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  • Humans  (24)
  • Cell Line  (6)
  • 1995-1999  (25)
  • 1945-1949
  • 1940-1944
  • 1
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    AIDS vaccine development (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-05-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Agosto, M -- Allan, J -- Benson, C -- Berger, E A -- Blumenthal, R -- Burton, D -- Clements, J -- Coffin, J -- Connor, R -- Cullen, B -- Desrosiers, R -- Dimitrov, D -- Doms, R -- Emerman, M -- Feinberg, M -- Fultz, P -- Gerard, C -- Gonsalves, G -- Haase, A -- Haigwood, N -- Hirsch, V -- Ho, D -- Hoxie, J A -- Hu, S L -- Zingale, D -- New York, N.Y. -- Science. 1998 May 8;280(5365):803, 804-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9599148" target="_blank"〉PubMed〈/a〉
    Keywords: *AIDS Vaccines/immunology ; Acquired Immunodeficiency Syndrome/prevention & control ; *Clinical Trials as Topic ; HIV Envelope Protein gp120/immunology ; HIV-1/immunology ; Humans ; National Institutes of Health (U.S.) ; United States
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Science over politics (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 3
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    Genome maps 10. Comparative genomics. Mammalian radiations. Wall chart (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉O'Brien, S J -- Eisenberg, J F -- Miyamoto, M -- Hedges, S B -- Kumar, S -- Wilson, D E -- Menotti-Raymond, M -- Murphy, W J -- Nash, W G -- Lyons, L A -- Menninger, J C -- Stanyon, R -- Wienberg, J -- Copeland, N G -- Jenkins, N A -- Gellin, J -- Yerle, M -- Andersson, L -- Womack, J -- Broad, T -- Postlethwait, J -- Serov, O -- Bailey, E -- James, M R -- Marshall Graves, J A -- New York, N.Y. -- Science. 1999 Oct 15;286(5439):463-78.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Cancer Institute, Frederick, MD, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10577209" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; *Chromosome Mapping ; Chromosome Painting ; *Genome ; *Genome, Human ; Humans ; Mammals/*genetics ; Nucleic Acid Hybridization ; Phylogeny
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    The RNA component of human telomerase (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-09-01
    Description: Eukaryotic chromosomes are capped with repetitive telomere sequences that protect the ends from damage and rearrangements. Telomere repeats are synthesized by telomerase, a ribonucleic acid (RNA)-protein complex. Here, the cloning of the RNA component of human telomerase, termed hTR, is described. The template region of hTR encompasses 11 nucleotides (5'-CUAACCCUAAC) complementary to the human telomere sequence (TTAGGG)n. Germline tissues and tumor cell lines expressed more hTR than normal somatic cells and tissues, which have no detectable telomerase activity. Human cell lines that expressed hTR mutated in the template region generated the predicted mutant telomerase activity. HeLa cells transfected with an antisense hTR lost telomeric DNA and began to die after 23 to 26 doublings. Thus, human telomerase is a critical enzyme for the long-term proliferation of immortal tumor cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Feng, J -- Funk, W D -- Wang, S S -- Weinrich, S L -- Avilion, A A -- Chiu, C P -- Adams, R R -- Chang, E -- Allsopp, R C -- Yu, J -- AG09383/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 1995 Sep 1;269(5228):1236-41.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Geron Corporation, Menlo Park, CA 94025, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7544491" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cell Death ; *Cell Division ; Cell Line ; Cloning, Molecular ; DNA Nucleotidylexotransferase/antagonists & ; inhibitors/chemistry/genetics/*metabolism ; HeLa Cells ; Humans ; Molecular Sequence Data ; Oligonucleotides, Antisense/pharmacology ; Polymerase Chain Reaction ; RNA/chemistry/genetics/*metabolism ; Templates, Genetic ; Transfection ; Tumor Cells, Cultured
    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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    Regulation of human gene therapy (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-07-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chase, G A -- DeLeon, P A -- Dronamraju, K R -- Erickson, R P -- Glorioso, J C 3rd -- Hirschhorn, R -- Lysaught, M T -- McGraw, K M -- Meyers, A S -- Miller, A D -- New York, N.Y. -- Science. 1995 Jul 7;269(5220):14-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7604272" target="_blank"〉PubMed〈/a〉
    Keywords: *Advisory Committees ; Clinical Protocols ; Clinical Trials, Phase I as Topic/legislation & jurisprudence ; Clinical Trials, Phase II as Topic/legislation & jurisprudence ; DNA, Recombinant ; Ethical Review ; Federal Government ; Genetic Therapy/*legislation & jurisprudence ; *Government Regulation ; Humans ; *National Institutes of Health (U.S.) ; 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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    Cloning and characterization of a G protein-activated human phosphoinositide-3 kinase (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-08-04
