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  • Mice  (1,066)
  • National Institutes of Health (U.S.)  (265)
  • American Association for the Advancement of Science (AAAS)  (1,327)
  • Annual Reviews
  • 1990-1994  (812)
  • 1980-1984  (515)
Collection
Keywords
Publisher
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Year
  • 1
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    Premature p34cdc2 activation required for apoptosis (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-02-25
    Description: Activation of the serine-threonine kinase p34cdc2 at an inappropriate time during the cell cycle leads to cell death that resembles apoptosis. Premature activation of p34cdc2 was shown to be required for apoptosis induced by a lymphocyte granule protease. The kinase was rapidly activated and tyrosine dephosphorylated at the initiation of apoptosis. DNA fragmentation and nuclear collapse could be prevented by blocking p34cdc2 activity with excess peptide substrate, or by inactivating p34cdc2 in a temperature-sensitive mutant. Premature p34cdc2 activation may be a general mechanism by which cells induced to undergo apoptosis initiate the disruption of the nucleus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shi, L -- Nishioka, W K -- Th'ng, J -- Bradbury, E M -- Litchfield, D W -- Greenberg, A H -- New York, N.Y. -- Science. 1994 Feb 25;263(5150):1143-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Manitoba Institute of Cell Biology, University of Manitoba, Winnipeg, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8108732" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; *Apoptosis ; CDC2 Protein Kinase/*metabolism ; DNA Damage ; Deoxyribonucleases/pharmacology ; Enzyme Activation ; Enzyme Induction ; Membrane Glycoproteins/pharmacology ; Mice ; Mitosis ; Molecular Sequence Data ; Perforin ; Phosphorylation ; Pore Forming Cytotoxic Proteins ; Serine Endopeptidases/pharmacology ; Tumor Cells, Cultured
    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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    Slow going for blood substitutes (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-12-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pool, R -- New York, N.Y. -- Science. 1990 Dec 21;250(4988):1655-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2270476" target="_blank"〉PubMed〈/a〉
    Keywords: *Blood Substitutes/adverse effects ; Hemoglobins/*therapeutic use ; Humans ; National Institutes of Health (U.S.) ; 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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  • 3
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    Mycoplasmas in the AIDS spotlight (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-05-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wright, K -- New York, N.Y. -- Science. 1990 May 11;248(4956):682-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2333519" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/*microbiology ; Animals ; HIV/isolation & purification/pathogenicity ; Humans ; Liver/microbiology ; Mycoplasma/*isolation & purification/pathogenicity ; National Institutes of Health (U.S.) ; Research/standards ; Research Design ; 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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  • 4
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    Human genome initiative (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-09-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sinsheimer, R L -- New York, N.Y. -- Science. 1990 Sep 21;249(4975):1359.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2402630" target="_blank"〉PubMed〈/a〉
    Keywords: *Human Genome Project ; 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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  • 5
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    Flying blind: the making of EMF policy (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-10-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pool, R -- New York, N.Y. -- Science. 1990 Oct 5;250(4977):23-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2218509" target="_blank"〉PubMed〈/a〉
    Keywords: *Electromagnetic Phenomena ; *Environmental Exposure ; Humans ; National Institutes of Health (U.S.) ; Neoplasms/*etiology ; 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
    Published by American Association for the Advancement of Science (AAAS)
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  • 6
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    Induction of cellular senescence in immortalized cells by human chromosome 1 (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-02-09
    Description: The control of cellular senescence by specific human chromosomes was examined in interspecies cell hybrids between diploid human fibroblasts and an immortal, Syrian hamster cell line. Most such hybrids exhibited a limited life span comparable to that of the human fibroblasts, indicating that cellular senescence is dominant in these hybrids. Karyotypic analyses of the hybrid clones that did not senesce revealed that all these clones had lost both copies of human chromosome 1, whereas all other human chromosomes were observed in at least some of the immortal hybrids. The application of selective pressure for retention of human chromosome 1 to the cell hybrids resulted in an increased percentage of hybrids that senesced. Further, the introduction of a single copy of human chromosome 1 to the hamster cells by microcell fusion caused typical signs of cellular senescence. Transfer of chromosome 11 had no effect on the growth of the cells. These findings indicate that human chromosome 1 may participate in the control of cellular senescence and further support a genetic basis for cellular senescence.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sugawara, O -- Oshimura, M -- Koi, M -- Annab, L A -- Barrett, J C -- New York, N.Y. -- Science. 1990 Feb 9;247(4943):707-10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2300822" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cell Survival/*genetics ; Chromosome Mapping ; *Chromosomes, Human, Pair 1 ; Clone Cells ; Cricetinae ; Diploidy ; Fibroblasts/*cytology ; Humans ; Hybrid Cells/*cytology ; Hypoxanthine Phosphoribosyltransferase/genetics ; Karyotyping ; Mice ; Ploidies ; Transfection ; Translocation, Genetic ; X Chromosome
    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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    T cell reactivity to MHC molecules: immunity versus tolerance (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-06-15
    Description: The specificity of mature CD8+ and CD4+ T lymphocytes is controlled by major histocompatibility complex (MHC) class I and class II molecules, respectively. The MHC class specificity of T cells is stringent in many assays, but is less evident when cells are supplemented with exogenous lymphokines. The repertoire of T cells is shaped through contact with MHC molecules in the thymus and involves a complex process of positive selection and negative selection (tolerance). Tolerance of immature T cells to MHC molecules can reflect either clonal deletion or anergy and results from intrathymic contact with several cell types, including epithelial cells and cells with antigen-presenting function. Unlike immature T cells, mature T cells are relatively resistant to tolerance induction. In certain situations partial unresponsiveness of mature T cells can be achieved by exposing T cells to foreign MHC molecules expressed on atypical antigen-presenting cells. Tolerance is rarely complete, however, and the precise requirements for tolerizing mature T cells are still unclear.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sprent, J -- Gao, E K -- Webb, S R -- AI21487/AI/NIAID NIH HHS/ -- CA25803/CA/NCI NIH HHS/ -- CA38355/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1990 Jun 15;248(4961):1357-63.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Research Institute of Scripps Clinic, La Jolla, CA 92037.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1694041" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen-Presenting Cells/immunology ; Bone Marrow/immunology ; CD4-Positive T-Lymphocytes/immunology ; Clone Cells/immunology ; Epitopes/immunology ; Histocompatibility Antigens/*immunology ; Histocompatibility Antigens Class II/immunology ; *Immune Tolerance ; *Immunity ; Interleukin-2/physiology ; Mice ; Mice, Transgenic ; Receptors, Antigen, T-Cell/immunology ; T-Lymphocytes/*immunology ; T-Lymphocytes, Regulatory/immunology ; Thymus Gland/immunology
    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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    Posttranslational glutamylation of alpha-tubulin (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-01-05
    Description: The high degree of tubulin heterogeneity in neurons is controlled mainly at the posttranslational level. Several variants of alpha-tubulin can be posttranslationally labeled after incubation of cells with [3H]acetate or [3H]glutamate. Peptides carrying the radioactive moiety were purified by high-performance liquid chromatography. Amino acid analysis, Edman degradation sequencing, and mass spectrometric analysis of these peptides led to the characterization of a posttranslational modification consisting of the successive addition of glutamyl units on the gamma-carboxyl group of a glutamate residue (Glu445). This modification, localized within a region of alpha-tubulin that is important in the interactions of tubulin with microtubule-associated proteins and calcium, could play a role in regulating microtubule dynamics.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Edde, B -- Rossier, J -- Le Caer, J P -- Desbruyeres, E -- Gros, F -- Denoulet, P -- New York, N.Y. -- Science. 1990 Jan 5;247(4938):83-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratoire de Biochimie Cellulaire, College de France, Paris.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1967194" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acids/analysis ; Animals ; Brain/*metabolism ; Chromatography, High Pressure Liquid ; Glutamates/*metabolism ; Glutamic Acid ; Mass Spectrometry ; Mice ; Neurons/*metabolism ; Peptide Fragments/analysis ; *Protein Processing, Post-Translational ; Tubulin/*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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  • 9
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    Clonal deletion versus clonal anergy: the role of the thymus in inducing self tolerance (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-06-15
    Description: During development in the thymus, T cells are rendered tolerant to self antigens. It is now apparent that thymocytes bearing self-reactive T cell receptors can be tolerized by processes that result in physical elimination (clonal deletion) or functional inactivation (clonal anergy). As these mechanisms have important clinical implications for transplantation and autoimmunity, current investigations are focused on understanding the cellular and molecular interactions that generate these forms of tolerance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ramsdell, F -- Fowlkes, B J -- New York, N.Y. -- Science. 1990 Jun 15;248(4961):1342-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Cellular and Molecular Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1972593" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Surface/immunology ; Autoantigens/immunology ; Autoimmunity/immunology ; Bone Marrow/immunology ; CD4-Positive T-Lymphocytes/immunology ; Chickens ; Chimera ; Clone Cells/*immunology ; H-2 Antigens/immunology ; Histocompatibility Antigens/immunology ; Histocompatibility Antigens Class II/immunology ; *Immune Tolerance ; Mice ; Mice, Transgenic ; Minor Lymphocyte Stimulatory Antigens ; Receptors, Antigen, T-Cell/*immunology ; T-Lymphocytes/*immunology ; T-Lymphocytes, Regulatory/immunology ; Thymus Gland/*immunology ; Xenopus
    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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    The dominant W42 spotting phenotype results from a missense mutation in the c-kit receptor kinase (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-01-12
    Description: The murine white spotting locus (W) is allelic with the proto-oncogene c-kit, which encodes a transmembrane tyrosine protein kinase receptor for an unknown ligand. Mutations at the W locus affect various aspects of hematopoiesis and the proliferation and migration of primordial germ cells and melanoblasts during development to varying degrees of severity. The W42 mutation has a particularly severe effect in both the homozygous and the heterozygous states. The molecular basis of the W42 mutation was determined. The c-kit protein products in homozygous mutant mast cells were expressed normally but displayed a defective tyrosine kinase activity in vitro. Nucleotide sequence analysis of mutant complementary DNAs revealed a missense mutation that replaces aspartic acid with asparagine at position 790 in the c-kit protein product. Aspartic acid-790 is a conserved residue in all protein kinases. These results provide an explanation for the dominant nature of the W42 mutation and provide insight into the mechanism of c-kit-mediated signal transduction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tan, J C -- Nocka, K -- Ray, P -- Traktman, P -- Besmer, P -- P01-CA-16599/CA/NCI NIH HHS/ -- R01-CA-32926/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1990 Jan 12;247(4939):209-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Biology Program, Sloan Kettering Institute, New York, NY 10021.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1688471" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cells, Cultured ; DNA/genetics ; Gene Expression ; Homozygote ; Liver/analysis/cytology/embryology ; Mast Cells/metabolism ; Mice ; Molecular Sequence Data ; *Mutation ; *Phenotype ; Polymerase Chain Reaction ; Protein-Tyrosine Kinases/*genetics ; Proto-Oncogene Proteins/*genetics ; Proto-Oncogene Proteins c-kit ; RNA/analysis ; Receptors, Cell Surface/genetics ; Signal Transduction
    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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  • 11
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    Use of prior vaccinations for the development of new vaccines (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-07-27
