; *Education, Graduate ; Employment ; Faculty ; *Fellowships and Scholarships ; Female ; Humans ; Male ; *Mathematics ; Salaries and Fringe Benefits ; Societies, Scientific ; Time Factors ; United States ; Universities
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-01-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Couzin, J -- New York, N.Y. -- Science. 1998 Dec 18;282(5397):2175-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9890822" target="_blank"〉PubMed〈/a〉
    Keywords: Budgets ; Cartilage ; *Complementary Therapies/economics/organization & administration ; Controlled Clinical Trials as Topic ; Humans ; Lung Neoplasms/therapy ; National Institutes of Health (U.S.)/economics/*organization & administration ; Research Support as Topic ; Tissue Extracts/therapeutic use ; United States
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-09-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wickelgren, I -- New York, N.Y. -- Science. 1999 Aug 13;285(5430):999.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10475850" target="_blank"〉PubMed〈/a〉
    Keywords: Biotechnology/history ; Genetics, Medical/history ; Genome, Human ; History, 20th Century ; Humans ; United States
    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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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-12-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Langan, P -- Schoenborn, B P -- New York, N.Y. -- Science. 1999 Nov 5;286(5442):1089.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10610521" target="_blank"〉PubMed〈/a〉
    Keywords: Crystallography/*instrumentation ; *Neutrons ; Proteins/*chemistry ; United States
    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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  • 7
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-07-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Laver, W G -- New York, N.Y. -- Science. 1999 Jun 25;284(5423):2089.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10409063" target="_blank"〉PubMed〈/a〉
    Keywords: Crystallization ; Neuraminidase/*chemistry ; *Space Flight ; *Spacecraft ; United States ; United States National Aeronautics and Space Administration ; *Weightlessness
    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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  • 8
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-01-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lawler, C -- Erbisch, F -- New York, N.Y. -- Science. 1999 Jan 1;283(5398):33-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9917260" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biotechnology ; Mice ; Mice, Transgenic ; *Patents as Topic ; Plants, Genetically Modified/*genetics ; United States
    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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  • 9
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-10-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shapiro, H T -- New York, N.Y. -- Science. 1999 Sep 24;285(5436):2065.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10523197" target="_blank"〉PubMed〈/a〉
    Keywords: Advisory Committees ; *Bioethical Issues ; Embryo Research ; Embryo, Mammalian/*cytology ; Ethics Committees ; Financing, Government ; Government Regulation ; Humans ; Private Sector ; *Public Policy ; Research/*standards ; Research Support as Topic ; *Stem Cells ; United States
    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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  • 10
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-06-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Colvin, M -- New York, N.Y. -- Science. 1999 May 28;284(5419):1480.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Duke Comprehensive Cancer Center, Durham, NC 27710, USA. colvi003@mc.duke.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10383327" target="_blank"〉PubMed〈/a〉
    Keywords: Chemistry, Pharmaceutical/history ; Drug Design ; History, 20th Century ; Nobel Prize ; United States
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  • 11
    Publication Date: 1999-11-05
    Description: The Brca1 (breast cancer gene 1) tumor suppressor protein is phosphorylated in response to DNA damage. Results from this study indicate that the checkpoint protein kinase ATM (mutated in ataxia telangiectasia) was required for phosphorylation of Brca1 in response to ionizing radiation. ATM resides in a complex with Brca1 and phosphorylated Brca1 in vivo and in vitro in a region that contains clusters of serine-glutamine residues. Phosphorylation of this domain appears to be functionally important because a mutated Brca1 protein lacking two phosphorylation sites failed to rescue the radiation hypersensitivity of a Brca1-deficient cell line. Thus, phosphorylation of Brca1 by the checkpoint kinase ATM may be critical for proper responses to DNA double-strand breaks and may provide a molecular explanation for the role of ATM in breast cancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cortez, D -- Wang, Y -- Qin, J -- Elledge, S J -- GM44664/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1999 Nov 5;286(5442):1162-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Verna and Mars McLean Department of Biochemistry and Molecular Biology, Howard Hughes Medical Institute, Department of Cell Biology, Baylor College of Medicine, Houston, TX 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10550055" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Ataxia Telangiectasia/genetics ; Ataxia Telangiectasia Mutated Proteins ; BRCA1 Protein/*metabolism ; Breast Neoplasms/genetics ; Cell Cycle Proteins ; Cell Line ; *DNA Damage ; *DNA Repair ; DNA, Complementary ; DNA-Binding Proteins ; Female ; Gamma Rays ; Genes, BRCA1 ; Genetic Predisposition to Disease ; HeLa Cells ; Heterozygote ; Humans ; Molecular Sequence Data ; Mutation ; Phosphorylation ; Protein-Serine-Threonine Kinases/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Tumor Suppressor Proteins
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
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  • 12
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-10-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sherley, J L -- New York, N.Y. -- Science. 1999 Sep 10;285(5434):1676-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10523183" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; *Gene Expression Regulation ; Genetic Vectors ; Operator Regions, Genetic ; Recombinant Fusion Proteins/metabolism ; Repressor Proteins/metabolism ; *Research Design ; Tetracycline/*pharmacology ; Trans-Activators/metabolism
    Print ISSN: 0036-8075
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  • 13
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-06-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Av-Gay, Y -- New York, N.Y. -- Science. 1999 Jun 4;284(5420):1621.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10383337" target="_blank"〉PubMed〈/a〉
    Keywords: Bacteria/*genetics/pathogenicity ; *Biotechnology ; *Containment of Biohazards ; Ecosystem ; *Genetic Engineering ; Guidelines as Topic ; Humans ; United States ; Viruses/*genetics/pathogenicity
    Print ISSN: 0036-8075
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  • 14
    Publication Date: 1999-08-28
    Description: Class II transactivator (CIITA) is a global transcriptional coactivator of human leukocyte antigen-D (HLA-D) genes. CIITA contains motifs similar to guanosine triphosphate (GTP)-binding proteins. This report shows that CIITA binds GTP, and mutations in these motifs decrease its GTP-binding and transactivation activity. Substitution of these motifs with analogous sequences from Ras restores CIITA function. CIITA exhibits little GTPase activity, yet mutations in CIITA that confer GTPase activity reduce transcriptional activity. GTP binding by CIITA correlates with nuclear import. Thus, unlike other GTP-binding proteins, CIITA is involved in transcriptional activation that uses GTP binding to facilitate its own nuclear import.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Harton, J A -- Cressman, D E -- Chin, K C -- Der, C J -- Ting, J P -- AI29564/AI/NIAID NIH HHS/ -- AI41751/AI/NIAID NIH HHS/ -- AI45580/AI/NIAID NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1999 Aug 27;285(5432):1402-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Lineberger Comprehensive Cancer Center, University of North Carolina-Chapel Hill, Chapel Hill, NC 27599, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10464099" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Animals ; Binding Sites ; COS Cells ; Cell Line ; Cell Nucleus/*metabolism ; GTP-Binding Proteins/chemistry/genetics/*metabolism ; *Genes, MHC Class II ; Guanosine Triphosphate/*metabolism ; HLA-DR Antigens/genetics ; Humans ; Mutation ; *Nuclear Proteins ; Promoter Regions, Genetic ; Temperature ; Trans-Activators/chemistry/genetics/*metabolism ; Transcription Factors/metabolism ; *Transcriptional Activation
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 15
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-12-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Curry, M -- Hazard-Daniel, A -- Daniel, H J -- New York, N.Y. -- Science. 1999 Dec 3;286(5446):1854-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10610573" target="_blank"〉PubMed〈/a〉
    Keywords: *Dietary Supplements/adverse effects ; Drug Prescriptions ; Drug-Related Side Effects and Adverse Reactions ; *Legislation, Drug ; *Legislation, Food ; United States ; United States Food and Drug Administration
    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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  • 16
    Publication Date: 1999-07-31
    Description: Many immune receptors are composed of separate ligand-binding and signal-transducing subunits. In natural killer (NK) and T cells, DAP10 was identified as a cell surface adaptor protein in an activating receptor complex with NKG2D, a receptor for the stress-inducible and tumor-associated major histocompatibility complex molecule MICA. Within the DAP10 cytoplasmic domain, an Src homology 2 (SH2) domain-binding site was capable of recruiting the p85 subunit of the phosphatidylinositol 3-kinase (PI 3-kinase), providing for NKG2D-dependent signal transduction. Thus, NKG2D-DAP10 receptor complexes may activate NK and T cell responses against MICA-bearing tumors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wu, J -- Song, Y -- Bakker, A B -- Bauer, S -- Spies, T -- Lanier, L L -- Phillips, J H -- AI30581/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1999 Jul 30;285(5428):730-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉DNAX Research Institute, 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/10426994" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Binding Sites ; Cell Line ; Cytotoxicity, Immunologic ; Humans ; Killer Cells, Natural/*immunology/metabolism ; Ligands ; *Lymphocyte Activation ; Membrane Proteins/chemistry/genetics/*metabolism ; Mice ; Molecular Sequence Data ; NK Cell Lectin-Like Receptor Subfamily K ; Neoplasms/immunology ; Phosphatidylinositol 3-Kinases/metabolism ; Phosphorylation ; Phosphotyrosine/metabolism ; Receptors, Immunologic/chemistry/genetics/*metabolism ; Receptors, Natural Killer Cell ; Signal Transduction ; T-Lymphocytes/*immunology/metabolism ; Tumor Cells, Cultured ; src Homology Domains
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 17
    Publication Date: 1999-04-09