    Description: Phosphoinositide-3 kinase activity is implicated in diverse cellular responses triggered by mammalian cell surface receptors and in the regulation of protein sorting in yeast. Receptors with intrinsic and associated tyrosine kinase activity recruit heterodimeric phosphoinositide-3 kinases that consist of p110 catalytic subunits and p85 adaptor molecules containing Src homology 2 (SH2) domains. A phosphoinositide-3 kinase isotype, p110 gamma, was cloned and characterized. The p110 gamma enzyme was activated in vitro by both the alpha and beta gamma subunits of heterotrimeric guanosine triphosphate (GTP)-binding proteins (G proteins) and did not interact with p85. A potential pleckstrin homology domain is located near its amino terminus. The p110 gamma isotype may link signaling through G protein-coupled receptors to the generation of phosphoinositide second messengers phosphorylated in the D-3 position.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stoyanov, B -- Volinia, S -- Hanck, T -- Rubio, I -- Loubtchenkov, M -- Malek, D -- Stoyanova, S -- Vanhaesebroeck, B -- Dhand, R -- Nurnberg, B -- New York, N.Y. -- Science. 1995 Aug 4;269(5224):690-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max Planck Research Unit in Growth Factor Signal Transduction, Medical Faculty, University of Jena, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7624799" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; *Cloning, Molecular ; Enzyme Activation ; GTP-Binding Proteins/*physiology ; Guanosine 5'-O-(3-Thiotriphosphate)/pharmacology ; Humans ; Hydrogen-Ion Concentration ; Molecular Sequence Data ; Phosphatidylinositol 3-Kinases ; Phosphatidylinositols/metabolism ; Phosphotransferases (Alcohol Group Acceptor)/chemistry/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Substrate Specificity ; Tumor Cells, Cultured
    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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    A region of adenylyl cyclase 2 critical for regulation by G protein beta gamma subunits (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-05-26
    Description: Receptor-mediated activation of heterotrimeric guanine nucleotide-binding proteins (G proteins) results in the dissociation of alpha from beta gamma subunits, thereby allowing both to regulate effectors. Little is known about the regions of effectors required for recognition of G beta gamma. A peptide encoding residues 956 to 982 of adenylyl cyclase 2 specifically blocked G beta gamma stimulation of adenylyl cyclase 2, phospholipase C-beta 3, potassium channels, and beta-adrenergic receptor kinase as well as inhibition of calmodulin-stimulated adenylyl cyclases, but had no effect on interactions between G beta gamma and G alpha o. Substitutions in this peptide identified a functionally important motif, Gln-X-X-Glu-Arg, that is also conserved in regions of potassium channels and beta-adrenergic receptor kinases that participate in G beta gamma interactions. Thus, the region defined by residues 956 to 982 of adenylyl cyclase 2 may contain determinants important for receiving signals from G beta gamma.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, J -- DeVivo, M -- Dingus, J -- Harry, A -- Li, J -- Sui, J -- Carty, D J -- Blank, J L -- Exton, J H -- Stoffel, R H -- CA-44998/CA/NCI NIH HHS/ -- DK-37219/DK/NIDDK NIH HHS/ -- DK-38761/DK/NIDDK NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1995 May 26;268(5214):1166-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, Mount Sinai School of Medicine, City University of New York, NY 10029, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7761832" target="_blank"〉PubMed〈/a〉
    Keywords: Adenylyl Cyclase Inhibitors ; Adenylyl Cyclases/*chemistry/metabolism ; Amino Acid Sequence ; Animals ; Cell Line ; Enzyme Activation/physiology ; GTP-Binding Proteins/chemistry/*physiology ; Guanosine Triphosphate/physiology ; In Vitro Techniques ; Molecular Sequence Data ; Peptide Fragments/chemical synthesis/chemistry/physiology ; Potassium Channels/physiology ; Rats ; Receptor Protein-Tyrosine Kinases/metabolism ; Receptors, Adrenergic, beta/metabolism ; Signal Transduction/physiology ; Structure-Activity Relationship ; Type C Phospholipases/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
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    A morbillivirus that caused fatal disease in horses and humans (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-04-07