    Description: There is currently a need for vaccine development to improve the immunogenicity of protective epitopes, which themselves are often poorly immunogenic. Although the immunogenicity of these epitopes can be enhanced by linking them to highly immunogenic carriers, such carriers derived from current vaccines have not proven to be generally effective. One reason may be related to epitope-specific suppression, in which prior vaccination with a protein can inhibit the antibody response to new epitopes linked to the protein. To circumvent such inhibition, a peptide from tetanus toxoid was identified that, when linked to a B cell epitope and injected into tetanus toxoid-primed recipients, retained sequences for carrier but not suppressor function. The antibody response to the B cell epitope was enhanced. This may be a general method for taking advantage of previous vaccinations in the development of new vaccines.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Etlinger, H M -- Gillessen, D -- Lahm, H W -- Matile, H -- Schonfeld, H J -- Trzeciak, A -- New York, N.Y. -- Science. 1990 Jul 27;249(4967):423-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Central Research Unit F. Hoffmann-La Roche, Basel, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1696030" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antigens, Protozoan/*immunology ; B-Lymphocytes/immunology ; Epitopes/*immunology ; Humans ; Mice ; Mice, Inbred BALB C ; Molecular Sequence Data ; Peptide Fragments/immunology ; Plasmodium falciparum/*immunology ; T-Lymphocytes/immunology ; T-Lymphocytes, Helper-Inducer/immunology ; T-Lymphocytes, Regulatory/immunology ; Tetanus Toxoid/*immunology ; *Vaccination ; Vaccines/*immunology
    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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  • 12
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    Acceleration of diabetes in young NOD mice with a CD4+ islet-specific T cell clone (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-09-21
    Description: Nonobese diabetic (NOD) mice develop an autoimmune form of diabetes, becoming hyperglycemic after 3 months of age. This process was accelerated by injecting young NOD mice with CD4+ islet-specific T cell clones derived from NOD mice. Overt diabetes developed in 10 of 19 experimental animals by 7 weeks of age, with the remaining mice showing marked signs of the disease in progress. Control mice did not become diabetic and had no significant pancreatic infiltration. This work demonstrates that a CD4 T cell clone is sufficient to initiate the disease process in the diabetes-prone NOD mouse.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Haskins, K -- McDuffie, M -- P01 DK40144/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1990 Sep 21;249(4975):1433-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Barbara Davis Center for Childhood Diabetes, University of Colorado Health Sciences Center, Denver 80262.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2205920" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD4/analysis/*immunology ; Clone Cells ; Diabetes Mellitus, Experimental/*immunology/pathology ; Female ; Islets of Langerhans/*immunology/pathology ; Male ; Mice ; Mice, Inbred Strains ; Mice, Mutant Strains ; T-Lymphocytes/*immunology/transplantation
    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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  • 13
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    Pinning down sequencing costs (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-12-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉New York, N.Y. -- Science. 1990 Dec 21;250(4988):1663.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2270479" target="_blank"〉PubMed〈/a〉
    Keywords: Cost Control ; DNA/*genetics ; Government Agencies ; Human Genome Project/*economics ; Humans ; National Institutes of Health (U.S.) ; United States
    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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  • 14
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    A meeting of the minds on the genome project? (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-11-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roberts, L -- New York, N.Y. -- Science. 1990 Nov 9;250(4982):756-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2237425" target="_blank"〉PubMed〈/a〉
    Keywords: Federal Government ; Government Agencies ; *Human Genome Project ; National Institutes of Health (U.S.) ; *Research Design ; Resource Allocation ; United States
    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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    Dominant negative regulation of the mouse alpha-fetoprotein gene in adult liver (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-12-21
    Description: Transcription of the mouse alpha-fetoprotein gene is activated in the developing fetal liver and gut and repressed in both tissues shortly after birth. With germline transformation in mice, a cis-acting element was identified upstream of the transcription initiation site of the alpha-fetoprotein gene that was responsible for repression of the gene in adult liver. This negative element acts as a repressor in a position-dependent manner.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vacher, J -- Tilghman, S M -- CA44976/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1990 Dec 21;250(4988):1732-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Biology, Princeton University, NJ 08544.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1702902" target="_blank"〉PubMed〈/a〉
    Keywords: Aging ; Animals ; Animals, Newborn ; Chromosome Deletion ; Cloning, Molecular ; DNA-Binding Proteins/metabolism ; Enhancer Elements, Genetic ; Fetus ; *Gene Expression Regulation ; Hepatocyte Nuclear Factor 1 ; Hepatocyte Nuclear Factor 1-alpha ; Hepatocyte Nuclear Factor 1-beta ; Liver/growth & development/*metabolism ; Mice ; *Nuclear Proteins ; Transcription Factors/metabolism ; Transcription, Genetic ; alpha-Fetoproteins/*genetics
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 16
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    "Superantigens" may shed light on immune puzzle (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-05-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hoffman, M -- New York, N.Y. -- Science. 1990 May 11;248(4956):685-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2333520" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Bacterial/*immunology ; Antigens, Viral/immunology ; Bacterial Toxins/*immunology ; Humans ; Immune System/*physiology ; Lymphocytes/*immunology ; Mice ; T-Lymphocytes/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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  • 17
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    RAG-1 and RAG-2, adjacent genes that synergistically activate V(D)J recombination (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-06-22
    Description: The vast repertoire of immunoglobulins and T cell receptors is generated, in part, by V(D)J recombination, a series of genomic rearrangements that occur specifically in developing lymphocytes. The recombination activating gene, RAG-1, which is a gene expressed exclusively in maturing lymphoid cells, was previously isolated. RAG-1 inefficiently induced V(D)J recombinase activity when transfected into fibroblasts, but cotransfection with an adjacent gene, RAG-2, has resulted in at least a 1000-fold increase in the frequency of recombination. The 2.1-kilobase RAG-2 complementary DNA encodes a putative protein of 527 amino acids whose sequence is unrelated to that of RAG-1. Like RAG-1, RAG-2 is conserved between species that carry out V(D)J recombination, and its expression pattern correlates precisely with that of V(D)J recombinase activity. In addition to being located just 8 kilobases apart, these convergently transcribed genes are unusual in that most, if not all, of their coding and 3' untranslated sequences are contained in single exons. RAG-1 and RAG-2 might activate the expression of the V(D)J recombinase but, more likely, they directly participate in the recombination reaction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Oettinger, M A -- Schatz, D G -- Gorka, C -- Baltimore, D -- GM39458/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1990 Jun 22;248(4962):1517-23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research, Cambridge, MA 02142.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2360047" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Biological Evolution ; Cattle ; Cell Line ; Chickens ; Cricetinae ; DNA/*genetics ; DNA Nucleotidyltransferases/*genetics ; *DNA-Binding Proteins ; Dogs ; Female ; *Gene Rearrangement, B-Lymphocyte ; *Gene Rearrangement, T-Lymphocyte ; *Homeodomain Proteins ; Humans ; Male ; Mice ; Molecular Sequence Data ; *Multigene Family ; Nuclear Proteins ; Nucleic Acid Hybridization ; Opossums ; Proteins/*genetics ; Rabbits ; Recombination, Genetic/*genetics ; Restriction Mapping ; Transfection ; Turtles ; VDJ Recombinases
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    What's holding up "aversives" report? (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-08-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Holden, C -- New York, N.Y. -- Science. 1990 Aug 31;249(4972):980-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2396100" target="_blank"〉PubMed〈/a〉
    Keywords: *Aversive Therapy ; Electroconvulsive Therapy ; Humans ; Intellectual Disability/*therapy ; National Institutes of Health (U.S.) ; Self Mutilation/prevention & control ; United States
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  • 19
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    Presentation of exogenous antigen with class I major histocompatibility complex molecules (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-08-24
    Description: Soluble antigens (Ags) in the extracellular fluids are excluded from the class I major histocompatibility complex (MHC)-restricted pathway of Ag presentation in most cells. However, an exogenous Ag can be internalized, processed, and presented in association with class I MHC molecules on specialized Ag-presenting cells (APCs). These APCs express class II molecules and can simultaneously present exogenous Ags to both class I and class II MHC-restricted T cells. These APCs may be important participants in the regulation of host immune responses. This APC activity may explain several phenomena of cytotoxic T lymphocyte (CTL) priming in vivo and might be exploited for eliciting CTL responses to protein vaccines.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rock, K L -- Gamble, S -- Rothstein, L -- AI-20248/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1990 Aug 24;249(4971):918-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Harvard Medical School, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2392683" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen-Presenting Cells/*immunology ; Azides/pharmacology ; Cell Line ; Histocompatibility Antigens Class I/*immunology ; Histocompatibility Antigens Class II/immunology ; Mice ; Mice, Inbred C57BL ; Ovalbumin/*immunology ; Spleen/immunology ; T-Lymphocytes/drug effects/immunology ; T-Lymphocytes, Cytotoxic/immunology
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  • 20
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    Genetic differences in the ethanol sensitivity of GABAA receptors expressed in Xenopus oocytes (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-07-20
    Description: Animal lines selected for differences in drug sensitivity can be used to help determine the molecular basis of drug action. Long-sleep (LS) and short-sleep (SS) mice differ markedly in their genetic sensitivity to ethanol. To investigate the molecular basis for this difference, mRNA from brains of LS and SS mice was expressed in Xenopus oocytes and the ethanol sensitivity of gamma-aminobutyric acid A (GABAA)- and N-methyl D-aspartate (NMDA)-activated ion channels was tested. Ethanol facilitated GABA responses in oocytes injected with mRNA from LS mice but antagonized responses in oocytes injected with mRNA from SS animals. Ethanol inhibited NMDA responses equally in the two lines. Thus, genes coding for the GABAA receptor or associated proteins may be critical determinants of individual differences in ethanol sensitivity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wafford, K A -- Burnett, D M -- Dunwiddie, T V -- Harris, R A -- AA03527/AA/NIAAA NIH HHS/ -- AA06399/AA/NIAAA NIH HHS/ -- New York, N.Y. -- Science. 1990 Jul 20;249(4966):291-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of Colorado Health Sciences Center, Denver.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1695761" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aspartic Acid/analogs & derivatives/pharmacology ; Brain/*metabolism ; Chloride Channels ; Chlorides/*physiology ; Diazepam/pharmacology ; Ethanol/*pharmacology ; Female ; Ion Channels/drug effects/physiology ; Membrane Proteins/*physiology ; Mice ; Mice, Inbred Strains ; Microinjections ; N-Methylaspartate ; Oocytes/*drug effects/*physiology ; RNA, Messenger/administration & dosage/genetics ; Receptors, GABA-A/drug effects/*genetics ; Xenopus ; gamma-Aminobutyric Acid/pharmacology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 21
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    Defective presentation of endogenous antigen by a cell line expressing class I molecules (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-04-20
    Description: Cytotoxic T lymphocytes (CTLs) recognize class I major histocompatibility complex (MHC) molecules associated with antigenic peptides derived from endogenously synthesized proteins. Binding to such peptides is a requirement for class I assembly in the endoplasmic reticulum (ER). A mutant human cell line, T2, assembles and transports to its surface some, but not all, class I MHC molecules. The class I molecules expressed on the surface of T2 do not present peptides derived from cytosolic antigens, although they can present exogenously added peptides to CTL. The transported class I molecules may interact weakly with an unknown retaining factor in the ER such that they can assemble despite the relative shortage of peptides.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hosken, N A -- Bevan, M J -- AI-19335/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1990 Apr 20;248(4953):367-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Research Institute of Scripps Clinic, La Jolla, CA 92037.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2326647" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen-Presenting Cells/*immunology ; Antigens/immunology ; Antigens, Viral/immunology ; B-Lymphocytes/immunology ; Capsid/immunology ; Cell Line ; Endoplasmic Reticulum/immunology ; Gene Expression ; H-2 Antigens/genetics/immunology ; HLA Antigens/genetics ; Histocompatibility Antigens Class I/*immunology ; Histocompatibility Antigens Class II/genetics ; Humans ; Mice ; Mutation ; Ovalbumin/immunology ; Peptides/immunology ; T-Lymphocytes, Cytotoxic/immunology ; Transfection ; Tumor Cells, Cultured ; Viral Core Proteins/immunology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 22