    Description: Phosphorylation of inhibitor of kappa B (IkappaB) proteins is an important step in the activation of the transcription nuclear factor kappa B (NF-kappaB) and requires two IkappaB kinases, IKK1 (IKKalpha) and IKK2 (IKKbeta). Mice that are devoid of the IKK2 gene had extensive liver damage from apoptosis and died as embryos, but these mice could be rescued by the inactivation of the gene encoding tumor necrosis factor receptor 1. Mouse embryonic fibroblast cells that were isolated from IKK2-/- embryos showed a marked reduction in tumor necrosis factor-alpha (TNF-alpha)- and interleukin-1alpha-induced NF-kappaB activity and an enhanced apoptosis in response to TNF-alpha. IKK1 associated with NF-kappaB essential modulator (IKKgamma/IKKAP1), another component of the IKK complex. These results show that IKK2 is essential for mouse development and cannot be substituted with IKK1.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Q -- Van Antwerp, D -- Mercurio, F -- Lee, K F -- Verma, I M -- New York, N.Y. -- Science. 1999 Apr 9;284(5412):321-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Salk Institute, La Jolla, CA 92037, USA. Signal Pharmaceuticals, San Diego, CA 92121, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10195897" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Cell Line ; DNA-Binding Proteins/metabolism ; Embryonic and Fetal Development ; Gene Targeting ; I-kappa B Kinase ; I-kappa B Proteins ; Interleukin-1/pharmacology ; Liver/cytology/*embryology ; Mice ; NF-kappa B/metabolism ; Phosphorylation ; Polymerase Chain Reaction ; Protein-Serine-Threonine Kinases/genetics/*metabolism ; Receptors, Tumor Necrosis Factor/genetics/metabolism ; Recombinant Fusion Proteins/metabolism ; Sequence Deletion ; Signal Transduction ; Transcription Factor RelA ; Transcription Factors/metabolism ; Tumor Necrosis Factor-alpha/pharmacology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 18
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-01-29
    Description: The protein encoded by the c-MYC proto-oncogene is a transcription factor that can both activate and repress the expression of target genes, but few of its transcriptional targets have been identified. Here, c-MYC is shown to repress the expression of the heavy subunit of the protein ferritin (H-ferritin), which sequesters intracellular iron, and to stimulate the expression of the iron regulatory protein-2 (IRP2), which increases the intracellular iron pool. Down-regulation of the expression of H-ferritin gene was required for cell transformation by c-MYC. These results indicate that c-MYC coordinately regulates genes controlling intracellular iron concentrations and that this function is essential for the control of cell proliferation and transformation by c-MYC.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wu, K J -- Polack, A -- Dalla-Favera, R -- CA-37165/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1999 Jan 29;283(5402):676-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Oncology, Department of Pathology, Columbia University, New York, NY 10032, USA. an.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9924025" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Division ; Cell Line ; Cell Line, Transformed ; Cell Transformation, Neoplastic ; DNA/biosynthesis ; Down-Regulation ; Ferritins/*genetics/metabolism ; *Gene Expression Regulation ; Genes, myc ; Homeostasis ; Iron/*metabolism ; Iron Regulatory Protein 2 ; Iron-Regulatory Proteins ; Iron-Sulfur Proteins/*genetics/metabolism ; Proto-Oncogene Proteins c-myc/*physiology ; RNA/metabolism ; RNA-Binding Proteins/*genetics/metabolism ; Receptors, Transferrin/genetics ; Transcription, Genetic ; Transfection
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 19
    Publication Date: 1999-09-18
    Description: Antithrombin, a member of the serpin family, functions as an inhibitor of thrombin and other enzymes. Cleavage of the carboxyl-terminal loop of antithrombin induces a conformational change in the molecule. Here it is shown that the cleaved conformation of antithrombin has potent antiangiogenic and antitumor activity in mouse models. The latent form of intact antithrombin, which is similar in conformation to the cleaved molecule, also inhibited angiogenesis and tumor growth. These data provide further evidence that the clotting and fibrinolytic pathways are directly involved in the regulation of angiogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉O'Reilly, M S -- Pirie-Shepherd, S -- Lane, W S -- Folkman, J -- P01-CA45548/CA/NCI NIH HHS/ -- R01-CA64481/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1999 Sep 17;285(5435):1926-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Surgery, Children's Hospital, Departments of Surgery and Cellular Biology, Harvard Microchemistry Facility, 16 Divinity Avenue, Cambridge, MA 02138, USA. oreilly@hub.tch.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10489375" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antineoplastic Agents/chemistry/isolation & purification/metabolism/*pharmacology ; Antithrombins/chemistry/isolation & purification/metabolism/*pharmacology ; Carcinoma, Small Cell/blood supply/drug therapy ; Cell Line ; Culture Media, Conditioned ; Drug Screening Assays, Antitumor ; Humans ; Lung Neoplasms/blood supply/drug therapy ; Mice ; Mice, SCID ; Neoplasm Transplantation ; Neovascularization, Pathologic/*drug therapy ; Peptide Fragments/chemistry/metabolism/pharmacology ; Protein Conformation ; Tumor Cells, Cultured
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  • 20
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-05-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Baker, M -- New York, N.Y. -- Science. 1999 Apr 16;284(5413):410.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10232978" target="_blank"〉PubMed〈/a〉
    Keywords: Academies and Institutes/*organization & administration ; Developing Countries ; History, 20th Century ; *Immunization Programs ; Korea ; United Nations ; United States ; *Vaccines ; World Health Organization
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  • 21
    Publication Date: 1999-09-18
    Description: The bacterial pathogen Yersinia uses a type III secretion system to inject several virulence factors into target cells. One of the Yersinia virulence factors, YopJ, was shown to bind directly to the superfamily of MAPK (mitogen-activated protein kinase) kinases (MKKs) blocking both phosphorylation and subsequent activation of the MKKs. These results explain the diverse activities of YopJ in inhibiting the extracellular signal-regulated kinase, c-Jun amino-terminal kinase, p38, and nuclear factor kappa B signaling pathways, preventing cytokine synthesis and promoting apoptosis. YopJ-related proteins that are found in a number of bacterial pathogens of animals and plants may function to block MKKs so that host signaling responses can be modulated upon infection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Orth, K -- Palmer, L E -- Bao, Z Q -- Stewart, S -- Rudolph, A E -- Bliska, J B -- Dixon, J E -- 18024/PHS HHS/ -- AI35175/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1999 Sep 17;285(5435):1920-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Chemistry, University of Michigan, Ann Arbor, MI 48109-0606, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10489373" target="_blank"〉PubMed〈/a〉
    Keywords: Bacterial Proteins/*physiology ; Calcium-Calmodulin-Dependent Protein Kinases/*antagonists & inhibitors ; Cell Line ; Enzyme Activation ; Enzyme Inhibitors/*pharmacology ; HeLa Cells ; Humans ; *MAP Kinase Kinase Kinase 1 ; NF-kappa B/metabolism ; Phosphorylation ; Protein Binding ; Protein-Serine-Threonine Kinases/genetics/metabolism ; Recombinant Fusion Proteins/genetics/metabolism ; Transfection ; Virulence ; Yersinia pseudotuberculosis/genetics/metabolism/pathogenicity/*physiology
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  • 22
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-07-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hemminki, E -- Hailey, D -- Koivusalo, M -- New York, N.Y. -- Science. 1999 Jul 9;285(5425):203-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Research and Development Centre for Welfare and Health, Helsinki, Finland. elina.hemminki@stakes.fi〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10428717" target="_blank"〉PubMed〈/a〉
    Keywords: Anticholesteremic Agents/therapeutic use ; Canada ; Commerce ; Contraceptive Agents, Female ; Drug Approval ; Finland ; International Cooperation ; Jurisprudence ; Levonorgestrel ; Publishing ; Technology Assessment, Biomedical/*legislation & jurisprudence ; United States
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  • 23
    Publication Date: 1999-10-16
    Description: Defensins contribute to host defense by disrupting the cytoplasmic membrane of microorganisms. This report shows that human beta-defensins are also chemotactic for immature dendritic cells and memory T cells. Human beta-defensin was selectively chemotactic for cells stably transfected to express human CCR6, a chemokine receptor preferentially expressed by immature dendritic cells and memory T cells. The beta-defensin-induced chemotaxis was sensitive to pertussis toxin and inhibited by antibodies to CCR6. The binding of iodinated LARC, the chemokine ligand for CCR6, to CCR6-transfected cells was competitively displaced by beta-defensin. Thus, beta-defensins may promote adaptive immune responses by recruiting dendritic and T cells to the site of microbial invasion through interaction with CCR6.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yang, D -- Chertov, O -- Bykovskaia, S N -- Chen, Q -- Buffo, M J -- Shogan, J -- Anderson, M -- Schroder, J M -- Wang, J M -- Howard, O M -- Oppenheim, J J -- N01-CO-56000/CO/NCI NIH HHS/ -- New York, N.Y. -- Science. 1999 Oct 15;286(5439):525-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Immunoregulation, Division of Basic Sciences, Intramural Research Support Program, SAIC Frederick, National Cancer Institute-Frederick Cancer Research and Development Center, Frederick, MD 21702-1201, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10521347" target="_blank"〉PubMed〈/a〉
    Keywords: Antibodies/immunology ; Binding, Competitive ; Cell Line ; Chemokine CCL20 ; Chemokines, CC/metabolism/pharmacology ; Chemotaxis ; Chemotaxis, Leukocyte ; Defensins ; Dendritic Cells/*immunology ; Humans ; *Immunity, Active ; *Immunity, Innate ; Immunologic Memory ; *Macrophage Inflammatory Proteins ; Pertussis Toxin ; Proteins/pharmacology/*physiology ; Receptors, CCR6 ; Receptors, Chemokine/genetics/*metabolism ; Recombinant Proteins/pharmacology ; T-Lymphocyte Subsets/*immunology ; Transfection ; Virulence Factors, Bordetella/pharmacology ; *beta-Defensins
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  • 24
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-02-26
    Description: Biological weapons have recently attracted the attention and the resources of the nation. Discerning the nature of the threat of bioweapons as well as appropriate responses to them requires greater attention to the biological characteristics of these instruments of war and terror. The dominant paradigm of a weapon as a nuclear device that explodes or a chemical cloud that is set adrift leaves us ill-equipped conceptually and practically to assess and thus to prevent the potentially devastating effects of bioterrorism. Strengthening the public health and infectious disease infrastructure is an effective step toward averting the suffering that could be wrought by a terrorist's use of a biological agent.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Henderson, D A -- New York, N.Y. -- Science. 1999 Feb 26;283(5406):1279-82.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Johns Hopkins Center for Civilian Biodefense Studies, Johns Hopkins School of Public Health, Suite 850, Candler Building, 111 Market Place, Baltimore, MD 21202, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10037590" target="_blank"〉PubMed〈/a〉