    Description: A morbillivirus has been isolated and added to an increasing list of emerging viral diseases. This virus caused an outbreak of fatal respiratory disease in horses and humans. Genetic analyses show it to be only distantly related to the classic morbilliviruses rinderpest, measles, and canine distemper. When seen by electron microscopy, viruses had 10- and 18-nanometer surface projections that gave them a "double-fringed" appearance. The virus induced syncytia that developed in the endothelium of blood vessels, particularly the lungs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Murray, K -- Selleck, P -- Hooper, P -- Hyatt, A -- Gould, A -- Gleeson, L -- Westbury, H -- Hiley, L -- Selvey, L -- Rodwell, B -- New York, N.Y. -- Science. 1995 Apr 7;268(5207):94-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉CSIRO Australian Animal Health Laboratory, East Geelong, Victoria.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7701348" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Amino Acid Sequence ; Animals ; Base Sequence ; Cercopithecus aethiops ; Disease Outbreaks/*veterinary ; Female ; Horse Diseases/epidemiology/mortality/*virology ; Horses ; Humans ; Kidney/virology ; Lung/virology ; Male ; Middle Aged ; Molecular Sequence Data ; Morbillivirus/genetics/*isolation & purification ; Morbillivirus Infections/epidemiology/mortality/*veterinary/*virology ; Pregnancy ; Queensland/epidemiology ; Respiratory Tract Infections/veterinary/virology ; Spleen/virology ; Vero Cells ; Virus Cultivation
    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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    Identification of a graft versus host disease-associated human minor histocompatibility antigen (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-06-09
    Description: Minor histocompatibility antigen disparities between human leukocyte antigen (HLA)-matched bone marrow donors and recipients are a major risk factor for graft versus host disease (GVHD). An HLA-A2.1-restricted cytotoxic T cell clone that recognized the minor histocompatibility antigen HA-2 was previously isolated from a patient with severe GVHD after HLA-identical bone marrow transplantation. The HLA-A2.1-bound peptide representing HA-2 has now been identified. This peptide appears to originate from a member of the non-filament-forming class I myosin family. Because HA-2 has a phenotype frequency of 95 percent in the HLA-A2.1-positive population, it is a candidate for immunotherapeutic intervention in bone marrow transplantation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉den Haan, J M -- Sherman, N E -- Blokland, E -- Huczko, E -- Koning, F -- Drijfhout, J W -- Skipper, J -- Shabanowitz, J -- Hunt, D F -- Engelhard, V H -- AI20963/AI/NIAID NIH HHS/ -- AI33993/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1995 Jun 9;268(5216):1476-80.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunohaematology, University Hospital, Leiden, Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7539551" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Bone Marrow Transplantation ; Epitopes ; Female ; Graft vs Host Disease/*immunology ; HLA-A2 Antigen/immunology ; Humans ; Mass Spectrometry ; Minor Histocompatibility Antigens/chemistry/*immunology ; Molecular Sequence Data ; Neoplasm Proteins/chemistry/*immunology ; Oligopeptides/chemistry/immunology ; T-Lymphocytes, Cytotoxic/immunology
    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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  • 10
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    Inactivation of the mouse Huntington's disease gene homolog Hdh (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-07-21
    Description: Huntington's disease (HD) is a dominant neurodegenerative disorder caused by expansion of a CAG repeat in the gene encoding huntingtin, a protein of unknown function. To distinguish between "loss of function" and "gain of function" models of HD, the murine HD homolog Hdh was inactivated by gene targeting. Mice heterozygous for Hdh inactivation were phenotypically normal, whereas homozygosity resulted in embryonic death. Homozygotes displayed abnormal gastrulation at embryonic day 7.5 and were resorbing by day 8.5. Thus, huntingtin is critical early in embryonic development, before the emergence of the nervous system. That Hdh inactivation does not mimic adult HD neuropathology suggests that the human disease involves a gain of function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Duyao, M P -- Auerbach, A B -- Ryan, A -- Persichetti, F -- Barnes, G T -- McNeil, S M -- Ge, P -- Vonsattel, J P -- Gusella, J F -- Joyner, A L -- NS16367/NS/NINDS NIH HHS/ -- NS32765/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1995 Jul 21;269(5222):407-10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Neurogenetics Unit, Massachusetts General Hospital, Charlestown 02129, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7618107" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cell Line ; Ectoderm/cytology ; Embryonic and Fetal Development ; Female ; Gene Targeting ; Genotype ; Heterozygote ; Homozygote ; Humans ; Huntington Disease/*genetics ; Male ; Mesoderm/cytology ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Nerve Tissue Proteins/*genetics/physiology ; Nuclear Proteins/*genetics/physiology ; Phenotype ; Stem Cells/metabolism
    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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