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    Expression of interleukin-10 activity by Epstein-Barr virus protein BCRF1 (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-11-09
    Description: Cytokine synthesis inhibitory factor (CSIF; interleukin-10), a product of mouse TH2 T cell clones that inhibits synthesis of cytokines by mouse TH1 T cell clones, exhibits extensive sequence similarity to an uncharacterized open reading frame in the Epstein-Barr virus BCRF1. Recombinant BCRF1 protein mimics the activity of interleukin-10, suggesting that BCRF1 may have a role in the interaction of the virus with the host's immune system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hsu, D H -- de Waal Malefyt, R -- Fiorentino, D F -- Dang, M N -- Vieira, P -- de Vries, J -- Spits, H -- Mosmann, T R -- Moore, K W -- New York, N.Y. -- Science. 1990 Nov 9;250(4982):830-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, DNAX Research Institute, Palo Alto, CA 94304.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2173142" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; DNA, Viral/genetics ; Electrophoresis, Polyacrylamide Gel ; *Gene Expression Regulation, Viral ; Herpesvirus 4, Human/genetics/*immunology ; Humans ; Interleukin-10 ; Interleukins/*biosynthesis ; Killer Cells, Natural/immunology ; Mice ; Radioimmunoprecipitation Assay ; T-Lymphocytes/immunology ; Viral Proteins/genetics/*immunology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Expanded HIV-1 cellular tropism by phenotypic mixing with murine endogenous retroviruses (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-02-16
    Description: In view of the current interest in in vivo murine models for acquired immunodeficiency syndrome (AIDS), the interaction between human immunodeficiency virus type 1 (HIV-1) and endogenous murine leukemia virus (MuLV)-related retroviruses was investigated with a human leukemic T cell line (PF-382x) that acquired xenotropic MuLV (X-MuLV) after in vivo passage in immunosuppressed mice. Despite similar levels of membrane CD4 expression and HIV-1 125I-labeled gp 120 binding, a dramatic acceleration in the time course of HIV-1 infection was observed in PF-382x compared to its X-MuLV-negative counterpart (PF-382). Moreover, PF-382 cells coinfected by X-MuLV and HIV-1 generated a progeny of phenotypically mixed viral particles, enabling HIV-1 to productively infect a panel of CD4- human cells, including B lymphoid cells and purified normal peripheral blood CD4-/CD8+ T lymphocytes. Mixed viral phenotypes were also produced by human CD4+ T cells coinfected with an amphotropic MuLV-related retrovirus (A-MuLV) and HIV-1. These data show that endogenous MuLV acquired by human cells transplanted into mice can significantly interact with HIV-1, thereby inducing important alterations of HIV-1 biological properties.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lusso, P -- di Marzo Veronese, F -- Ensoli, B -- Franchini, G -- Jemma, C -- DeRocco, S E -- Kalyanaraman, V S -- Gallo, R C -- New York, N.Y. -- Science. 1990 Feb 16;247(4944):848-52.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Tumor Cell Biology, National Cancer Institute, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2305256" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/immunology ; Animals ; Antibodies, Monoclonal ; Antigens, CD4/analysis ; Cell Line ; Cell Transformation, Viral ; Disease Models, Animal ; HIV-1/*genetics/physiology ; Hematopoietic Stem Cells/cytology/microbiology ; Humans ; Mice ; Phenotype ; Retroviridae/*genetics ; Viral Proteins/analysis ; Virus Replication
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  • 24
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    Characterization of naturally occurring minor histocompatibility peptides including H-4 and H-Y (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-07-20
    Description: Minor histocompatibility (H) antigens can be peptides derived from cellular proteins that are presented on the cell surface by major histocompatibility complex (MHC) class I molecules. This is similar to viral antigens, because in both cases cytotoxic T lymphocytes (CTLs) recognize artificially produced peptides loaded on target cells. Naturally processed minor H peptides were found to be similar to those artificial CTL-epitopes, as far as size and hydrophobicity is concerned. The peptides studied were isolated from a transfectant that expressed a model CTL-defined antigen, beta-galactosidase, from male cells that express H-Y, which has been known operationally since 1955, and from cells that express H-4, known since 1961.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rotzschke, O -- Falk, K -- Wallny, H J -- Faath, S -- Rammensee, H G -- New York, N.Y. -- Science. 1990 Jul 20;249(4966):283-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max-Planck-Institut fur Biologie, Abteilung Immungenetik, Tubingen, Federal Republic of Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1695760" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Epitopes/isolation & purification ; Female ; H-Y Antigen/*analysis/immunology ; Male ; Mice ; Mice, Inbred Strains ; Minor Histocompatibility Antigens/*analysis/immunology ; Molecular Sequence Data ; Peptides/chemical synthesis ; Species Specificity ; Spleen/immunology ; T-Lymphocytes, Cytotoxic/*immunology
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    The untold story of HUT78 (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-06-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rubinstein, E -- New York, N.Y. -- Science. 1990 Jun 22;248(4962):1499-507.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2193399" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/history/*microbiology ; *Biomedical Research ; *Cell Line ; *Ethics ; Federal Government ; Government Regulation ; HIV/*isolation & purification ; History, 20th Century ; Humans ; *Information Dissemination ; National Institutes of Health (U.S.) ; United States
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  • 26
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    Recovery of mitogenic activity of a growth factor mutant with a nuclear translocation sequence (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-09-28
    Description: Heparin-binding growth factor-1 (HBGF-1) is an angiogenic polypeptide mitogen for mesoderm- and neuroectoderm-derived cells in vitro and remains biologically active after truncation of the amino-terminal domain (HBGF-1 alpha) of the HBGF-1 beta precursor. Polymerase chain reaction mutagenesis and prokaryotic expression systems were used to prepare a mutant of HBGF-1 alpha lacking a putative nuclear translocation sequence (amino acid residues 21 to 27; HBGF-1U). Although HBGF-1U retains its ability to bind to heparin, HBGF-1U fails to induce DNA synthesis and cell proliferation at concentrations sufficient to induce intracellular receptor-mediated tyrosine phosphorylation and c-fos expression. Attachment of the nuclear translocation sequence from yeast histone 2B at the amino terminus of HBGF-1U yields a chimeric polypeptide (HBGF-1U2) with mitogenic activity in vitro and indicates that nuclear translocation is important for this biological response.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Imamura, T -- Engleka, K -- Zhan, X -- Tokita, Y -- Forough, R -- Roeder, D -- Jackson, A -- Maier, J A -- Hla, T -- Maciag, T -- HL 32348/HL/NHLBI NIH HHS/ -- HL 35627/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1990 Sep 28;249(4976):1567-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Biology, Jerome H. Holland Laboratory for the Biomedical Sciences, American Red Cross, Rockville, MD 20855.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1699274" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Binding, Competitive ; Cattle ; Cell Division/drug effects ; Cell Line ; Cell Nucleus/metabolism ; Cells, Cultured ; DNA Replication/drug effects ; Endothelium, Vascular/drug effects/metabolism ; Fibroblast Growth Factor 1/*genetics/metabolism/pharmacology ; Kinetics ; Mice ; Mitogens/pharmacology ; Molecular Sequence Data ; *Mutation ; Oligonucleotide Probes ; Receptors, Mitogen/metabolism ; Receptors, Vascular Endothelial Growth Factor ; Recombinant Proteins/metabolism/pharmacology ; Transcription, Genetic/drug effects
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    Medicine from plants (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-02-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Abelson, P H -- New York, N.Y. -- Science. 1990 Feb 2;247(4942):513.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2300807" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antineoplastic Agents/pharmacology ; Drug Evaluation, Preclinical ; Drug Screening Assays, Antitumor ; Humans ; National Institutes of Health (U.S.) ; *Plants, Medicinal ; Tumor Cells, Cultured/drug effects ; United States
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  • 28
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    Hypertriglyceridemia as a result of human apo CIII gene expression in transgenic mice (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-08-17
    Description: Primary and secondary hypertriglyceridemia is common in the general population, but the biochemical basis for this disease is largely unknown. With the use of transgenic technology, two lines of mice were created that express the human apolipoprotein CIII gene. One of these mouse lines with 100 copies of the gene was found to express large amounts of the protein and to be severely hypertriglyceridemic. The other mouse line with one to two copies of the gene expressed low amounts of the protein, but nevertheless manifested mild hypertriglyceridemia. Thus, overexpression of apolipoprotein CIII can be a primary cause of hypertriglyceridemia in vivo and may provide one possible etiology for this common disorder in humans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ito, Y -- Azrolan, N -- O'Connell, A -- Walsh, A -- Breslow, J L -- HL 36461/HL/NHLBI NIH HHS/ -- HL33435/HL/NHLBI NIH HHS/ -- HL33714/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1990 Aug 17;249(4970):790-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Rockefeller University, New York, NY 10021.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2167514" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apolipoprotein C-III ; Apolipoproteins C/blood/*genetics ; Chylomicrons/blood ; Cloning, Molecular ; DNA Restriction Enzymes/metabolism ; DNA, Recombinant/metabolism ; *Gene Expression ; Humans ; Hypertriglyceridemia/blood/*genetics ; Lipoproteins, VLDL/blood ; Mice ; Mice, Inbred C57BL ; Mice, Inbred CBA ; Mice, Transgenic ; Nucleic Acid Hybridization ; RNA, Messenger/genetics ; Triglycerides/blood
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  • 29
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    Human sickle hemoglobin in transgenic mice (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-02-02
    Description: DNA molecules that contain the human alpha- and beta s-globin genes inserted downstream of erythroid-specific, deoxyribonuclease I super-hypersensitive sites were coinjected into fertilized mouse eggs and a transgenic mouse line was established that synthesizes human sickle hemoglobin (Hb S). These animals were bred to beta-thalassemic mice to reduce endogenous mouse globin levels. When erythrocytes from these mice were deoxygenated, greater than 90 percent of the cells displayed the same characteristic sickled shapes as erythrocytes from humans with sickle cell disease. Compared to controls the mice have decreased hematocrits, elevated reticulocyte counts, lower hemoglobin concentrations, and splenomegaly, which are all indications of the anemia associated with human sickle cell disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ryan, T M -- Townes, T M -- Reilly, M P -- Asakura, T -- Palmiter, R D -- Brinster, R L -- Behringer, R R -- HD-09172/HD/NICHD NIH HHS/ -- HL-35559/HL/NHLBI NIH HHS/ -- HL43508/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1990 Feb 2;247(4942):566-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, School of Medicine, University of Alabama, Birmingham 35294.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2154033" target="_blank"〉PubMed〈/a〉
    Keywords: Anemia, Sickle Cell/blood/genetics ; Animals ; DNA/genetics ; DNA Transposable Elements ; Erythrocytes/ultrastructure ; Genes ; Globins/*genetics ; Hemoglobin, Sickle/*genetics/isolation & purification ; Humans ; Mice ; Mice, Transgenic ; Microscopy, Electron ; Microscopy, Electron, Scanning
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  • 30
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    Cloning of an interleukin-3 receptor gene: a member of a distinct receptor gene family (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-01-19
    Description: Interleukin-3 (IL-3) binds to its receptor with high and low affinities, induces tyrosine phosphorylation, and promotes the proliferation and differentiation of hematopoietic cells. A binding component of the IL-3 receptor was cloned. Fibroblasts transfected with the complementary DNA bound IL-3 with a low affinity [dissociation constant (Kd) of 17.9 +/- 3.6 nM]. No consensus sequence for a tyrosine kinase was present in the cytoplasmic domain. Thus, additional components are required for a functional high affinity IL-3 receptor. A sequence comparison of the IL-3 receptor with other cytokine receptors (erythropoietin, IL-4, IL-6, and the beta chain IL-2 receptor) revealed a common motif of a distinct receptor gene family.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Itoh, N -- Yonehara, S -- Schreurs, J -- Gorman, D M -- Maruyama, K -- Ishii, A -- Yahara, I -- Arai, K -- Miyajima, A -- New York, N.Y. -- Science. 1990 Jan 19;247(4940):324-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, DNAX Research Institute of Molecular and Cellular Biology, Palo Alto, CA 94304.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2404337" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; *Cloning, Molecular ; DNA/genetics ; DNA Probes ; Escherichia coli/genetics ; Fibroblasts/metabolism ; Interleukin-3/metabolism ; Mice ; Molecular Sequence Data ; Nucleic Acid Hybridization ; Plasmids ; Protein-Tyrosine Kinases/metabolism ; Receptors, Immunologic/*genetics/metabolism ; Receptors, Interleukin-3 ; Sequence Homology, Nucleic Acid ; Transfection
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    Biomedical funds: IOM strikes back (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-12-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Palca, J -- New York, N.Y. -- Science. 1990 Dec 7;250(4986):1332.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2255903" target="_blank"〉PubMed〈/a〉
    Keywords: *Institute of Medicine (U.S.) ; National Institutes of Health (U.S.) ; *Research Support as Topic ; United States