    Keywords: Anthrax/epidemiology/prevention & control/therapy/transmission ; *Biological Warfare/prevention & control ; Disaster Planning ; Disease Outbreaks ; Humans ; *Public Health ; Smallpox/epidemiology/prevention & control/therapy/transmission ; United States ; Vaccination ; *Violence/prevention & control
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  • 25
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-06-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lipman, N S -- Nguyen, H -- Perkins, S -- New York, N.Y. -- Science. 1999 May 14;284(5417):1123.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10366341" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Laboratory/virology ; Blood/*virology ; China ; *Ectromelia virus ; Ectromelia, Infectious/epidemiology/*transmission ; Mice/*virology ; Rodent Diseases/epidemiology/*transmission ; United States
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  • 26
    Publication Date: 1999-04-09
    Description: IkappaB [inhibitor of nuclear factor kappaB (NF-kappaB)] kinase (IKK) phosphorylates IkappaB inhibitory proteins, causing their degradation and activation of transcription factor NF-kappaB, a master activator of inflammatory responses. IKK is composed of three subunits-IKKalpha and IKKbeta, which are highly similar protein kinases, and IKKgamma, a regulatory subunit. In mammalian cells, phosphorylation of two sites at the activation loop of IKKbeta was essential for activation of IKK by tumor necrosis factor and interleukin-1. Elimination of equivalent sites in IKKalpha, however, did not interfere with IKK activation. Thus, IKKbeta, not IKKalpha, is the target for proinflammatory stimuli. Once activated, IKKbeta autophosphorylated at a carboxyl-terminal serine cluster. Such phosphorylation decreased IKK activity and may prevent prolonged activation of the inflammatory response.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Delhase, M -- Hayakawa, M -- Chen, Y -- Karin, M -- R01 AI43477/AI/NIAID NIH HHS/ -- R37 ES04151/ES/NIEHS NIH HHS/ -- New York, N.Y. -- Science. 1999 Apr 9;284(5412):309-13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Gene Regulation and Signal Transduction, Department of Pharmacology, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0636, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10195894" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Amino Acid Substitution ; Cell Line ; DNA-Binding Proteins/metabolism ; Enzyme Activation ; HeLa Cells ; Helix-Loop-Helix Motifs ; Humans ; I-kappa B Kinase ; I-kappa B Proteins ; Interleukin-1/pharmacology ; Leucine Zippers ; *MAP Kinase Kinase Kinase 1 ; Molecular Sequence Data ; Mutation ; Phosphorylation ; Phosphoserine/metabolism ; Protein-Serine-Threonine Kinases/chemistry/genetics/*metabolism ; Transfection ; Tumor Necrosis Factor-alpha/pharmacology
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  • 27
    Publication Date: 1999-01-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pardes, H -- Manton, K G -- Lander, E S -- Tolley, H D -- Ullian, A D -- Palmer, H -- New York, N.Y. -- Science. 1999 Jan 1;283(5398):36-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Faculty of Medicine, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA. hp2@columbia.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9917262" target="_blank"〉PubMed〈/a〉
    Keywords: Aged ; *Biotechnology/economics ; *Delivery of Health Care ; Disabled Persons ; Drug Industry ; *Economics, Medical ; *Health Care Costs ; Health Status ; Humans ; Longevity ; *Research ; United States
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  • 28
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-06-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Balter, M -- New York, N.Y. -- Science. 1999 May 28;284(5419):1453, 1455.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10383320" target="_blank"〉PubMed〈/a〉
    Keywords: Animal Husbandry ; Animals ; Carcinogens/*analysis ; Cattle ; Drug Residues/adverse effects/*analysis ; Estradiol/adverse effects/*analysis ; European Union ; *Food Contamination ; Gonadal Steroid Hormones/adverse effects/*analysis ; Humans ; Meat/adverse effects/*analysis ; Mutagens/analysis ; Neoplasms/chemically induced ; United States ; United States Food and Drug Administration
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  • 29
    Publication Date: 1999-11-05
    Description: Focal adhesions (FAs) are clustered integrins and associated proteins that mediate cell adhesion and signaling. A green fluorescent protein-beta1 integrin chimera was used to label FAs in living cells. In stationary cells, FAs were highly motile, moving linearly for several plaque lengths toward the cell center. FA motility was independent of cell density and resulted from contraction of associated actin fibers. In migrating cells, FAs were stationary and only moved in the tail. FA motility in stationary cells suggests that cell movement may be regulated by a clutch-like mechanism by which the affinity of integrins to substrate may be altered in response to migratory cues.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Smilenov, L B -- Mikhailov, A -- Pelham, R J -- Marcantonio, E E -- Gundersen, G G -- GM42026/GM/NIGMS NIH HHS/ -- GM44585/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1999 Nov 5;286(5442):1172-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Columbia University, New York, NY 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10550057" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Actins/physiology ; Animals ; Antigens, CD29/*metabolism ; *Cell Adhesion ; Cell Count ; Cell Line ; *Cell Movement ; Fibroblasts/*cytology/metabolism ; Fluorescence ; Green Fluorescent Proteins ; Luminescent Proteins ; Mice ; Microscopy, Interference ; Rats ; Recombinant Fusion Proteins/metabolism
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  • 30
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-06-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉DeLucas, L J -- New York, N.Y. -- Science. 1999 Jun 4;284(5420):1621.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10383336" target="_blank"〉PubMed〈/a〉
    Keywords: Cryopreservation ; Crystallization ; Crystallography, X-Ray ; Drug Design ; Drug Industry ; Enzyme Inhibitors ; Neuraminidase/antagonists & inhibitors/*chemistry ; *Spacecraft ; United States ; United States National Aeronautics and Space Administration ; *Weightlessness
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  • 31
    Publication Date: 1999-05-21
    Description: Bile acids regulate the transcription of genes that control cholesterol homeostasis through molecular mechanisms that are poorly understood. Physiological concentrations of free and conjugated chenodeoxycholic acid, lithocholic acid, and deoxycholic acid activated the farnesoid X receptor (FXR; NR1H4), an orphan nuclear receptor. As ligands, these bile acids and their conjugates modulated interaction of FXR with a peptide derived from steroid receptor coactivator 1. These results provide evidence for a nuclear bile acid signaling pathway that may regulate cholesterol homeostasis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Parks, D J -- Blanchard, S G -- Bledsoe, R K -- Chandra, G -- Consler, T G -- Kliewer, S A -- Stimmel, J B -- Willson, T M -- Zavacki, A M -- Moore, D D -- Lehmann, J M -- F32 DK09793/DK/NIDDK NIH HHS/ -- R01 DK53366/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1999 May 21;284(5418):1365-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biochemistry, Glaxo Wellcome Research and Development, Research Triangle Park NC, 27709, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10334993" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bile Acids and Salts/chemistry/*metabolism/pharmacology ; Carrier Proteins/metabolism ; Cell Line ; Chenodeoxycholic Acid/*metabolism/pharmacology ; Cholesterol/metabolism ; DNA-Binding Proteins/chemistry/genetics/*metabolism ; Deoxycholic Acid/metabolism/pharmacology ; Histone Acetyltransferases ; Homeostasis ; Humans ; Ligands ; Lithocholic Acid/metabolism/pharmacology ; Mice ; Nuclear Receptor Coactivator 1 ; *Organic Anion Transporters, Sodium-Dependent ; Protein Conformation ; Receptors, Cytoplasmic and Nuclear/chemistry/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Structure-Activity Relationship ; *Symporters ; Transcription Factors/chemistry/genetics/*metabolism ; Transfection
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  • 32
    Publication Date: 1999-10-26
    Description: T cell receptor (TCR)-induced apoptosis of thymocytes is mediated by calcium-dependent expression of the steroid receptors Nur77 and Nor1. Nur77 expression is controlled by the transcription factor myocyte enhancer factor 2 (MEF2), but how MEF2 is activated by calcium signaling is still obscure. Cabin1, a calcineurin inhibitor, was found to regulate MEF2. MEF2 was normally sequestered by Cabin1 in a transcriptionally inactive state. TCR engagement led to an increase in intracellular calcium concentration and the dissociation of MEF2 from Cabin1, as a result of competitive binding of activated calmodulin to Cabin1. The interplay between Cabin1, MEF2, and calmodulin defines a distinct signaling pathway from the TCR to the Nur77 promoter during T cell apoptosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Youn, H D -- Sun, L -- Prywes, R -- Liu, J O -- GM55783/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1999 Oct 22;286(5440):790-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Cancer Research, Department of Biology, Department of Chemistry, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10531067" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; *Apoptosis ; Calcineurin/chemistry/genetics/metabolism/pharmacology ; Calcium/metabolism ; *Calcium Signaling ; Calmodulin/metabolism ; Cell Line ; DNA-Binding Proteins/chemistry/genetics/*metabolism ; Gene Expression ; Genes, Reporter ; Humans ; Jurkat Cells ; MEF2 Transcription Factors ; Myogenic Regulatory Factors ; Nuclear Receptor Subfamily 4, Group A, Member 1 ; Phosphoproteins/chemistry/genetics/metabolism/pharmacology ; Receptors, Antigen, T-Cell/metabolism ; Receptors, Cytoplasmic and Nuclear ; Receptors, Steroid ; T-Lymphocytes/*cytology/*metabolism ; Transcription Factors/chemistry/genetics/*metabolism ; Transcription, Genetic ; Two-Hybrid System Techniques
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  • 33
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-09-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lovins, A B -- New York, N.Y. -- Science. 1999 Sep 3;285(5433):1489-91; author reply 1492.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10498532" target="_blank"〉PubMed〈/a〉
    Keywords: Agriculture/*methods ; Crops, Agricultural/*genetics ; Directed Molecular Evolution ; *Food ; *Plants, Genetically Modified ; United States ; United States Department of Agriculture ; United States Environmental Protection Agency ; United States Food and Drug Administration
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  • 34
    Publication Date: 1999-05-29