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    A storm over steroid therapy (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-11-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Palca, J -- New York, N.Y. -- Science. 1990 Nov 30;250(4985):1196-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2244205" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/*complications ; Health Policy ; Humans ; National Institutes of Health (U.S.) ; Periodicals as Topic ; Pneumonia, Pneumocystis/complications/*drug therapy ; Steroids/adverse effects/*therapeutic use ; United States
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    Toxoplasma gondii: fusion competence of parasitophorous vacuoles in Fc receptor-transfected fibroblasts (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-08-10
    Description: After actively entering its host cells, the protozoan parasite Toxoplasma gondii resides in an intracellular vacuole that is completely unable to fuse with other endocytic or biosynthetic organelles. The fusion blocking requires entry of viable organisms but is irreversible: fusion competence of the vacuole is not restored if the parasite is killed after entry. The fusion block can be overcome, however, by altering the parasite's route of entry. Thus, phagocytosis of viable antibody-coated T. gondii by Chinese hamster ovary cells transfected with macrophage-lymphocyte Fc receptors results in the formation of vacuoles that are capable of both fusion and acidification. Phagocytosis and fusion appear to involve a domain of the Fc receptor cytoplasmic tail distinct from that required for localization at clathrin-coated pits. These results suggest that the mechanism of fusion inhibition is likely to reflect a modification of the vacuole membrane at the time of its formation, as opposed to the secretion of a soluble inhibitor by the parasite.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Joiner, K A -- Fuhrman, S A -- Miettinen, H M -- Kasper, L H -- Mellman, I -- New York, N.Y. -- Science. 1990 Aug 10;249(4969):641-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Yale University School of Medicine, New Haven, CT 06510.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2200126" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Fibroblasts/parasitology/physiology/ultrastructure ; Fluorescent Antibody Technique ; Lysosomes/physiology/ultrastructure ; Macrophages/immunology ; Membrane Fusion ; Mice ; Mice, Inbred BALB C ; Phagocytosis ; Receptors, Fc/genetics/*physiology ; Toxoplasma/growth & development/*physiology ; *Transfection ; Vacuoles/*parasitology/physiology/ultrastructure
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    Effect of phospholipase C-gamma overexpression on PDGF-induced second messengers and mitogenesis (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-05-04
    Description: Platelet-derived growth factor (PDGF) stimulates phospholipase C (PLC) activity and the phosphorylation of the gamma isozyme of PLC (PLC-gamma) in vitro and in living cells. The role of PLC-gamma in the phosphoinositide signaling pathway was addressed by examining the effect of overexpression of PLC-gamma on cellular responses to PDGF. Overexpression of PLC-gamma correlated with PDGF-induced tyrosine phosphorylation of PLC-gamma and with PDGF-induced breakdown of phosphatidylinositol 4,5-bisphosphate (PIP2). However, neither bradykinin- nor lysophosphatidic acid-induced phosphoinositide metabolism was enhanced in the transfected cells, suggesting that the G protein-coupled phosphoinositide responses to these ligands are mediated by other PLC isozymes. The enhanced PDGF-induced generation of inositol trisphosphate (IP3) did not enhance intracellular calcium signaling or influence PDGF-induced DNA synthesis. Thus, enzymes other than PLC-gamma may limit PDGF-induced calcium signaling and DNA synthesis. Alternatively, PDGF-induced calcium signaling and DNA synthesis may use biochemical pathways other than phosphoinositide metabolism for signal transduction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Margolis, B -- Zilberstein, A -- Franks, C -- Felder, S -- Kremer, S -- Ullrich, A -- Rhee, S G -- Skorecki, K -- Schlessinger, J -- New York, N.Y. -- Science. 1990 May 4;248(4955):607-10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Rorer Biotechnology, King of Prussia, PA 19406.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2333512" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/physiology ; Cattle ; Cell Division/*drug effects ; Cells, Cultured ; DNA Replication/drug effects ; Genetic Vectors ; Inositol Phosphates/metabolism ; Isoenzymes/biosynthesis/*genetics/metabolism ; Kinetics ; Mice ; Platelet-Derived Growth Factor/*pharmacology ; Second Messenger Systems/*drug effects ; Transfection ; Type C Phospholipases/biosynthesis/*genetics/metabolism
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    A mouse model of the aniridia-Wilms tumor deletion syndrome (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-11-09
    Description: Deletion of chromosome 11p13 in humans produces the WAGR syndrome, consisting of aniridia (an absence or malformation of the iris), Wilms tumor (nephroblastoma), genitourinary malformations, and mental retardation. An interspecies backcross between Mus musculus/domesticus and Mus spretus was made in order to map the homologous chromosomal region in the mouse genome and to define an animal model of this syndrome. Nine evolutionarily conserved DNA clones from proximal human 11p were localized on mouse chromosome 2 near Small-eyes (Sey), a semidominant mutation that is phenotypically similar to aniridia. Analysis of Dickie's Small-eye (SeyDey), a poorly viable allele that has pleiotropic effects, revealed the deletion of three clones, f3, f8, and k13, which encompass the aniridia (AN2) and Wilms tumor susceptibility genes in man. Unlike their human counterparts, SeyDey/+ mice do not develop nephroblastomas. These findings suggest that the Small-eye defect is genetically equivalent to human aniridia, but that loss of the murine homolog of the Wilms tumor gene is not sufficient for tumor initiation. A comparison among Sey alleles suggests that the AN2 gene product is required for induction of the lens and nasal placodes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Glaser, T -- Lane, J -- Housman, D -- 2 T32 GMO7753-11/GM/NIGMS NIH HHS/ -- GM27882/GM/NIGMS NIH HHS/ -- T32 GM007753/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1990 Nov 9;250(4982):823-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Cancer Research, Massachusetts Institute of Technology, Cambridge 02139.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2173141" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aniridia/*genetics ; Blotting, Southern ; Chromosome Deletion ; Chromosome Mapping ; DNA/analysis ; *Disease Models, Animal ; Eye/embryology/pathology ; Female ; Genes, Wilms Tumor/*genetics ; Genetic Markers ; Kidney Neoplasms/*genetics ; Male ; Mice ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Muridae ; Mutation ; Phenotype ; Polymorphism, Genetic ; Syndrome ; Wilms Tumor/*genetics
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    Thymic epithelium tolerizes for histocompatibility antigens (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-03-23
    Description: The role of thymic epithelium in the establishment of tissue tolerance was analyzed with a murine chimeric system. All T cells differentiated from birth onward in a thymus comprising allogeneic epithelium and syngeneic hematopoietic cells. Embryonic thymic rudiments that contained no hematopoietic cells from C3H (H-2k) donors were grafted to newborn athymic (nude) BALB/c (H-2d) mice. Chimeras that had normal T cell numbers and function rejected third-party skin grafts, but permanently accepted grafts syngeneic to the thymic epithelium. In vitro functional assays did not always correlate with the state of tolerance in vivo. Thus, pure thymic epithelium induces tolerance to histocompatibility antigens.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Salaun, J -- Bandeira, A -- Khazaal, I -- Calman, F -- Coltey, M -- Coutinho, A -- Le Douarin, N M -- New York, N.Y. -- Science. 1990 Mar 23;247(4949 Pt 1):1471-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Instit d'Embryologie cellulaire et moleculaire du CNRS, College de France, Nogent-sur-Marne.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2321009" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chimera ; Epithelium/immunology ; Graft Rejection/immunology ; Graft Survival/*immunology ; Histocompatibility Antigens/*immunology ; Immune Tolerance/immunology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Mice, Nude ; Thymus Gland/*immunology
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    Hair analysis (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-11-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Martinez, F -- Poet, T S -- Watson, R R -- New York, N.Y. -- Science. 1990 Nov 23;250(4984):1070.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2251495" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cocaine/metabolism/pharmacokinetics ; Hair/*chemistry/metabolism ; Humans ; Male ; Mice ; Morphine/metabolism/pharmacokinetics ; *Substance Abuse Detection
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    Subtle cerebellar phenotype in mice homozygous for a targeted deletion of the En-2 homeobox (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-03-08
    Description: The two mouse genes, En-1 and En-2, that are homologs of the Drosophila segmentation gene engrailed, show overlapping spatially restricted patterns of expression in the neural tube during embryogenesis, suggestive of a role in regional specification. Mice homozygous for a targeted mutation that deletes the homeobox were viable and showed no obvious defects in embryonic development. This may be due to functional redundancy of En-2 and the related En-1 gene product during embryogenesis. Consistent with this hypothesis, the mutant mice showed abnormal foliation in the adult cerebellum, where En-2, and not En-1, is normally expressed.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Joyner, A L -- Herrup, K -- Auerbach, B A -- Davis, C A -- Rossant, J -- HD25334/HD/NICHD NIH HHS/ -- NS18381/NS/NINDS NIH HHS/ -- NS20591/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1991 Mar 8;251(4998):1239-43.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, Ontario, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1672471" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blastocyst ; Cell Line ; Cerebellum/*anatomy & histology/embryology/pathology ; Chimera ; *Chromosome Deletion ; Female ; *Genes, Homeobox ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Nervous System/embryology ; Phenotype
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    Negative regulation of CD45 protein tyrosine phosphatase activity by ionomycin in T cells (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-09-20
    Description: CD45 is a leukocyte-specific, transmembrane protein tyrosine phosphatase (PTPase) required for T cell responsiveness. How the activity of PTPases is regulated in vivo is unclear. Treatment of murine thymocytes and a variety of murine T cell lines with the calcium ionophore ionomycin decreased CD45 PTPase activity. Ionomycin treatment also led to a decreased phosphorylation of serine residues in CD45. These results indicate that increased intracellular calcium modulates CD45 PTPase activity, demonstrating regulation of CD45 PTPase activity in vivo, and also implicate serine dephosphorylation as a possible mechanism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ostergaard, H L -- Trowbridge, I S -- CA-17733/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1991 Sep 20;253(5026):1423-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cancer Biology, Salk Institute, San Diego, CA 92186.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1654595" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD/*metabolism ; Antigens, CD45 ; Cell Line ; Histocompatibility Antigens/*metabolism ; Ionomycin/*pharmacology ; Kinetics ; Mice ; Mice, Inbred BALB C ; Phosphoprotein Phosphatases/*metabolism ; Protein Tyrosine Phosphatases ; Spleen/drug effects/enzymology/immunology ; T-Lymphocytes/drug effects/*enzymology/immunology ; Thymus Gland/immunology
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    Differentiation of 3T3-L1 fibroblasts to adipocytes induced by transfection of ras oncogenes (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-08-02
    Description: Mammalian 3T3-L1 cells differentiate into adipocytes after continuous exposure to pharmacological doses of insulin or physiological doses of insulin-like growth factor I (IGF-1). Expression of transfected ras oncogenes led to differentiation of these cells into adipocytes in the absence of externally added insulin or IGF-I. Cells transfected with normal ras genes or the tyrosine kinase trk oncogene did not differentiate. Transfection with a dominant inhibitory ras mutant resulted in inhibition of differentiation. Exposure of untransfected 3T3-L1 cells to insulin stimulated formation of the active Ras.GTP complex. These observations indicate that Ras proteins participate in signal transduction pathways initiated by insulin and IGF-I in these cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Benito, M -- Porras, A -- Nebreda, A R -- Santos, E -- New York, N.Y. -- Science. 1991 Aug 2;253(5019):565-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Microbiology, National Institute of Allergy and Infectious Diseases, National Institute of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1857988" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue/*cytology ; Animals ; Blotting, Northern ; *Cell Differentiation ; Cell Line ; *Cell Transformation, Neoplastic ; Fibroblasts/cytology ; *Genes, ras ; Mice ; RNA, Messenger/analysis/genetics ; *Transfection
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    An unexpectedly efficient catalytic antibody operating by ping-pong and induced fit mechanisms (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-05-03
    Description: A transition state analogue was used to produce a mouse antibody that catalyzes transesterification in water. The antibody behaves as a highly efficient catalyst with a covalent intermediate and the characteristic of induced fit. While some features of the catalytic pathway were programmed when the hapten was designed and reflect favorable substrate-antibody interactions, other features are a manifestation of the chemical potential of antibody diversity. The fact that antibodies recapitulate mechanisms and pathways previously thought to be a characteristic of highly evolved enzymes suggests that once an appropriate binding cavity is achieved, reaction pathways commensurate with the intrinsic chemical potential of proteins ensue.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wirsching, P -- Ashley, J A -- Benkovic, S J -- Janda, K D -- Lerner, R A -- GM43858-01/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1991 May 3;252(5006):680-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry, Scripps Research Institute, La Jolla, CA 92037.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2024120" target="_blank"〉PubMed〈/a〉
    Keywords: Acylation ; Alcohols/metabolism ; Animals ; Antibodies, Monoclonal/immunology/*metabolism ; Antibody Specificity ; Binding Sites, Antibody ; *Catalysis ; Enzymes/metabolism ; Esterification ; Haptens ; Kinetics ; Mice ; Water
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    Breast cancer: stalemate in the war on cancer (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-12-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marshall, E -- New York, N.Y. -- Science. 1991 Dec 20;254(5039):1719-20.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1763320" target="_blank"〉PubMed〈/a〉
    Keywords: Breast Neoplasms/*economics/prevention & control/therapy ; Female ; Government Agencies ; Humans ; National Institutes of Health (U.S.) ; Research Support as Topic ; United States
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  • 43
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    Lateral movements of membrane glycoproteins restricted by dynamic cytoplasmic barriers (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-11-29
    Description: Cell membranes often are patchy, composed of lateral domains. These domains may be formed by barriers within or on either side of the membrane bilayer. Major histocompatibility complex (MHC) class 1 molecules that were either transmembrane- (H-2Db) or glycosylphosphatidylinositol (GPI)-anchored (Qa2) were labeled with antibody-coated gold particles and moved across the cell surface with a laser optical tweezers until they encountered a barrier, the barrier-free path length (BFP). At room temperature, the BFPs of Qa2 and H-2Db were 1.7 +/- 0.2 and 0.6 +/- 0.1 (micrometers +/- SEM), respectively. Barriers persisted at 34 degrees C, although the BFP for both MHC molecules was fivefold greater at 34 degrees C than at 23 degrees C. This indicates that barriers to lateral movement are primarily on the cytoplasmic half of the membrane and are dynamic.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Edidin, M -- Kuo, S C -- Sheetz, M P -- AL14584/PHS HHS/ -- GM 36277/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1991 Nov 29;254(5036):1379-82.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Johns Hopkins University, Baltimore, MD 21218.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1835798" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal ; Cell Line ; Glycolipids/physiology ; Glycosylphosphatidylinositols ; Gold ; H-2 Antigens/*physiology ; Histocompatibility Antigens Class I/*physiology ; *Lipid Bilayers ; Membrane Glycoproteins/*physiology ; Mice ; Phosphatidylinositols/physiology ; Thermodynamics ; Transfection
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    Split anergy in a CD8+ T cell: receptor-dependent cytolysis in the absence of interleukin-2 production (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-03-08
    Description: Engagement of the antigen-specific receptor (TCR) of CD4+ T lymphocytes without a second (costimulatory) signal prevents the subsequent production of interleukin-2 (IL-2) by these cells. Because IL-2 is a key immunoregulatory lymphokine and is also produced by a subset of CD8+ T cells that are able to kill target cells, the effect of engaging the TCR of one such clone in the absence of costimulatory signals was examined. The capacity for TCR-dependent IL-2 production was lost, indicating comparable costimulator-dependent signaling requirements for IL-2 production in CD4+ and CD8+ T cells. However, TCR-mediated cytotoxicity was not impaired, implying that costimulation is required for only certain TCR-dependent effector functions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Otten, G R -- Germain, R N -- New York, N.Y. -- Science. 1991 Mar 8;251(4998):1228-31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Lymphocyte Biology Section, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1900952" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/immunology ; Antigen-Presenting Cells/immunology ; Antigens, CD8 ; Antigens, Differentiation, T-Lymphocyte/*immunology ; Female ; Interleukin-2/biosynthesis/*physiology ; Kinetics ; Lymphocyte Activation ; Mice ; Mice, Inbred Strains ; Ovalbumin/immunology ; Rats ; Receptors, Antigen, T-Cell/*immunology ; Spleen/immunology/radiation effects ; T-Lymphocytes/*immunology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Gallo concedes contamination (again) (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-06-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Palca, J -- New York, N.Y. -- Science. 1991 Jun 7;252(5011):1369.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2047847" target="_blank"〉PubMed〈/a〉
    Keywords: *Hiv ; History, 20th Century ; Humans ; Male ; National Institutes of Health (U.S.) ; United States ; Virus Cultivation
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    Lysyl oxidase and rrg messenger RNA (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-08-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kenyon, K -- Contente, S -- Trackman, P C -- Tang, J -- Kagan, H M -- Friedman, R M -- P01 HL13262/HL/NHLBI NIH HHS/ -- R01 CA37351-04A1/CA/NCI NIH HHS/ -- R37 AR18880/AR/NIAMS NIH HHS/ -- New York, N.Y. -- Science. 1991 Aug 16;253(5021):802.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Uniformed Services University of the Health Sciences, Bethesda, MD 20814.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1678898" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blotting, Northern ; Cell Line ; *Cell Transformation, Neoplastic ; Gene Expression ; *Genes, Tumor Suppressor ; In Vitro Techniques ; Mice ; Protein-Lysine 6-Oxidase/*physiology ; RNA, Messenger/genetics
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    Direct molecular identification of the mouse pink-eyed unstable mutation by genome scanning (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-04-26
    Description: DNA sequences associated with the mouse pink-eyed unstable mutation were identified in the absence of closely linked molecular markers and without prior knowledge of the encoded gene product. This was accomplished by "genome scanning," a technique in which high-resolution Southern blots of genomic DNAs were hybridized to a dispersed and moderately repetitive DNA sequence. In this assay, pink-eyed unstable DNA was distinguished from the DNA of wild-type and revertant mice by enhanced hybridization to one of several hundred resolved fragments. The fragment showing enhanced hybridization in pink-eyed unstable DNA was cloned and found to lie within a DNA duplication that is located close to, or within, the pink-eyed dilution locus. The duplication associated with the mouse pink-eyed unstable mutation may mediate the high reversion frequency characteristic of this mutation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brilliant, M H -- Gondo, Y -- Eicher, E M -- CA06927/CA/NCI NIH HHS/ -- GM43840/GM/NIGMS NIH HHS/ -- RR05529/RR/NCRR NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1991 Apr 26;252(5005):566-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Cancer Research, Fox Chase Cancer Center, Philadelphia, PA 19111.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1673574" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Blotting, Southern/methods ; DNA/genetics/isolation & purification ; Eye Color/*genetics ; *Genes ; Homozygote ; Mice ; Mice, Inbred C57BL ; Mice, Mutant Strains ; *Mutation ; Restriction Mapping ; Tyrosine 3-Monooxygenase/genetics
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Hints emerge from the Gallo Probe (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-08-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hamilton, D P -- New York, N.Y. -- Science. 1991 Aug 16;253(5021):728-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1876829" target="_blank"〉PubMed〈/a〉
    Keywords: Hiv-1 ; History, 20th Century ; National Institutes of Health (U.S.) ; Patents as Topic ; *Scientific Misconduct ; United States
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    Linkage of faulty major histocompatibility complex class I to autoimmune diabetes (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-12-20
    Description: Pancreatic islet cells are the targets of an autoimmune response in type I diabetes. In the nonobese diabetic (NOD) mouse model of autoimmune diabetes, expression of major histocompatibility complex (MHC) class I proteins was inversely correlated with diabetes; in this mouse a mutation in the MHC class II-linked gene for the putative MHC class I peptide transporter was also present. Mice deficient in MHC class I expression because they do not produce beta 2-microglobulin also developed late onset autoimmune diabetes. In cells from humans with type I diabetes expression of MHC class I was decreased; subsets of prediabetics categorized as most likely to become hyperglycemic also had low MHC class I. T cell responses to self antigens are faulty in diabetics. In sets of genetically identical twins that are discordant for diabetes, the defect appeared to reside with the antigen presenting cell. Thus, a lack of surface MHC class I protein is associated with autoimmune diabetes; the concomitant defect in antigen presentation may impair the development of self tolerance, which could result in autoimmune disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Faustman, D -- Li, X P -- Lin, H Y -- Fu, Y E -- Eisenbarth, G -- Avruch, J -- Guo, J -- New York, N.Y. -- Science. 1991 Dec 20;254(5039):1756-61.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Harvard Medical School, Massachusetts General Hospital, Charlestown 02129.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1763324" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autoimmune Diseases/*genetics ; Cytotoxicity, Immunologic ; Diabetes Mellitus, Type 1/genetics/*immunology ; Diseases in Twins ; Flow Cytometry ; Gene Expression ; *Genes, MHC Class I ; Humans ; *Lymphocyte Activation ; Lymphocytes/*immunology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Inbred NOD ; Prediabetic State/genetics/immunology ; Spleen/immunology ; T-Lymphocytes/immunology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Putting AIDS research in perspective (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-03-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Palca, J -- New York, N.Y. -- Science. 1991 Mar 8;251(4998):1172.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2006406" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/*economics ; Behavioral Research ; *Biomedical Research ; Federal Government ; Humans ; National Institutes of Health (U.S.) ; *Research Support as Topic ; *Resource Allocation ; United States
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    How peptide hormones get ready for work (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-05-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J -- New York, N.Y. -- Science. 1991 May 10;252(5007):779-80.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1674172" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Gene Expression Regulation, Enzymologic ; Hormones/*metabolism ; Mice ; Neurotransmitter Agents/metabolism ; Pro-Opiomelanocortin/metabolism ; Proprotein Convertase 2 ; Proprotein Convertases ; Protein Precursors/metabolism ; *Protein-Tyrosine Kinases ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins c-fes ; Serine Endopeptidases/*physiology
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    Function of the homeodomain protein GHF1 in pituitary cell proliferation (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-07-12
    Description: Mutations that cause pituitary dwarfism in the mouse reside in the gene encoding the transcription factor growth hormone factor 1 (GHF1 or pit1). These dwarf mice (dw and dwJ) are deficient in growth hormone (GH) and prolactin (PRL) synthesis and exhibit pituitary hypoplasia, suggesting a stem cell defect. With antisense oligonucleotide technology, a cell culture model of this genetic defect was developed. Specific inhibition of GHF1 synthesis by complementary oligonucleotides led to a marked decrease in GH and PRL expression and to a marked decrease in proliferation of somatotrophic cell lines. These results provide direct evidence that the homeodomain protein GHF1 is required not only for the establishment and maintenance of the differentiated phenotype but for cell proliferation as well.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Castrillo, J L -- Theill, L E -- Karin, M -- DK38527/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1991 Jul 12;253(5016):197-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, School of Medicine, University of California, San Diego, La Jolla 92093.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1677216" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antisense Elements (Genetics) ; Base Sequence ; *Cell Division ; Cells, Cultured ; DNA/biosynthesis ; DNA-Binding Proteins/*physiology ; Dwarfism/genetics ; Gene Expression Regulation ; *Genes, Homeobox ; Growth Hormone/genetics ; In Vitro Techniques ; Mice ; Molecular Sequence Data ; Pituitary Gland/*cytology/physiology ; Prolactin/genetics ; Transcription Factor Pit-1 ; Transcription Factors/*physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    ACh receptor-rich membrane domains organized in fibroblasts by recombinant 43-kildalton protein (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-02-01
    Description: Neurotransmitter receptors are generally clustered in the postsynaptic membrane. The mechanism of clustering was analyzed with fibroblast cell lines that were stably transfected with the four subunits for fetal (alpha, beta, gamma, delta) or adult (alpha, beta, epsilon, delta) type mouse muscle nicotinic acetylcholine receptors (AChRs). Immunofluorescent staining indicated that AChRs were dispersed on the surface of these cells. When transiently transfected with an expression construct encoding a 43-kilodalton protein that is normally concentrated under the postsynaptic membrane, AChRs expressed in these cells became aggregated in large cell-surface clusters, colocalized with the 43-kilodalton protein. This suggests that 43-kilodalton protein can induce AChR clustering and that cluster induction involves direct contact between AChR and 43-kilodalton protein.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Phillips, W D -- Kopta, C -- Blount, P -- Gardner, P D -- Steinbach, J H -- Merlie, J P -- R01 NS022356/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1991 Feb 1;251(4993):568-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, Washington University School of Medicine, St. Louis, MO 63110.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1703661" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcholine/pharmacology ; Animals ; Cell Membrane/physiology ; Fetus ; Fibroblasts/cytology/physiology ; Fluorescent Antibody Technique ; Ion Channels/drug effects/physiology ; Macromolecular Substances ; Mice ; Molecular Weight ; Muscles/physiology ; Receptors, Nicotinic/analysis/genetics/*physiology ; Recombinant Proteins/analysis/metabolism ; Transfection