    Description: Inositol 1,4,5-trisphosphate (IP3) is a second messenger that elicits complex spatiotemporal patterns of calcium ion (Ca2+) mobilization and has essential roles in the regulation of many cellular functions. In Madin-Darby canine kidney epithelial cells, green fluorescent protein-tagged pleckstrin homology domain translocated from the plasma membrane to the cytoplasm in response to increased concentration of IP3. The detection of translocation enabled monitoring of IP3 concentration changes within single cells and revealed spatiotemporal dynamics in the concentration of IP3 synchronous with Ca2+ oscillations and intracellular and intercellular IP3 waves that accompanied Ca2+ waves. Such changes in IP3 concentration may be fundamental to Ca2+ signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hirose, K -- Kadowaki, S -- Tanabe, M -- Takeshima, H -- Iino, M -- New York, N.Y. -- Science. 1999 May 28;284(5419):1527-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, Faculty of Medicine, University of Tokyo and CREST, Japan Science and Technology Corporation, Tokyo 113-8654, Japan. hirose@calcium.cmp.m.u-tokyo.ac.jp〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10348740" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/pharmacology ; Animals ; Calcium/*metabolism ; *Calcium Signaling ; Cell Line ; Cell Membrane/metabolism ; Cell Nucleus/metabolism ; Cytoplasm/metabolism ; Dogs ; Green Fluorescent Proteins ; Inositol 1,4,5-Trisphosphate/*metabolism ; Inositol Phosphates/metabolism ; Isoenzymes/chemistry/metabolism ; Ligands ; Luminescent Proteins ; Microscopy, Confocal ; Phosphatidylinositol 4,5-Diphosphate/metabolism ; Phospholipase C delta ; Recombinant Fusion Proteins/metabolism ; Time Factors ; Type C Phospholipases/chemistry/metabolism
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  • 35
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-10-16
    Description: The Mammalian Gene Collection (MGC) project is a new effort by the NIH to generate full-length complementary DNA (cDNA) resources. This project will provide publicly accessible resources to the full research community. The MGC project entails the production of libraries, sequencing, and database and repository development, as well as the support of library construction, sequencing, and analytic technologies dedicated to the goal of obtaining a full set of human and other mammalian full-length (open reading frame) sequences and clones of expressed genes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Strausberg, R L -- Feingold, E A -- Klausner, R D -- Collins, F S -- New York, N.Y. -- Science. 1999 Oct 15;286(5439):455-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Cancer Institute, National Human Genome Research 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/10521335" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Computational Biology ; DNA, Complementary ; Databases, Factual ; Expressed Sequence Tags ; *Gene Library ; *Genome ; *Genome, Human ; Humans ; Mammals/*genetics ; Mice ; National Institutes of Health (U.S.) ; Private Sector ; Public Sector ; *Sequence Analysis, DNA ; United States
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-10-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marshall, E -- New York, N.Y. -- Science. 1999 Sep 24;285(5436):2047.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10523193" target="_blank"〉PubMed〈/a〉
    Keywords: *Acquired Immunodeficiency Syndrome ; Humans ; National Institutes of Health (U.S.)/*organization & administration ; *Peer Review, Research ; *Research ; United States
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  • 37
    Publication Date: 1999-07-31
    Description: Many psychotropic drugs interfere with the reuptake of dopamine, norepinephrine, and serotonin. Transport capacity is regulated by kinase-linked pathways, particularly those involving protein kinase C (PKC), resulting in transporter phosphorylation and sequestration. Phosphorylation and sequestration of the serotonin transporter (SERT) were substantially impacted by ligand occupancy. Ligands that can permeate the transporter, such as serotonin or the amphetamines, prevented PKC-dependent SERT phosphorylation. Nontransported SERT antagonists such as cocaine and antidepressants were permissive for SERT phosphorylation but blocked serotonin effects. PKC-dependent SERT sequestration was also blocked by serotonin. These findings reveal activity-dependent modulation of neurotransmitter reuptake and identify previously unknown consequences of amphetamine, cocaine, and antidepressant action.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ramamoorthy, S -- Blakely, R D -- DA07390/DA/NIDA NIH HHS/ -- New York, N.Y. -- Science. 1999 Jul 30;285(5428):763-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology and Center for Molecular Neuroscience, School of Medicine, Vanderbilt University, Nashville, TN 37232-6420, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10427004" target="_blank"〉PubMed〈/a〉
    Keywords: Antidepressive Agents/metabolism/pharmacology ; Biogenic Monoamines/metabolism/pharmacology ; Biotinylation ; Carrier Proteins/antagonists & inhibitors/*metabolism ; Cell Line ; Central Nervous System Agents/metabolism/*pharmacology ; Cocaine/metabolism/pharmacology ; Dextroamphetamine/metabolism/pharmacology ; Enzyme Activation ; Humans ; Ligands ; Membrane Glycoproteins/antagonists & inhibitors/*metabolism ; *Membrane Transport Proteins ; Models, Biological ; *Nerve Tissue Proteins ; Neurotransmitter Agents/metabolism/*pharmacology ; Phosphorylation ; Protein Kinase C/metabolism ; Protein Kinases/metabolism ; Serotonin/*metabolism/pharmacology ; Serotonin Antagonists/pharmacology ; Serotonin Plasma Membrane Transport Proteins ; Serotonin Uptake Inhibitors/metabolism/pharmacology ; Tetradecanoylphorbol Acetate/pharmacology
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  • 38
    Publication Date: 1999-10-09
    Description: Ubiquitination of receptor protein-tyrosine kinases (RPTKs) terminates signaling by marking active receptors for degradation. c-Cbl, an adapter protein for RPTKs, positively regulates RPTK ubiquitination in a manner dependent on its variant SRC homology 2 (SH2) and RING finger domains. Ubiquitin-protein ligases (or E3s) are the components of ubiquitination pathways that recognize target substrates and promote their ligation to ubiquitin. The c-Cbl protein acted as an E3 that can recognize tyrosine-phosphorylated substrates, such as the activated platelet-derived growth factor receptor, through its SH2 domain and that recruits and allosterically activates an E2 ubiquitin-conjugating enzyme through its RING domain. These results reveal an SH2-containing protein that functions as a ubiquitin-protein ligase and thus provide a distinct mechanism for substrate targeting in the ubiquitin system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Joazeiro, C A -- Wing, S S -- Huang, H -- Leverson, J D -- Hunter, T -- Liu, Y C -- CA39780/CA/NCI NIH HHS/ -- R01 DK56558/DK/NIDDK NIH HHS/ -- T32CA09523/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1999 Oct 8;286(5438):309-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Salk Institute, Molecular Biology and Virology Laboratory, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10514377" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Cell Line ; Humans ; Ligases/chemistry/*metabolism ; Molecular Sequence Data ; Phosphotyrosine/metabolism ; Point Mutation ; Proto-Oncogene Proteins/chemistry/genetics/*metabolism ; Proto-Oncogene Proteins c-cbl ; Receptor Protein-Tyrosine Kinases/*metabolism ; Receptor, Platelet-Derived Growth Factor beta/metabolism ; Recombinant Fusion Proteins/metabolism ; Sequence Alignment ; Signal Transduction ; *Ubiquitin-Conjugating Enzymes ; Ubiquitin-Protein Ligases ; Ubiquitins/*metabolism ; src Homology Domains
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  • 39
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-07-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bloom, F E -- New York, N.Y. -- Science. 1999 Jul 9;285(5425):197.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10428715" target="_blank"〉PubMed〈/a〉
    Keywords: Costs and Cost Analysis ; *Internet ; *National Institutes of Health (U.S.) ; Peer Review, Research ; Periodicals as Topic ; *Publishing/economics ; Research Support as Topic ; Societies, Scientific/economics ; United States
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  • 40
    Publication Date: 1999-01-08
    Description: Cochlear frequency selectivity in lower vertebrates arises in part from electrical tuning intrinsic to the sensory hair cells. The resonant frequency is determined largely by the gating kinetics of calcium-activated potassium (BK) channels encoded by the slo gene. Alternative splicing of slo from chick cochlea generated kinetically distinct BK channels. Combination with accessory beta subunits slowed the gating kinetics of alpha splice variants but preserved relative differences between them. In situ hybridization showed that the beta subunit is preferentially expressed by low-frequency (apical) hair cells in the avian cochlea. Interaction of beta with alpha splice variants could provide the kinetic range needed for electrical tuning of cochlear hair cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ramanathan, K -- Michael, T H -- Jiang, G J -- Hiel, H -- Fuchs, P A -- DC00276/DC/NIDCD NIH HHS/ -- New York, N.Y. -- Science. 1999 Jan 8;283(5399):215-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Hearing Sciences, Department of Biomedical Engineering, 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/9880252" target="_blank"〉PubMed〈/a〉
    Keywords: Alternative Splicing ; Animals ; Calcium/metabolism ; Cell Line ; Electrophysiology ; Gene Expression ; Hair Cells, Auditory/*physiology ; Humans ; In Situ Hybridization ; *Ion Channel Gating ; Kinetics ; Large-Conductance Calcium-Activated Potassium Channel beta Subunits ; Large-Conductance Calcium-Activated Potassium Channels ; Membrane Potentials ; Patch-Clamp Techniques ; Potassium Channels/genetics/*physiology ; *Potassium Channels, Calcium-Activated ; Quail ; RNA, Messenger/genetics/metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Transfection
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  • 41
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-07-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bowman, J E -- New York, N.Y. -- Science. 1999 Jul 2;285(5424):47; author reply 49-50.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10428699" target="_blank"〉PubMed〈/a〉
    Keywords: African Americans/*history ; Alabama ; Ethics Committees, Research ; Ethics, Medical/*history ; History, 20th Century ; Human Experimentation/*history ; Humans ; Metaphor ; *Persons ; Pregnant Women ; Syphilis/*history ; United States ; United States Public Health Service ; *Vulnerable Populations ; Withholding Treatment
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  • 42
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-07-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lurie, P -- Wolfe, S M -- New York, N.Y. -- Science. 1999 Jul 2;285(5424):47-8; author reply 49-50.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10428701" target="_blank"〉PubMed〈/a〉
    Keywords: Anti-HIV Agents/therapeutic use ; *Clinical Trials as Topic ; *Ethics, Medical ; HIV Infections/prevention & control/transmission ; *Human Experimentation ; Humans ; Infectious Disease Transmission, Vertical ; Metaphor ; Needle-Exchange Programs ; Syphilis ; United States ; United States Public Health Service ; Zidovudine/therapeutic use
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  • 43
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-04-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Solter, D -- Gearhart, J -- New York, N.Y. -- Science. 1999 Mar 5;283(5407):1468-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Developmental Biology, Max Planck Institute of Immunology, Freiburg, Germany. solter@immunbio.mpg.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10206877" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bioethics ; Blastocyst/*cytology ; *Cell Differentiation ; Cell Line ; Cells, Cultured ; Cloning, Organism ; Cytoplasm/physiology ; Embryo, Mammalian/cytology ; Humans ; Mice ; Nuclear Transfer Techniques ; Stem Cells/*cytology
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  • 44
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-05-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jones, E G -- Mendell, L M -- New York, N.Y. -- Science. 1999 Apr 30;284(5415):739.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10336393" target="_blank"〉PubMed〈/a〉
    Keywords: *Brain ; Humans ; *Neurosciences/economics/manpower ; *Research ; Research Support as Topic ; United States
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  • 45
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-10-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Malakoff, D -- New York, N.Y. -- Science. 1999 Oct 1;286(5437):19, 21.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10532880" target="_blank"〉PubMed〈/a〉
    Keywords: *Budgets ; Financing, Government ; National Institutes of Health (U.S.)/*economics ; Politics ; *Research Support as Topic ; United States
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  • 46
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-07-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Malakoff, D -- New York, N.Y. -- Science. 1999 Jun 25;284(5423):2063, 2065.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10409055" target="_blank"〉PubMed〈/a〉
    Keywords: *Biological Science Disciplines ; Costs and Cost Analysis ; *Internet ; *Libraries ; *Periodicals as Topic/economics ; *Publishing/economics ; *Societies, Scientific/economics ; United States
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  • 47
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-09-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- Kaiser, J -- New York, N.Y. -- Science. 1999 Aug 20;285(5431):1189-90.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10484725" target="_blank"〉PubMed〈/a〉
    Keywords: California ; Electromagnetic Fields/adverse effects ; Financing, Government ; *National Institutes of Health (U.S.)/economics ; *Research Support as Topic ; *Scientific Misconduct ; United States ; *Universities/economics
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  • 48
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-07-03
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Malakoff, D -- New York, N.Y. -- Science. 1999 Jun 11;284(5421):1742.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10391783" target="_blank"〉PubMed〈/a〉
    Keywords: Academies and Institutes ; Budgets ; *Computational Biology/economics/manpower ; *Databases, Factual ; Financing, Government ; National Institutes of Health (U.S.)/*economics ; *Research Support as Topic ; Software ; United States ; Universities
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  • 49
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-07-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaiser, J -- New York, N.Y. -- Science. 1999 Jul 9;285(5425):177-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10428707" target="_blank"〉PubMed〈/a〉
    Keywords: Humans ; Maximum Allowable Concentration ; *National Academy of Sciences (U.S.) ; Public Policy ; *Radiation Dosage ; Radiation Injuries/*etiology ; *Radiation, Ionizing ; United States
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  • 50
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-01-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sikorski, R -- Peters, R -- New York, N.Y. -- Science. 1998 Dec 18;282(5397):2213.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9890829" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Brain Tissue Transplantation ; Cell Differentiation ; Cell Line ; Cell Movement ; Cerebellum/cytology ; Cerebral Ventricles/cytology/embryology ; *Fetal Tissue Transplantation ; Humans ; Mice ; Neuroglia/cytology ; Neurons/cytology ; *Stem Cell Transplantation ; Stem Cells/cytology/enzymology ; beta-N-Acetylhexosaminidases/genetics
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  • 51
    Publication Date: 1999-04-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lanza, R P -- Arrow, K J -- Axelrod, J -- Baltimore, D -- Benacerraf, B -- Bloch, K E -- Bloembergen, N -- Brown, H C -- Brown, M S -- Cibelli, J B -- Cohen, S -- Cooper, L N -- Corey, E J -- Dulbecco, R -- Fischer, E H -- Fitch, V L -- Friedmen, M -- Friedman, M -- Furchgott, R F -- Gell-Mann, M -- Glaser, D A -- Glashow, S L -- Gilbert, W -- Goldstein, J L -- Wilson, R W -- New York, N.Y. -- Science. 1999 Mar 19;283(5409):1849-50.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10206888" target="_blank"〉PubMed〈/a〉
    Keywords: *Bioethics ; Biomedical Research ; *Embryo Research ; Embryo, Mammalian/*cytology ; Federal Government ; Government Regulation ; Humans ; Politics ; Research/*legislation & jurisprudence ; Research Support as Topic/legislation & jurisprudence ; *Risk Assessment ; *Stem Cells ; United States ; United States Dept. of Health and Human Services
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  • 52
    Publication Date: 1999-03-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hannon, G J -- Sun, P -- Carnero, A -- Xie, L Y -- Maestro, R -- Conklin, D S -- Beach, D -- New York, N.Y. -- Science. 1999 Feb 19;283(5405):1129-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10075573" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cloning, Molecular/*methods ; DNA, Complementary ; Gene Expression ; Gene Library ; Genes, p53 ; Genes, ras ; *Genetic Techniques ; Genetic Vectors ; Mammals ; Phenotype ; Proviruses/genetics ; Retroviridae/genetics ; Transformation, Genetic
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  • 53
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-10-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lasley, E N -- New York, N.Y. -- Science. 1999 Sep 10;285(5434):1649-50.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10523176" target="_blank"〉PubMed〈/a〉
    Keywords: *Animal Experimentation ; *Animal Welfare ; Animals ; *Animals, Laboratory ; Federal Government ; Government Regulation ; National Institutes of Health (U.S.) ; New Mexico ; *Pan troglodytes ; Research ; United States ; United States Department of Agriculture
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  • 54
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-04-30
    Description: Morphological analysis was performed on multilegged deformed frogs representing five species from 12 different localities in California, Oregon, Arizona, and New York. The pattern of duplicated limbs was consistent with mechanical perturbation by trematode infestation but not with the effects of retinoids.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sessions, S K -- Franssen, R A -- Horner, V L -- New York, N.Y. -- Science. 1999 Apr 30;284(5415):800-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Hartwick College, Oneonta, NY 13820, USA. sessionss@hartwick.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10221911" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anura/*abnormalities/*parasitology ; Forelimb/*abnormalities ; Gene Expression Regulation, Developmental/drug effects ; Hindlimb/*abnormalities/parasitology ; Limb Buds/drug effects/metabolism ; Ranidae/abnormalities/parasitology ; Trematode Infections/parasitology/*veterinary ; Tretinoin/*toxicity ; United States
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-05-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Malakoff, D -- New York, N.Y. -- Science. 1999 Apr 9;284(5412):230.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10232965" target="_blank"〉PubMed〈/a〉
    Keywords: *Animal Experimentation ; *Animal Rights ; *Animal Testing Alternatives ; Animals ; Animals, Laboratory/immunology ; Antibodies, Monoclonal/*biosynthesis ; Ascites ; Culture Techniques ; Federal Government ; Government Regulation ; Hybridomas ; Internationality ; *Mice/immunology ; *National Institutes of Health (U.S.)/legislation & jurisprudence ; United States
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  • 56
    Publication Date: 1999-04-24
    Description: Control of cyclin levels is critical for proper cell cycle regulation. In yeast, the stability of the G1 cyclin Cln1 is controlled by phosphorylation-dependent ubiquitination. Here it is shown that this reaction can be reconstituted in vitro with an SCF E3 ubiquitin ligase complex. Phosphorylated Cln1 was ubiquitinated by SCF (Skp1-Cdc53-F-box protein) complexes containing the F-box protein Grr1, Rbx1, and the E2 Cdc34. Rbx1 promotes association of Cdc34 with Cdc53 and stimulates Cdc34 auto-ubiquitination in the context of Cdc53 or SCF complexes. Rbx1, which is also a component of the von Hippel-Lindau tumor suppressor complex, may define a previously unrecognized class of E3-associated proteins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Skowyra, D -- Koepp, D M -- Kamura, T -- Conrad, M N -- Conaway, R C -- Conaway, J W -- Elledge, S J -- Harper, J W -- AG11085/AG/NIA NIH HHS/ -- GM41628/GM/NIGMS NIH HHS/ -- GM54137/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1999 Apr 23;284(5414):662-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Verna and Marrs McLean Department of Biochemistry, Howard Hughes Medical Institute, Baylor College of Medicine, Houston, TX 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10213692" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Anaphase-Promoting Complex-Cyclosome ; Animals ; Carrier Proteins/chemistry/*metabolism ; Cell Cycle Proteins/metabolism ; Cell Line ; *Cullin Proteins ; Cyclins/*metabolism ; F-Box Proteins ; Fungal Proteins/*metabolism ; Ligases/metabolism ; Molecular Sequence Data ; Peptide Synthases/*metabolism ; Phosphorylation ; Recombinant Fusion Proteins/metabolism ; S-Phase Kinase-Associated Proteins ; SKP Cullin F-Box Protein Ligases ; Saccharomyces cerevisiae/metabolism ; *Saccharomyces cerevisiae Proteins ; Sequence Alignment ; Ubiquitin-Conjugating Enzymes ; *Ubiquitin-Protein Ligase Complexes ; Ubiquitin-Protein Ligases ; Ubiquitins/*metabolism
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-06-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Enserink, M -- New York, N.Y. -- Science. 1999 May 28;284(5419):1445.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10383318" target="_blank"〉PubMed〈/a〉
    Keywords: Financing, Government ; Intellectual Property ; *National Institutes of Health (U.S.) ; Publishing ; Research Support as Topic ; *Technology Transfer ; United States
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  • 58
    Publication Date: 1999-11-05
    Description: Peptide-major histocompatibility complex protein complexes (pMHCs) on antigen-presenting cells (APCs) are central to T cell activation. Within minutes of peptide-specific T cells interacting with APCs, pMHCs on APCs formed clusters at the site of T cell contact. Thereafter, these clusters were acquired by T cells and internalized through T cell receptor-mediated endocytosis. During this process, T cells became sensitive to peptide-specific lysis by neighboring T cells (fratricide). This form of immunoregulation could explain the "exhaustion" of T cell responses that is induced by high viral loads and may serve to down-regulate immune responses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huang, J F -- Yang, Y -- Sepulveda, H -- Shi, W -- Hwang, I -- Peterson, P A -- Jackson, M R -- Sprent, J -- Cai, Z -- New York, N.Y. -- Science. 1999 Oct 29;286(5441):952-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉R. W. Johnson Pharmaceutical Research Institute, 3210 Merryfield Row, San Diego, CA 92121, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10542149" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Drosophila ; *Endocytosis ; Flow Cytometry ; Histocompatibility Antigens/*immunology ; Macromolecular Substances ; Peptides/*immunology ; Receptors, Antigen, T-Cell/*immunology ; Recombinant Fusion Proteins/genetics/immunology ; T-Lymphocytes/*immunology/metabolism ; T-Lymphocytes, Cytotoxic/immunology