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    Protection against malaria by vaccination with sporozoite surface protein 2 plus CS protein (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-05-03
    Description: The circumsporozoite (CS) protein has been the target for development of malaria sporozoite vaccines for a decade. However, immunization with subunit vaccines based on the CS protein has never given the complete protection found after immunization with irradiated sporozoites. BALB/c mice immunized with irradiated Plasmodium yoelii sporozoites produced antibodies and cytotoxic T cells against a 140-kilodalton protein, sporozoite surface protein 2 (SSP2). Mice immunized with P815 cells that had been transfected with either SSP2 or CS genes were partially protected, and those immunized with a mixture of SSP2 and CS transfectants were completely protected against malaria. These studies emphasize the importance of vaccine delivery systems in achieving protection and define a multi-antigen sporozoite vaccine.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Khusmith, S -- Charoenvit, Y -- Kumar, S -- Sedegah, M -- Beaudoin, R L -- Hoffman, S L -- New York, N.Y. -- Science. 1991 May 3;252(5006):715-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Malaria Program, Naval Medical Research Institute, Bethesda, MD 20889.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1827210" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/immunology ; Antibodies, Protozoan/immunology ; Antigens, Protozoan/genetics/*immunology ; Immunization ; Malaria/*prevention & control ; Mice ; Mice, Inbred BALB C ; Molecular Weight ; Plasmodium yoelii/*immunology ; Protozoan Proteins/genetics/*immunology ; *Protozoan Vaccines ; T-Lymphocytes, Cytotoxic/immunology ; T-Lymphocytes, Helper-Inducer/immunology ; T-Lymphocytes, Regulatory/immunology ; Transfection ; *Vaccination
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    In vitro and in vivo consequences of VLA-2 expression on rhabdomyosarcoma cells (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-03-29
    Description: Cloned integrin alpha 2 subunit complementary DNA was expressed on human rhabdomyosarcoma (RD) cells to give a functional VLA-2 (alpha 2 beta 1) adhesion receptor. The VLA-2-positive RDA2 cells not only showed increased adhesion to collagen and laminin in vitro, but also formed substantially more metastatic tumor colonies in nude mice after either intravenous or subcutaneous injection. These results show that a specific adhesion receptor (VLA-2) can markedly enhance both experimental and spontaneous metastasis. In contrast to the metastasis results, there was no difference in either the in vitro growth rate or apparent in vivo tumorigenicity of RD and RDA2 cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chan, B M -- Matsuura, N -- Takada, Y -- Zetter, B R -- Hemler, M E -- CA 37393/CA/NCI NIH HHS/ -- GM 38903/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1991 Mar 29;251(5001):1600-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2011740" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Adhesion ; Cell Line ; Collagen ; Fibronectins ; Humans ; Kinetics ; Laminin ; Lung Neoplasms/pathology/secondary ; Mice ; Mice, Nude ; Neoplasm Metastasis ; Neoplasm Transplantation ; Receptors, Very Late Antigen/genetics/*physiology ; Rhabdomyosarcoma/*pathology ; Transplantation, Heterologous
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    Overhead costs (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-05-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉New York, N.Y. -- Science. 1991 May 24;252(5009):1046.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2031175" target="_blank"〉PubMed〈/a〉
    Keywords: Costs and Cost Analysis ; National Institutes of Health (U.S.) ; *Research Support as Topic ; United States
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    Deregulation of a homeobox gene, HOX11, by the t(10;14) in T cell leukemia (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-07-05
    Description: Molecular cloning of the t(10;14)(q24;q11) recurrent breakpoint of T cell acute lymphoblastic leukemia has demonstrated a transcript for the candidate gene TCL3. Characterization of this gene from chromosome segment 10q24 revealed it to be a new homeobox, HOX11. The HOX11 homeodomain is most similar to that of the murine gene Hlx and possesses a markedly glycine-rich variable region and an acidic carboxyl terminus. HOX11, while expressed in liver, was not detected in normal thymus or T cells. This lineage-restricted homeobox gene is deregulated upon translocation into the T cell receptor locus where it may act as an oncogene.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hatano, M -- Roberts, C W -- Minden, M -- Crist, W M -- Korsmeyer, S J -- 1 PO1 CA49712/CA/NCI NIH HHS/ -- CA 21765/CA/NCI NIH HHS/ -- CA 30969/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1991 Jul 5;253(5015):79-82.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Washington University School of Medicine, St. Louis, MO 63110.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1676542" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Blotting, Northern ; Chromosomes, Human, Pair 10 ; Chromosomes, Human, Pair 14 ; Cloning, Molecular ; *Gene Expression Regulation, Neoplastic ; *Genes, Homeobox ; Humans ; Leukemia-Lymphoma, Adult T-Cell/*genetics ; Mice ; Molecular Sequence Data ; Receptors, Antigen, T-Cell/genetics ; Restriction Mapping ; Sequence Homology, Nucleic Acid ; *Translocation, Genetic
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Recognition of self antigens by skin-derived T cells with invariant gamma delta antigen receptors (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-06-07
    Description: Thy-1+ dendritic epidermal T cells (dECs) express invariant gamma delta antigen receptors and are found in intimate contact with keratinocytes in murine epidermis--thus raising the possibility that keratinocytes express a ligand for the antigen receptor of these T cells. Thy-1+ dECs were stimulated to produce lymphokines by interaction with keratinocytes in vitro. This stimulation was mediated through the dEC antigen receptor and did not appear to be restricted by the major histocompatibility complex. Thus, dECs can recognize self antigens and may participate in immune surveillance for cellular damage rather than for foreign antigens.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Havran, W L -- Chien, Y H -- Allison, J P -- AI26942/AI/NIAID NIH HHS/ -- CA40041/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1991 Jun 7;252(5011):1430-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cell Biology, University of California, Berkeley 94720.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1828619" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autoantigens/*immunology ; Cell Line ; Dendrites/immunology ; Epidermis ; *Immunity, Cellular ; In Vitro Techniques ; Interleukin-2/secretion ; Keratinocytes/physiology ; Mice ; Mice, Inbred BALB C ; Receptors, Antigen, T-Cell/*physiology ; Receptors, Antigen, T-Cell, gamma-delta ; T-Lymphocytes/*immunology
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    The best of times, the worst of times (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-06-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koshland, D E Jr -- New York, N.Y. -- Science. 1991 May 31;252(5010):1229.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1925529" target="_blank"〉PubMed〈/a〉
    Keywords: National Institutes of Health (U.S.) ; Research Support as Topic/*trends ; *Science ; United States
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    Carcinogens and human health: Part 2 (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-01-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rall, D P -- New York, N.Y. -- Science. 1991 Jan 4;251(4989):10-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1986406" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carcinogenicity Tests/standards ; Carcinogens/*toxicity ; Humans ; National Institutes of Health (U.S.) ; Neoplasms/*chemically induced ; *Toxicology ; United States
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Expression cDNA cloning of the KGF receptor by creation of a transforming autocrine loop (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-01-04
    Description: An expression cloning strategy was devised to isolate the keratinocyte growth factor (KGF) receptor complementary DNA. NIH/3T3 fibroblasts, which secrete this epithelial cell-specific mitogen, were transfected with a keratinocyte expression complementary DNA library. Among several transformed foci identified, one demonstrated the acquisition of specific high-affinity KGF binding sites. The pattern of binding competition by related fibroblast growth factors (FGFs) indicated that this receptor had high affinity for acidic FGF as well as KGF. The rescued 4.2-kilobase complementary DNA was shown to encode a predicted membrane-spanning tyrosine kinase related to but distinct from the basic FGF receptor. This expression cloning approach may be generally applicable to the isolation of genes that constitute limiting steps in mitogenic signaling pathways.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miki, T -- Fleming, T P -- Bottaro, D P -- Rubin, J S -- Ron, D -- Aaronson, S A -- New York, N.Y. -- Science. 1991 Jan 4;251(4989):72-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Cellular and Molecular Biology, National Cancer Institute, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1846048" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Binding, Competitive ; Cell Line ; *Cloning, Molecular ; DNA/*genetics ; Fibroblast Growth Factor 10 ; Fibroblast Growth Factor 7 ; Fibroblast Growth Factors/metabolism ; Fibroblasts/metabolism ; *Gene Expression ; Growth Substances/metabolism ; Mice ; Molecular Sequence Data ; Nucleic Acid Hybridization ; Plasmids ; Receptor, Fibroblast Growth Factor, Type 2 ; Receptors, Cell Surface/*genetics/metabolism ; *Receptors, Fibroblast Growth Factor ; Recombinant Proteins/metabolism ; Transfection ; Transformation, Genetic
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    Requirement of heparan sulfate for bFGF-mediated fibroblast growth and myoblast differentiation (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-06-21
    Description: Basic fibroblast growth factor (bFGF) binds to heparan sulfate proteoglycans at the cell surface and to receptors with tyrosine kinase activity. Prevention of binding between cell surface heparan sulfate and bFGF (i) substantially reduces binding of fibroblast growth factor to its cell-surface receptors, (ii) blocks the ability of bFGF to support the growth of Swiss 3T3 fibroblasts, and (iii) induces terminal differentiation of MM14 skeletal muscle cells, which is normally repressed by fibroblast growth factor. These results indicate that cell surface heparan sulfate is directly involved in bFGF cell signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rapraeger, A C -- Krufka, A -- Olwin, B B -- 5T32H007118/PHS HHS/ -- AR39467/AR/NIAMS NIH HHS/ -- HD21881/HD/NICHD NIH HHS/ -- R01 AR039467/AR/NIAMS NIH HHS/ -- R01 HD021881/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1991 Jun 21;252(5013):1705-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, University of Wisconsin, Madison 53706.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1646484" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cell Division ; Cell Line ; Chlorates/pharmacology ; Fibroblast Growth Factor 2/*metabolism ; Fibroblasts/*cytology ; Heparitin Sulfate/*physiology ; In Vitro Techniques ; Mice ; Muscles/*cytology ; Polysaccharide-Lyases/pharmacology ; Protein Binding ; Receptors, Cell Surface/metabolism ; Structure-Activity Relationship
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Science funding (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-04-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉New York, N.Y. -- Science. 1991 Apr 26;252(5005):490-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2020847" target="_blank"〉PubMed〈/a〉
    Keywords: Government Agencies ; National Institutes of Health (U.S.) ; *Research Support as Topic ; United States
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Generation of cAMP-activated chloride currents by expression of CFTR (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-02-08
    Description: Mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) cause cystic fibrosis. In order to evaluate its function, CFTR was expressed in HeLa, Chinese hamster ovary (CHO), and NIH 3T3 fibroblast cells, and anion permeability was assessed with a fluorescence microscopic assay and the whole-cell patch-clamp technique. Adenosine 3',5'-monophosphate (cAMP) increased anion permeability and chloride currents in cells expressing CFTR, but not in cells expressing a mutant CFTR (delta F508) or in nontransfected cells. The simplest interpretation of these observations is that CFTR is itself a cAMP-activated chloride channel. The alternative interpretation, that CFTR directly or indirectly regulates chloride channels, requires that these cells have endogenous cryptic, chloride channels that are stimulated by cAMP only in the presence of CFTR.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Anderson, M P -- Rich, D P -- Gregory, R J -- Smith, A E -- Welsh, M J -- New York, N.Y. -- Science. 1991 Feb 8;251(4994):679-82.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Internal Medicine, University of Iowa College of Medicine, Iowa City 52242.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1704151" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Chloride Channels ; Chlorides/*metabolism ; Cricetinae ; Cyclic AMP/*physiology ; Cystic Fibrosis Transmembrane Conductance Regulator ; Humans ; Membrane Proteins/*metabolism/*physiology ; Mice ; Mutation ; Recombinant Proteins ; Structure-Activity Relationship
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Putting new muscle into gene therapy (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-12-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hoffman, M -- New York, N.Y. -- Science. 1991 Dec 6;254(5037):1455-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1962203" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Genetic Therapy/*methods ; Growth Hormone/administration & dosage ; Mice ; Muscles/*cytology/secretion ; Recombinant Proteins/administration & dosage