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  • 59
    Publication Date: 1999-12-03
    Description: 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〉
    Keywords: 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
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  • 60
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-05-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Perpich, J G -- New York, N.Y. -- Science. 1999 Apr 23;284(5414):591-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10328741" target="_blank"〉PubMed〈/a〉
    Keywords: *Academies and Institutes ; *Education, Graduate ; Education, Medical, Graduate ; Fellowships and Scholarships ; *Physicians ; *Research ; *Research Personnel ; Research Support as Topic ; United States
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  • 61
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-11-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marshall, E -- New York, N.Y. -- Science. 1999 Oct 22;286(5440):655-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10577213" target="_blank"〉PubMed〈/a〉
    Keywords: *Internet ; National Institutes of Health (U.S.) ; *Peer Review, Research ; Periodicals as Topic ; *Publishing ; United States
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 62
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-08-14
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marshall, E -- New York, N.Y. -- Science. 1999 Jul 23;285(5427):519.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10447481" target="_blank"〉PubMed〈/a〉
    Keywords: China ; *International Cooperation ; Lobbying ; *National Institutes of Health (U.S.) ; *Research ; Research Support as Topic ; United States
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  • 63
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-11-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bloom, F E -- New York, N.Y. -- Science. 1999 Oct 22;286(5440):679.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10577220" target="_blank"〉PubMed〈/a〉
    Keywords: Databases, Factual ; *Internet ; Medline ; National Library of Medicine (U.S.) ; *Online Systems ; *Periodicals as Topic ; *Publishing ; Signal Transduction ; United States
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  • 64
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-09-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bloom, F E -- New York, N.Y. -- Science. 1999 Aug 20;285(5431):1207.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10484728" target="_blank"〉PubMed〈/a〉
    Keywords: *Periodicals as Topic ; Publishing/*organization & administration ; *Societies, Medical ; *Societies, Scientific ; United States
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 65
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-06-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marshall, E -- New York, N.Y. -- Science. 1999 May 21;284(5418):1246.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10383299" target="_blank"〉PubMed〈/a〉
    Keywords: Academic Medical Centers/*standards ; Bioethics ; Clinical Trials as Topic/*standards ; Ethics Committees, Research ; Federal Government ; *Government Regulation ; Humans ; Informed Consent ; National Institutes of Health (U.S.) ; North Carolina ; Professional Staff Committees ; Research/*standards ; Research Support as Topic ; United States
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  • 66
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-12-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ferber, D -- New York, N.Y. -- Science. 1999 Nov 26;286(5445):1662-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10610557" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacterial Proteins/genetics/toxicity ; *Bacterial Toxins ; *Biotechnology ; Butterflies/physiology ; Crops, Agricultural/adverse effects/*genetics ; Drug Resistance, Microbial/genetics ; Endotoxins/genetics/toxicity ; Food Hypersensitivity ; *Genetic Engineering ; Hemolysin Proteins ; Humans ; *Plants, Genetically Modified/adverse effects ; Pollen/genetics ; Public Opinion ; Risk Assessment ; United States ; United States Department of Agriculture ; United States Environmental Protection Agency ; United States Food and Drug Administration
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  • 67
    Publication Date: 1999
    Description: The temporal program of gene expression during a model physiological response of human cells, the response of fibroblasts to serum, was explored with a complementary DNA microarray representing about 8600 different human genes. Genes could be clustered into groups on the basis of their temporal patterns of expression in this program. Many features of the transcriptional program appeared to be related to the physiology of wound repair, suggesting that fibroblasts play a larger and richer role in this complex multicellular response than had previously been appreciated.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Iyer, V R -- Eisen, M B -- Ross, D T -- Schuler, G -- Moore, T -- Lee, J C -- Trent, J M -- Staudt, L M -- Hudson, J Jr -- Boguski, M S -- Lashkari, D -- Shalon, D -- Botstein, D -- Brown, P O -- CA 77097/CA/NCI NIH HHS/ -- HG00450/HG/NHGRI NIH HHS/ -- T32 HG00450/HG/NHGRI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1999 Jan 1;283(5398):83-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, 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/9872747" target="_blank"〉PubMed〈/a〉
    Keywords: *Blood ; Calcium-Calmodulin-Dependent Protein Kinases/genetics/metabolism ; Cell Cycle/*genetics ; Cell Line ; Cholesterol/biosynthesis ; Culture Media ; Culture Media, Serum-Free ; Expressed Sequence Tags ; Fibroblasts/cytology/*physiology ; Fluorescent Dyes ; *Gene Expression Regulation ; Genes, Immediate-Early ; Humans ; Oligonucleotide Array Sequence Analysis ; Polymerase Chain Reaction/methods ; Software ; Time Factors ; Transcription Factors/genetics ; *Transcription, Genetic ; Wound Healing/*genetics
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  • 68
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-07-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marshall, E -- New York, N.Y. -- Science. 1999 Jun 25;284(5423):2067, 2069.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10409058" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Chimera ; *Embryo, Mammalian ; Humans ; Pan troglodytes ; *Patents as Topic ; United States
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  • 69
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-06-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fairchild, A L -- Bayer, R -- New York, N.Y. -- Science. 1999 May 7;284(5416):919-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program in the History of Public Health and Medicine, Division of Sociomedical Sciences, The Joseph L. Mailman School of Public Health, Columbia University, New York, NY 10032-2625, USA. alf4@columbia.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10357678" target="_blank"〉PubMed〈/a〉
    Keywords: African Americans/history ; Alabama ; Anonymous Testing ; Anti-HIV Agents/*therapeutic use ; Clinical Trials as Topic ; Developing Countries ; Disclosure ; Ethics, Medical ; Female ; HIV Infections/prevention & control/*transmission ; *HIV Seroprevalence ; History, 20th Century ; *Human Experimentation/history ; Humans ; Infectious Disease Transmission, Vertical/*prevention & control ; Informed Consent/history ; Male ; *Needle-Exchange Programs ; *Persons ; Pregnant Women ; Syphilis/history ; *Trust ; United States ; *Vulnerable Populations ; Withholding Treatment
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  • 70
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-07-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marshall, E -- New York, N.Y. -- Science. 1999 Jun 25;284(5423):2062-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10409054" target="_blank"〉PubMed〈/a〉
    Keywords: Costs and Cost Analysis ; Europe ; Financing, Government ; History, 20th Century ; *Internet ; National Institutes of Health (U.S.) ; Peer Review, Research ; *Periodicals as Topic ; *Publishing/economics ; Societies, Scientific ; United States
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  • 71
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-05-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fears, R -- Poste, G -- New York, N.Y. -- Science. 1999 Apr 9;284(5412):267-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉SmithKline Beecham, New Frontiers Science Park, Harlow, Essex CM19 5AW, UK. robin_b_fears@sbphrd.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10232974" target="_blank"〉PubMed〈/a〉
    Keywords: Bioethics ; Confidentiality ; Databases, Factual ; *Databases, Nucleic Acid ; *Delivery of Health Care ; *Genetic Privacy ; *Genetic Research ; *Genetics, Medical ; *Genetics, Population ; Great Britain ; Humans ; Informed Consent ; Medical Informatics ; Medical Records Systems, Computerized ; Private Sector ; Public Sector ; *Research ; Research Subjects ; *Resource Allocation ; Social Control, Formal ; *State Medicine/organization & administration ; United States
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  • 72
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-05-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marshall, E -- New York, N.Y. -- Science. 1999 Apr 16;284(5413):406-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10232976" target="_blank"〉PubMed〈/a〉
    Keywords: Chromosome Mapping ; *Databases, Factual ; *Drug Industry ; Genetic Predisposition to Disease ; *Genome, Human ; Humans ; *Information Dissemination ; *Mutation ; National Institutes of Health (U.S.) ; *Polymorphism, Genetic ; Private Sector ; Public Sector ; Sequence Analysis, DNA ; United States
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  • 73
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-03-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marshall, E -- New York, N.Y. -- Science. 1999 Feb 26;283(5406):1234-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10084920" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anthrax/prevention & control/therapy ; *Biological Warfare/prevention & control ; *Financing, Government ; Government Agencies/economics ; Humans ; Military Medicine/economics ; *Public Health/economics ; Research Support as Topic ; Smallpox/prevention & control/therapy ; United States ; United States Public Health Service/economics ; *Violence/prevention & control
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  • 74
    Publication Date: 1999-07-03
    Description: Most isolates of hepatitis C virus (HCV) infections are resistant to interferon, the only available therapy, but the mechanism underlying this resistance has not been defined. Here it is shown that the HCV envelope protein E2 contains a sequence identical with phosphorylation sites of the interferon-inducible protein kinase PKR and the translation initiation factor eIF2alpha, a target of PKR. E2 inhibited the kinase activity of PKR and blocked its inhibitory effect on protein synthesis and cell growth. This interaction of E2 and PKR may be one mechanism by which HCV circumvents the antiviral effect of interferon.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Taylor, D R -- Shi, S T -- Romano, P R -- Barber, G N -- Lai, M M -- AI 40038/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1999 Jul 2;285(5424):107-10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Microbiology and Immunology and Howard Hughes Medical Institute, University of Southern California, School of Medicine, Los Angeles, CA 90089, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10390359" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Chloramphenicol O-Acetyltransferase/biosynthesis ; Drug Resistance, Microbial ; Endoplasmic Reticulum/metabolism ; Enzyme Induction ; Eukaryotic Initiation Factor-2/chemistry/metabolism ; HeLa Cells ; *Hepacivirus/drug effects ; Humans ; Interferon-alpha/*pharmacology ; Phosphorylation ; Protein Biosynthesis ; Recombinant Fusion Proteins/metabolism/pharmacology ; Saccharomyces cerevisiae/genetics/growth & development/metabolism ; Transfection ; Transformation, Genetic ; Viral Envelope Proteins/chemistry/metabolism/pharmacology/*physiology ; eIF-2 Kinase/*antagonists & inhibitors/chemistry/metabolism
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-10-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Martin, J B -- New York, N.Y. -- Science. 1999 Sep 10;285(5434):1671.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10523179" target="_blank"〉PubMed〈/a〉
    Keywords: Academic Medical Centers/*economics ; Budgets ; Hospitals, Teaching/economics ; Managed Care Programs ; Medical Indigency ; National Institutes of Health (U.S.) ; *Research ; *Research Support as Topic ; United States
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-10-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zeisel, S H -- New York, N.Y. -- Science. 1999 Sep 17;285(5435):1853-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Public Health, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599-7400, USA. stevenvzeisel@unc.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10515789" target="_blank"〉PubMed〈/a〉
    Keywords: Consumer Product Safety ; *Dietary Supplements/economics ; Food ; Humans ; *Legislation, Drug ; *Legislation, Food ; National Institutes of Health (U.S.) ; United States ; United States Food and Drug Administration
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-05-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marshall, E -- New York, N.Y. -- Science. 1999 Apr 16;284(5413):413, 415.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10232981" target="_blank"〉PubMed〈/a〉
    Keywords: Aborted Fetus ; Advisory Committees ; *Bioethics ; *Embryo Research ; Embryo, Mammalian/*cytology ; Federal Government ; Fetal Research ; Financing, Government ; *Government Regulation ; Guidelines as Topic ; Humans ; Informed Consent ; *National Institutes of Health (U.S.) ; Public Policy ; *Research ; Research Support as Topic ; *Stem Cells ; United States
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  • 78
    Publication Date: 1999-01-23
    Description: Tumor necrosis factor receptor type 1 (TNF-R1) contains a cytoplasmic death domain that is required for the signaling of TNF activities such as apoptosis and nuclear factor kappa B (NF-kappaB) activation. Normally, these signals are generated only after TNF-induced receptor aggregation. However, TNF-R1 self-associates and signals independently of ligand when overexpressed. This apparent paradox may be explained by silencer of death domains (SODD), a widely expressed approximately 60-kilodalton protein that was found to be associated with the death domain of TNF-R1. TNF treatment released SODD from TNF-R1, permitting the recruitment of proteins such as TRADD and TRAF2 to the active TNF-R1 signaling complex. SODD also interacted with death receptor-3 (DR3), another member of the TNF receptor superfamily. Thus, SODD association may be representative of a general mechanism for preventing spontaneous signaling by death domain-containing receptors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jiang, Y -- Woronicz, J D -- Liu, W -- Goeddel, D V -- New York, N.Y. -- Science. 1999 Jan 22;283(5401):543-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Tularik, Two Corporate Drive, South San Francisco, CA 94080, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9915703" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptor Proteins, Signal Transducing ; Amino Acid Sequence ; Antigens, CD/chemistry/genetics/*metabolism ; Apoptosis ; Carrier Proteins/chemistry/genetics/*metabolism ; Cell Line ; Fas-Associated Death Domain Protein ; Humans ; Jurkat Cells ; Molecular Sequence Data ; Mutation ; NF-kappa B/metabolism ; Protein Binding ; Proteins/metabolism ; Receptor Aggregation ; Receptor-Interacting Protein Serine-Threonine Kinases ; Receptors, Tumor Necrosis Factor/chemistry/genetics/*metabolism ; Receptors, Tumor Necrosis Factor, Member 25 ; Receptors, Tumor Necrosis Factor, Type I ; Recombinant Fusion Proteins/metabolism ; *Signal Transduction ; TNF Receptor-Associated Factor 1 ; TNF Receptor-Associated Factor 2 ; Transfection ; Tumor Necrosis Factor-alpha/pharmacology ; U937 Cells
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-04-03
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marshall, E -- New York, N.Y. -- Science. 1999 Mar 12;283(5408):1610-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10189309" target="_blank"〉PubMed〈/a〉
    Keywords: *Internet ; *National Institutes of Health (U.S.) ; Peer Review, Research ; *Publishing ; Societies, Scientific ; United States
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 80
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-03-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marshall, E -- New York, N.Y. -- Science. 1999 Feb 12;283(5404):913-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10075554" target="_blank"〉PubMed〈/a〉
    Keywords: Biomedical Research ; Federal Government ; Government Regulation ; Scientific Misconduct/*legislation & jurisprudence ; Texas ; United States ; United States Dept. of Health and Human Services ; Universities
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  • 81
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-02-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marshall, E -- New York, N.Y. -- Science. 1999 Jan 22;283(5401):465, 467.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9988645" target="_blank"〉PubMed〈/a〉
    Keywords: Advisory Committees ; Bioethics ; Cell Line ; *Embryo Research ; Embryo, Mammalian/*cytology ; Federal Government ; *Government Regulation ; Humans ; National Institutes of Health (U.S.)/economics/*legislation & jurisprudence ; Research ; Research Support as Topic/*legislation & jurisprudence ; *Stem Cells ; United States
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  • 82
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-08-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fiske, M R -- New York, N.Y. -- Science. 1999 Aug 6;285(5429):837-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10454934" target="_blank"〉PubMed〈/a〉
    Keywords: *Crystallization ; Proteins/*chemistry ; Societies, Scientific ; Space Flight ; United States ; *United States National Aeronautics and Space Administration ; *Weightlessness
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  • 83
    Publication Date: 1999-01-29
    Description: The Ras-dependent activation of mitogen-activated protein (MAP) kinase pathways by many receptors coupled to heterotrimeric guanine nucleotide binding proteins (G proteins) requires the activation of Src family tyrosine kinases. Stimulation of beta2 adrenergic receptors resulted in the assembly of a protein complex containing activated c-Src and the receptor. Src recruitment was mediated by beta-arrestin, which functions as an adapter protein, binding both c-Src and the agonist-occupied receptor. beta-Arrestin 1 mutants, impaired either in c-Src binding or in the ability to target receptors to clathrin-coated pits, acted as dominant negative inhibitors of beta2 adrenergic receptor-mediated activation of the MAP kinases Erk1 and Erk2. These data suggest that beta-arrestin binding, which terminates receptor-G protein coupling, also initiates a second wave of signal transduction in which the "desensitized" receptor functions as a critical structural component of a mitogenic signaling complex.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Luttrell, L M -- Ferguson, S S -- Daaka, Y -- Miller, W E -- Maudsley, S -- Della Rocca, G J -- Lin, F -- Kawakatsu, H -- Owada, K -- Luttrell, D K -- Caron, M G -- Lefkowitz, R J -- DK02352/DK/NIDDK NIH HHS/ -- DK55524/DK/NIDDK NIH HHS/ -- HL16037/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1999 Jan 29;283(5402):655-61.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Medicine, Duke University Medical Center, Durham, NC 27710, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9924018" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenergic beta-Agonists/metabolism/pharmacology ; Animals ; Arrestins/genetics/*metabolism ; Calcium-Calmodulin-Dependent Protein Kinases/metabolism ; Cell Line ; Cell Membrane/metabolism ; Enzyme Activation ; GTP-Binding Proteins/metabolism ; Humans ; Isoproterenol/metabolism/pharmacology ; Mitogen-Activated Protein Kinase 1 ; Mitogen-Activated Protein Kinase 3 ; *Mitogen-Activated Protein Kinases ; Models, Biological ; Phosphorylation ; Point Mutation ; Precipitin Tests ; Proto-Oncogene Proteins pp60(c-src)/*metabolism ; Receptor Cross-Talk ; Receptors, Adrenergic, beta-2/*metabolism ; Receptors, Cell Surface/metabolism ; *Signal Transduction ; Transfection ; src Homology Domains
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  • 84
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-10-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Doniach, S -- New York, N.Y. -- Science. 1999 Sep 17;285(5435):1850.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10515787" target="_blank"〉PubMed〈/a〉
    Keywords: National Institutes of Health (U.S.)/*organization & administration ; *Peer Review, Research ; Research Support as Topic ; United States
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  • 85
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-12-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sorenson, S B -- New York, N.Y. -- Science. 1999 Nov 19;286(5444):1481-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Public Health, University of California, Los Angeles, Los Angeles, CA 90095-1772, USA. sorenson@ucla.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10610547" target="_blank"〉PubMed〈/a〉
    Keywords: *Consumer Product Safety/legislation & jurisprudence ; Firearms/legislation & jurisprudence/*standards ; Public Opinion ; Public Policy ; Safety ; United States
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  • 86
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-09-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dovichi, N -- New York, N.Y. -- Science. 1999 Aug 13;285(5430):1016.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10475843" target="_blank"〉PubMed〈/a〉
    Keywords: Canada ; Financing, Government ; Human Genome Project ; Research Support as Topic ; Sequence Analysis, DNA/*instrumentation ; United States
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  • 87
    Publication Date: 1999-05-21