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Another sex survey bites the dust (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-09-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Moffat, A S -- New York, N.Y. -- Science. 1991 Sep 27;253(5027):1483.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1896855" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/prevention & control ; Adolescent ; Adult ; Female ; *Health Surveys ; Humans ; Male ; National Institutes of Health (U.S.) ; *Sexual Behavior ; Sexually Transmitted Diseases/prevention & control ; United States
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    A layer by layer look at the skin blister disease (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-11-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hoffman, M -- New York, N.Y. -- Science. 1991 Nov 22;254(5035):1111-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1720260" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Collagen/physiology ; Epidermis/*physiology ; Epidermolysis Bullosa/*physiopathology ; Humans ; Keratins/*physiology ; Mice ; Mice, Transgenic
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    AIDS vaccine meeting: international trials soon (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-11-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, J -- New York, N.Y. -- Science. 1991 Nov 1;254(5032):647.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1948042" target="_blank"〉PubMed〈/a〉
    Keywords: *AIDS Vaccines ; Acquired Immunodeficiency Syndrome/prevention & control ; Animals ; Clinical Trials as Topic ; Humans ; National Institutes of Health (U.S.) ; United States
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    OSTP to wade into gene patent quagmire (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-11-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roberts, L -- New York, N.Y. -- Science. 1991 Nov 22;254(5035):1104-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1957160" target="_blank"〉PubMed〈/a〉
    Keywords: Biotechnology ; *Dna ; *Human Genome Project ; Humans ; National Institutes of Health (U.S.) ; *Patents as Topic ; United States
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Maintenance of normoglycemia in diabetic mice by subcutaneous xenografts of encapsulated islets (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-12-20
    Description: The goal of islet transplantation in human diabetes is to maintain the islet grafts in the recipients without the use of immunosuppression. One approach is to encapsulate the donor islets in permselective membranes. Hollow fibers fabricated from an acrylic copolymer were used to encapsulate small numbers of rat islets that were immobilized in an alginate hydrogel for transplantation in diabetic mice. The fibers were biocompatible, prevented rejection, and maintained normoglycemia when transplanted intraperitoneally; hyperglycemia returned when the fibers were removed at 60 days. Normoglycemia was also maintained by subcutaneous implants that had an appropriately constructed outer surface on the fibers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lacy, P E -- Hegre, O D -- Gerasimidi-Vazeou, A -- Gentile, F T -- Dionne, K E -- DK01226/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1991 Dec 20;254(5039):1782-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Washington University School of Medicine, St. Louis, MO 63110.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1763328" target="_blank"〉PubMed〈/a〉
    Keywords: *Acrylic Resins ; Animals ; Animals, Newborn ; Blood Glucose/*metabolism ; Diabetes Mellitus, Experimental/blood/*surgery ; In Vitro Techniques ; Insulin/secretion ; Islets of Langerhans/*secretion ; Islets of Langerhans Transplantation/*physiology ; Male ; Membranes, Artificial ; Mice ; Mice, Inbred C57BL ; *Polyvinyl Chloride ; Rats ; Rats, Inbred WF ; Time Factors ; Transplantation, Heterologous
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    Phosphorylation of c-Src on tyrosine 527 by another protein tyrosine kinase (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-10-25
    Description: The protein tyrosine kinase activity of the cellular Src protein is negatively regulated by phosphorylation at tyrosine residue 527 (Tyr527). It has not been established whether this regulatory modification of Src is mediated by autophosphorylation or by another cellular protein kinase. The phosphorylation of a modified form of c-Src that lacks kinase activity was examined in mouse cells that do not express endogenous Src (because of the targeted disruption of both src alleles). Phosphorylation of the inactive form of Src on Tyr527 occurred to a similar extent in cells lacking endogenous Src as it did in cells expressing Src. Therefore, Tyr527 phosphorylation, and thus negative control of Src kinase activity, is mediated by another cellular protein tyrosine kinase.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thomas, J E -- Soriano, P -- Brugge, J S -- New York, N.Y. -- Science. 1991 Oct 25;254(5031):568-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Microbiology, University of Pennsylvania, School of Medicine, Philadelphia 19104.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1719633" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cells, Cultured ; Cyanogen Bromide ; Embryo, Mammalian ; Mice ; Peptide Mapping ; Phosphopeptides/isolation & purification ; Phosphorylation ; Protein-Tyrosine Kinases ; Proto-Oncogene Proteins pp60(c-src)/*metabolism ; *Tyrosine
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    Gene trees and the origins of inbred strains of mice (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-10-25
    Description: Extensive data on genetic divergence among 24 inbred strains of mice provide an opportunity to examine the concordance of gene trees and species trees, especially whether structured subsamples of loci give congruent estimates of phylogenetic relationships. Phylogenetic analyses of 144 separate loci reproduce almost exactly the known genealogical relationships among these 24 strains. Partitioning these loci into structured subsets representing loci coding for proteins, the immune system and endogenous viruses give incongruent phylogenetic results. The gene tree based on protein loci provides an accurate picture of the genealogical relationships among strains; however, gene trees based upon immune and viral data show significant deviations from known genealogical affinities.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Atchley, W R -- Fitch, W M -- GM-45344/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1991 Oct 25;254(5031):554-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, North Carolina State University, Raleigh 27695.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1948030" target="_blank"〉PubMed〈/a〉
    Keywords: Algorithms ; Alleles ; Analysis of Variance ; Animals ; Genes, Immunoglobulin ; Genotype ; Mice ; Mice, Inbred Strains/*genetics ; *Phylogeny ; Probability ; Proteins/genetics
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    France set to reopen AIDS pact? (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-09-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Coles, P -- New York, N.Y. -- Science. 1991 Sep 27;253(5027):1479.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1896853" target="_blank"〉PubMed〈/a〉
    Keywords: *Acquired Immunodeficiency Syndrome ; France ; HIV/isolation & purification ; Humans ; National Institutes of Health (U.S.) ; *Publishing ; Scientific Misconduct ; United States
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    Report card on the genome project (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-07-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roberts, L -- New York, N.Y. -- Science. 1991 Jul 26;253(5018):376.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1862337" target="_blank"〉PubMed〈/a〉
    Keywords: Chromosome Mapping ; Chromosomes, Human, Pair 19 ; *Human Genome Project ; Humans ; National Institutes of Health (U.S.) ; United States ; Universities
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    Whom do yew trust? (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-06-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Langreth, R -- New York, N.Y. -- Science. 1991 Jun 28;252(5014):1780.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1676541" target="_blank"〉PubMed〈/a〉
    Keywords: Alkaloids/*isolation & purification/therapeutic use ; Antineoplastic Agents, Phytogenic/*isolation & purification ; Environment ; Female ; Humans ; National Institutes of Health (U.S.) ; Neoplasms/*drug therapy ; Oregon ; Ovarian Neoplasms/drug therapy ; Paclitaxel ; Trees ; United States
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    Hughes investigators rile NIH peer reviewers (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-11-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gibbons, A -- New York, N.Y. -- Science. 1991 Nov 15;254(5034):933.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1948077" target="_blank"〉PubMed〈/a〉
    Keywords: Foundations ; National Institutes of Health (U.S.) ; *Research Support as Topic ; United States
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    Human immunodeficiency virus infection of human-PBL-SCID mice (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-02-15
    Description: Severe combined immunodeficient (SCID) mice reconstituted with human peripheral blood leukocytes (hu-PBL-SCID mice) have inducible human immune function and may be useful as a small animal model for acquired immunodeficiency syndrome (AIDS) research. Hu-PBL-SCID mice infected with human immunodeficiency virus-1 (HIV-1) contained virus that was recoverable by culture from the peritoneal cavity, spleen, peripheral blood, and lymph nodes for up to 16 weeks after infection; viral sequences were also detected by in situ hybridization and by amplification with the polymerase chain reaction (PCR). Mice could be infected with multiple strains of HIV-1, including LAV-1/Bru, IIIB, MN, SF2, and SF13. HIV-1 infection affected the concentration of human immunoglobulin and the number of CD4+ T cells in the mice. These results support the use of the hu-PBL-SCID mouse for studies of the pathogenesis and treatment of AIDS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mosier, D E -- Gulizia, R J -- Baird, S M -- Wilson, D B -- Spector, D H -- Spector, S A -- AI-27703/AI/NIAID NIH HHS/ -- AI-29182/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1991 Feb 15;251(4995):791-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Immunology, Medical Biology Institute, La Jolla, CA 92037.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1990441" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Transfusion ; Chimera/*immunology ; *Disease Models, Animal ; *HIV Infections/immunology ; *HIV-1/isolation & purification ; Humans ; Immunologic Deficiency Syndromes/genetics/*immunology ; Lymphocyte Transfusion ; Mice ; Mice, Mutant Strains/*immunology ; Spleen/microbiology
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    LBL genome center to try leadership by committee (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-04-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roberts, L -- New York, N.Y. -- Science. 1991 Apr 26;252(5005):500-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2020850" target="_blank"〉PubMed〈/a〉
    Keywords: California ; Human Genome Project/*organization & administration ; Humans ; National Institutes of Health (U.S.) ; United States
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    DOE's genome project comes of age (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-04-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roberts, L -- New York, N.Y. -- Science. 1991 Apr 26;252(5005):498-501.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2020849" target="_blank"〉PubMed〈/a〉
    Keywords: Government Agencies ; Human Genome Project/*organization & administration ; Humans ; National Institutes of Health (U.S.) ; 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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    Antibody-mediated clearance of alphavirus infection from neurons (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-11-08
    Description: Humoral immunity is important for protection against viral infection and neutralization of extracellular virus, but clearance of virus from infected tissues is thought to be mediated solely by cellular immunity. However, in a SCID mouse model of persistent alphavirus encephalomyelitis, adoptive transfer of hyperimmune serum resulted in clearance of infectious virus and viral RNA from the nervous system, whereas adoptive transfer of sensitized T lymphocytes had no effect on viral replication. Three monoclonal antibodies to two different epitopes on the E2 envelope glycoprotein mediated viral clearance. Treatment of alphavirus-infected primary cultured rat neurons with these monoclonal antibodies to E2 resulted in decreased viral protein synthesis, followed by gradual termination of mature infectious virion production. Thus, antibody can mediate clearance of alphavirus infection from neurons by restricting viral gene expression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Levine, B -- Hardwick, J M -- Trapp, B D -- Crawford, T O -- Bollinger, R C -- Griffin, D E -- NS29234/NS/NINDS NIH HHS/ -- T32-NS-07000/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1991 Nov 8;254(5033):856-60.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1658936" target="_blank"〉PubMed〈/a〉
    Keywords: Alphavirus/immunology/isolation & purification/*physiology ; Animals ; Antibodies, Monoclonal/*therapeutic use ; Central Nervous System/immunology/*microbiology ; Encephalomyelitis/*immunology/microbiology/therapy ; *Immunotherapy, Adoptive ; Mice ; Mice, Inbred Strains ; Mice, SCID ; Neurons/immunology/*microbiology ; RNA, Viral/isolation & purification ; T-Lymphocytes/*immunology ; Togaviridae Infections/*immunology/therapy ; Virus Replication
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  • 81
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    The Gallo factor: questions remain (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-08-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rubinstein, E -- New York, N.Y. -- Science. 1991 Aug 16;253(5021):732.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1876831" target="_blank"〉PubMed〈/a〉
    Keywords: Hiv-1 ; History, 20th Century ; National Institutes of Health (U.S.) ; *Scientific Misconduct ; United States
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  • 82
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    CCAAT-enhancer binding protein: a component of a differentiation switch (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-01-18