    Description: Bile acids are essential for the solubilization and transport of dietary lipids and are the major products of cholesterol catabolism. Results presented here show that bile acids are physiological ligands for the farnesoid X receptor (FXR), an orphan nuclear receptor. When bound to bile acids, FXR repressed transcription of the gene encoding cholesterol 7alpha-hydroxylase, which is the rate-limiting enzyme in bile acid synthesis, and activated the gene encoding intestinal bile acid-binding protein, which is a candidate bile acid transporter. These results demonstrate a mechanism by which bile acids transcriptionally regulate their biosynthesis and enterohepatic transport.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Makishima, M -- Okamoto, A Y -- Repa, J J -- Tu, H -- Learned, R M -- Luk, A -- Hull, M V -- Lustig, K D -- Mangelsdorf, D J -- Shan, B -- New York, N.Y. -- Science. 1999 May 21;284(5418):1362-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Pharmacology, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75235-9050, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10334992" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bile Acids and Salts/biosynthesis/*metabolism ; Biological Transport ; Carrier Proteins/*genetics/metabolism ; Cell Line ; Chenodeoxycholic Acid/*metabolism ; Cholesterol/metabolism ; Cholesterol 7-alpha-Hydroxylase/*genetics ; DNA-Binding Proteins/chemistry/genetics/*metabolism ; Gene Expression Regulation ; Histone Acetyltransferases ; Homeostasis ; Humans ; *Hydroxysteroid Dehydrogenases ; Ligands ; Liver/metabolism ; *Membrane Glycoproteins ; Mice ; Nuclear Receptor Coactivator 1 ; *Organic Anion Transporters, Sodium-Dependent ; Receptors, Cytoplasmic and Nuclear/chemistry/genetics/*metabolism ; *Symporters ; Transcription Factors/chemistry/genetics/*metabolism ; Transfection ; Tumor Cells, Cultured
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  • 88
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-09-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Holden, C -- New York, N.Y. -- Science. 1999 Aug 20;285(5431):1186-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10484724" target="_blank"〉PubMed〈/a〉
    Keywords: *Biological Evolution ; Curriculum ; Kansas ; Religion and Science ; Science/*education ; United States
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  • 89
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-12-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Malakoff, D -- New York, N.Y. -- Science. 1999 Dec 3;286(5446):1836.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10610571" target="_blank"〉PubMed〈/a〉
    Keywords: *Budgets ; Government Agencies/economics ; National Institutes of Health (U.S.)/*economics ; Research/*economics ; *Research Support as Topic ; United States
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  • 90
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-12-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Trull, F L -- New York, N.Y. -- Science. 1999 Nov 19;286(5444):1477.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10610546" target="_blank"〉PubMed〈/a〉
    Keywords: *Animal Rights ; Animals ; Animals, Laboratory ; *Organizations ; *Research Personnel ; United States ; *Violence
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  • 91
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-11-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaiser, J -- New York, N.Y. -- Science. 1999 Oct 29;286(5441):883.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10577232" target="_blank"〉PubMed〈/a〉
    Keywords: *Government Regulation ; *Scientific Misconduct ; United States ; United States Office of Research Integrity/*organization & administration
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  • 92
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-12-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaiser, J -- New York, N.Y. -- Science. 1999 Nov 5;286(5442):1059.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10610514" target="_blank"〉PubMed〈/a〉
    Keywords: *Animal Rights ; Animals ; Animals, Laboratory ; *Primates ; *Research Personnel ; United States ; *Violence
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  • 93
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-02-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brinkley, W R -- New York, N.Y. -- Science. 1999 Feb 5;283(5403):791.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10049119" target="_blank"〉PubMed〈/a〉
    Keywords: *Career Choice ; *Education, Medical, Graduate ; Humans ; National Institutes of Health (U.S.) ; *Physicians/statistics & numerical data ; Research/*manpower ; *Research Personnel/education/statistics & numerical data ; Research Support as Topic ; Societies, Scientific ; Training Support ; United States
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  • 94
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-01-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaiser, J -- New York, N.Y. -- Science. 1999 Jan 1;283(5398):18-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9917257" target="_blank"〉PubMed〈/a〉
    Keywords: Advisory Committees ; *Bioethics ; Federal Government ; *Human Experimentation ; No-Observed-Adverse-Effect Level ; *Nontherapeutic Human Experimentation ; Pesticides/*toxicity ; *Toxicity Tests/standards ; United States ; *United States Environmental Protection Agency
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  • 95
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-10-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Varmus, H -- New York, N.Y. -- Science. 1999 Sep 10;285(5434):1654-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10523178" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome ; Budgets ; Computational Biology ; Embryo, Mammalian/cytology ; Humans ; Internet ; *National Institutes of Health (U.S.)/economics/organization & administration ; Peer Review, Research ; Public Policy ; Publishing ; Research ; Stem Cells ; United States
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  • 96
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-01-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rosenberg, L -- New York, N.Y. -- Science. 1999 Jan 15;283(5400):331-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Princeton University, NJ 08544, USA. lrosenberg@molbiol.princeton.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9925491" target="_blank"〉PubMed〈/a〉
    Keywords: Academic Medical Centers ; *Career Choice ; Drug Industry ; *Education, Medical, Graduate ; Fellowships and Scholarships ; Financing, Government ; Foundations ; Health Care Sector ; National Institutes of Health (U.S.) ; *Physicians/statistics & numerical data/trends ; Public Policy ; Research/*manpower ; *Research Personnel ; Research Support as Topic ; United States
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  • 97
    Publication Date: 1999-11-27
    Description: Extracellular signals often result in simultaneous activation of both the Raf-MEK-ERK and PI3K-Akt pathways (where ERK is extracellular-regulated kinase, MEK is mitogen-activated protein kinase or ERK kinase, and PI3K is phosphatidylinositol 3-kinase). However, these two signaling pathways were shown to exert opposing effects on muscle cell hypertrophy. Furthermore, the PI3K-Akt pathway was shown to inhibit the Raf-MEK-ERK pathway; this cross-regulation depended on the differentiation state of the cell: Akt activation inhibited the Raf-MEK-ERK pathway in differentiated myotubes, but not in their myoblast precursors. The stage-specific inhibitory action of Akt correlated with its stage-specific ability to form a complex with Raf, suggesting the existence of differentially expressed mediators of an inhibitory Akt-Raf complex.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rommel, C -- Clarke, B A -- Zimmermann, S -- Nunez, L -- Rossman, R -- Reid, K -- Moelling, K -- Yancopoulos, G D -- Glass, D J -- New York, N.Y. -- Science. 1999 Nov 26;286(5445):1738-41.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Regeneron Pharmaceuticals, 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/10576741" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cell Line ; Cyclin-Dependent Kinase Inhibitor p21 ; Cyclins/genetics ; Enzyme Activation ; Enzyme Inhibitors/pharmacology ; Flavonoids/pharmacology ; Insulin-Like Growth Factor I/pharmacology ; MAP Kinase Signaling System/drug effects ; Mice ; Mitogen-Activated Protein Kinases/*antagonists & inhibitors/metabolism ; Muscle, Skeletal/*cytology/*metabolism ; Myogenin/genetics ; Phenotype ; Phosphatidylinositol 3-Kinases/metabolism ; Phosphorylation ; Protein-Serine-Threonine Kinases/*metabolism ; Proto-Oncogene Proteins/*metabolism ; Proto-Oncogene Proteins c-akt ; Proto-Oncogene Proteins c-raf/*antagonists & inhibitors/metabolism ; Signal Transduction ; Transfection ; Transgenes
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  • 98
    Publication Date: 1999-10-26
    Description: Progressive damage to mitochondrial DNA (mtDNA) during life is thought to contribute to aging processes. However, this idea has been difficult to reconcile with the small fraction of mtDNA so far found to be altered. Here, examination of mtDNA revealed high copy point mutations at specific positions in the control region for replication of human fibroblast mtDNA from normal old, but not young, individuals. Furthermore, in longitudinal studies, one or more mutations appeared in an individual only at an advanced age. Some mutations appeared in more than one individual. Most strikingly, a T414G transversion was found, in a generally high proportion (up to 50 percent) of mtDNA molecules, in 8 of 14 individuals above 65 years of age (57 percent) but was absent in 13 younger individuals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Michikawa, Y -- Mazzucchelli, F -- Bresolin, N -- Scarlato, G -- Attardi, G -- AG-12117-03/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 1999 Oct 22;286(5440):774-9.〈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/10531063" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Aged ; Aged, 80 and over ; Aging/*genetics ; Cell Line ; Child ; Child, Preschool ; DNA Damage ; DNA Repair ; DNA Replication/*genetics ; DNA, Mitochondrial/biosynthesis/chemistry/*genetics ; Fetus ; Fibroblasts ; Humans ; Infant ; Infant, Newborn ; Longitudinal Studies ; Middle Aged ; Mitochondria/*genetics ; Nucleic Acid Conformation ; Nucleic Acid Heteroduplexes ; *Point Mutation ; Polymerase Chain Reaction ; Pseudogenes
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  • 99
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-10-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Merrill, S A -- McGeary, M -- New York, N.Y. -- Science. 1999 Sep 10;285(5434):1679-80.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Research Council's Board on Science, Technology, and Economic Policy (STEP), Washington, DC 20418, USA. smerrill@nas.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10523184" target="_blank"〉PubMed〈/a〉
    Keywords: Budgets ; Government Agencies/economics ; National Institutes of Health (U.S.)/economics ; *Research ; *Research Support as Topic ; United States
    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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  • 100
    Publication Date: 1999-12-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Velculescu, V E -- New York, N.Y. -- Science. 1999 Nov 19;286(5444):1491-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Johns Hopkins Oncology Center, Baltimore, MD 21231, USA. velculescu@jhmi.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10610550" target="_blank"〉PubMed〈/a〉
    Keywords: *Awards and Prizes ; Gene Expression ; *Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Genes, ras ; *Genome ; History, 20th Century ; Humans ; Neoplasms/genetics ; RNA, Messenger/*genetics ; Saccharomyces cerevisiae/genetics ; United States
    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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