    Description: The CCAAT-enhancer binding protein (C/EBP) has now been found to promote the terminal differentiation of adipocytes. During the normal course of adipogenesis, C/EBP expression is restricted to a terminal phase wherein proliferative growth is arrested, and specialized cell phenotype is first manifested. A conditional form of C/EBP was developed, making it feasible to test its capacity to regulate the differentiation of cultured adipocytes. Premature expression of C/EBP in adipoblasts caused a direct cessation of mitotic growth. Moreover, when abetted by the effects of three adipogenic hormones, C/EBP promoted terminal cell differentiation. Since C/EBP is expressed in a variety of tissues, it may have a fundamental role in regulating the balance between cell growth and differentiation in higher animals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Umek, R M -- Friedman, A D -- McKnight, S L -- New York, N.Y. -- Science. 1991 Jan 18;251(4991):288-92.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Research Laboratories, Department of Embryology, Carnegic Institution of Washington, Baltimore, MD 21210.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1987644" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue/*cytology ; Animals ; CCAAT-Enhancer-Binding Proteins ; *Cell Differentiation ; Cell Division ; DNA-Binding Proteins/*physiology ; Gene Expression Regulation ; L Cells (Cell Line) ; Mice ; Nuclear Proteins/*physiology ; Receptors, Steroid/physiology ; Regulatory Sequences, Nucleic Acid ; Structure-Activity Relationship
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  • 83
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    Cystic fibrosis research (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-02-01
    Description: In Virginia Morell's Research News article "New light on writing in the Americas" (18 Jan., p. 268), the illustrations on page 268 should have been credited to George Stuart of the National Geographic Society.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gorden, P -- New York, N.Y. -- Science. 1991 Feb 1;251(4993):500.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1990423" target="_blank"〉PubMed〈/a〉
    Keywords: *Cystic Fibrosis ; Humans ; National Institutes of Health (U.S.) ; *Research ; United States
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  • 84
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    Increased osteoclast development after estrogen loss: mediation by interleukin-6 (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-07-03
    Description: Osteoclasts, the cells that resorb bone, develop from hematopoietic precursors of the bone marrow under the control of factors produced in their microenvironment. The cytokine interleukin-6 can promote hematopoiesis and osteoclastogenesis. Interleukin-6 production by bone and marrow stromal cells is suppressed by 17 beta-estradiol in vitro. In mice, estrogen loss (ovariectomy) increased the number of colony-forming units for granulocytes and macrophages, enhanced osteoclast development in ex vivo cultures of marrow, and increased the number of osteoclasts in trabecular bone. These changes were prevented by 17 beta-estradiol or an antibody to interleukin-6. Thus, estrogen loss results in an interleukin-6-mediated stimulation of osteoclastogenesis, which suggests a mechanism for the increased bone resorption in postmenopausal osteoporosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jilka, R L -- Hangoc, G -- Girasole, G -- Passeri, G -- Williams, D C -- Abrams, J S -- Boyce, B -- Broxmeyer, H -- Manolagas, S C -- AI21761/AI/NIAID NIH HHS/ -- AR41313/AR/NIAMS NIH HHS/ -- CA36464/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1992 Jul 3;257(5066):88-91.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Veterans Affairs Medical Center, Indiana University School of Medicine, Indianapolis 46202.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1621100" target="_blank"〉PubMed〈/a〉
    Keywords: Analysis of Variance ; Animals ; Antibodies, Monoclonal ; Bone Marrow Cells ; Cells, Cultured ; Estradiol/*pharmacology ; Female ; Granulocyte-Macrophage Colony-Stimulating Factor/pharmacology ; Immunoglobulin G ; Interleukin-6/immunology/*physiology ; Mice ; Osteoclasts/*cytology/drug effects ; *Ovariectomy ; Recombinant Proteins/pharmacology ; Spleen/cytology ; Stem Cells/cytology/drug effects
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    AIDS vaccines. Testing target date looms, but will the vaccines be ready? (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-09-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Palca, J -- New York, N.Y. -- Science. 1992 Sep 11;257(5076):1472-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1523403" target="_blank"〉PubMed〈/a〉
    Keywords: *AIDS Vaccines ; Acquired Immunodeficiency Syndrome/immunology/*prevention & control ; HIV/immunology ; Humans ; National Institutes of Health (U.S.) ; Recombinant Proteins ; Safety ; United States ; Vaccines, Synthetic
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  • 86
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    Minority health. NIH spells out plans for a $45 million initiative (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-04-03
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Palca, J -- New York, N.Y. -- Science. 1992 Apr 3;256(5053):24.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1566053" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Child ; Female ; *Health Promotion ; Humans ; Infant ; Infant Mortality ; Male ; Middle Aged ; *Minority Groups ; National Institutes of Health (U.S.) ; *Research Support as Topic ; United States
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    Exaggerated carcinogenicity of chemicals (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-06-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Abelson, P H -- New York, N.Y. -- Science. 1992 Jun 19;256(5064):1609.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1609271" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Butadienes/*toxicity ; *Carcinogenicity Tests ; Haplorhini ; Humans ; Mice ; Neoplasms/*chemically induced ; Rats ; Risk
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  • 88
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    The genome project: life after Watson (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-05-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Palca, J -- New York, N.Y. -- Science. 1992 May 15;256(5059):956-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1589774" target="_blank"〉PubMed〈/a〉
    Keywords: Chromosome Mapping ; History, 20th Century ; Human Genome Project/economics/*organization & administration ; National Institutes of Health (U.S.) ; Research Support as Topic ; United States
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  • 89
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    Repression of the insulin-like growth factor II gene by the Wilms tumor suppressor WT1 (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-07-31
    Description: The Wilms tumor suppressor gene wt1 encodes a zinc finger DNA binding protein, WT1, that functions as a transcriptional repressor. The fetal mitogen insulin-like growth factor II (IGF-II) is overexpressed in Wilms tumors and may have autocrine effects in tumor progression. The major fetal IGF-II promoter was defined in transient transfection assays as a region spanning from nucleotides -295 to +135, relative to the transcription start site. WT1 bound to multiple sites in this region and functioned as a potent repressor of IGF-II transcription in vivo. Maximal repression was dependent on the presence of WT1 binding sites on each side of the transcriptional initiation site. These findings provide a molecular basis for overexpression of IGF-II in Wilms tumors and suggest that WT1 negatively regulates blastemal cell proliferation by limiting the production of a fetal growth factor in the developing vertebrate kidney.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Drummond, I A -- Madden, S L -- Rohwer-Nutter, P -- Bell, G I -- Sukhatme, V P -- Rauscher, F J 3rd -- CA 10817/CA/NCI NIH HHS/ -- CA 47983/CA/NCI NIH HHS/ -- CA 52009/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1992 Jul 31;257(5070):674-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, University of Chicago, IL 60637.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1323141" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Binding Sites ; Blotting, Northern ; DNA/chemistry/metabolism ; DNA-Binding Proteins/*metabolism ; Deoxyribonuclease I/metabolism ; *Gene Expression Regulation, Neoplastic ; Genes, Wilms Tumor/*physiology ; Humans ; Insulin-Like Growth Factor II/*genetics ; Kidney/embryology/metabolism ; Mice ; Molecular Sequence Data ; Promoter Regions, Genetic ; Rats ; Sequence Homology, Nucleic Acid ; Transfection ; WT1 Proteins ; Wilms Tumor/genetics/metabolism ; Zinc Fingers
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  • 90
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    Enhanced degradation of the ferritin repressor protein during induction of ferritin messenger RNA translation (1992)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1992-05-01
    Description: Induction of ferritin synthesis in cultured cells by heme or iron is accompanied by degradation of the ferritin repressor protein (FRP). Intermediates in the degradative pathway apparently include FRP covalently linked in larger aggregates. The effect of iron on FRP degradation is enhanced by porphyrin precursors but is decreased by inhibitors of porphyrin synthesis, which implies that heme is an active agent. These results suggest that translational induction in this system may be caused by enhanced repressor degradation. While unique among translational regulatory systems, this process is common to a variety of other biosynthetic control mechanisms.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Goessling, L S -- Daniels-McQueen, S -- Bhattacharyya-Pakrasi, M -- Lin, J J -- Thach, R E -- AI 20484/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1992 May 1;256(5057):670-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Washington University, St. Louis, MO 63130.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1316633" target="_blank"〉PubMed〈/a〉
    Keywords: 5-Aminolevulinate Synthetase/genetics ; Aminolevulinic Acid/pharmacology ; Animals ; Cell Line ; Cell Line, Transformed ; Ferritins/biosynthesis/*genetics ; Fibroblasts/metabolism ; Iron/pharmacology ; Iron Regulatory Protein 1 ; Iron-Regulatory Proteins ; Mice ; Papillomaviridae ; Porphobilinogen/pharmacology ; *Protein Biosynthesis ; RNA, Messenger/*genetics ; RNA-Binding Proteins/*metabolism ; Rabbits
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  • 91
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    Activation of mitogen-activated protein kinase kinase by v-Raf in NIH 3T3 cells and in vitro (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-09-04
    Description: Mitogen-activated protein (MAP) kinases are 42- and 44-kD serine-threonine protein kinases that are activated by tyrosine and threonine phosphorylation in cells stimulated with mitogens and growth factors. MAP kinase and the protein kinase that activates it (MAP kinase kinase) were constitutively activated in NIH 3T3 cells infected with viruses containing either of two oncogenic forms (p35EC12, p3722W) of the c-Raf-1 protein kinase. The v-Raf proteins purified from cells infected with EC12 or 22W viruses activated MAP kinase kinase from skeletal muscle in vitro. Furthermore, a bacterially expressed v-Raf fusion protein (glutathione S-transferase-p3722W) also activated MAP kinase kinase in vitro. These findings suggest that one function of c-Raf-1 in mitogenic signaling is to phosphorylate and activate MAP kinase kinase.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dent, P -- Haser, W -- Haystead, T A -- Vincent, L A -- Roberts, T M -- Sturgill, T W -- CA50661/CA/NCI NIH HHS/ -- DK41077/DK/NIDDK NIH HHS/ -- HD24926/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1992 Sep 4;257(5075):1404-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Internal Medicine, University of Virginia, Charlottesville 22908.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1326789" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Animals ; Cell Line ; Cell Line, Transformed ; Enzyme Activation/drug effects ; Immunosorbent Techniques ; Mice ; Mitogen-Activated Protein Kinase Kinases ; Muscles/enzymology ; Oncogene Proteins v-raf ; Phosphorylation ; Protein Kinases/*metabolism ; Proto-Oncogene Proteins/pharmacology ; Proto-Oncogene Proteins c-raf ; Recombinant Fusion Proteins/pharmacology ; Retroviridae Proteins, Oncogenic/genetics/*pharmacology
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  • 92
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    Role of CD8+ T cells in murine experimental allergic encephalomyelitis (1992)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1992-05-22
    Description: The course of experimental allergic encephalomyelitis (EAE), an animal model for multiple sclerosis, is affected by immunoregulatory T lymphocytes. When animals are immunized with encephalitogenic peptide of myelin basic protein and recover from the first episode of EAE, they become resistant to a second induction of this disease. Animals depleted of CD8+ T cells by antibody-mediated clearance were used to examine the role of CD8+ T cells in EAE. These cells were found to be major participants in the resistance to a second induction of EAE but were not essential for spontaneous recovery from the first episode of the disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jiang, H -- Zhang, S I -- Pernis, B -- New York, N.Y. -- Science. 1992 May 22;256(5060):1213-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, College of Physicians and Surgeons, Columbia University, New York, NY 10032.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1375398" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/immunology ; Antigens, CD4/immunology ; Antigens, CD8/*immunology ; Encephalomyelitis, Autoimmune, Experimental/*immunology/physiopathology/therapy ; Immunization ; Lymphocyte Depletion ; Mice ; Mice, Inbred Strains ; Myelin Basic Protein/immunology ; T-Lymphocyte Subsets/*immunology
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    Homobatrachotoxin in the genus Pitohui: chemical defense in birds? (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-10-30
    Description: Three passerine species in the genus Pitohui, endemic to the New Guinea subregion, contain the steroidal alkaloid homobatrachotoxin, apparently as a chemical defense. Toxin concentrations varied among species but were always highest in the skin and feathers. Homobatrachotoxin is a member of a class of compounds collectively called batrachotoxins that were previously considered to be restricted to neotropical poison-dart frogs of the genus Phyllobates. The occurrence of homobatrachotoxin in pitohuis suggests that birds and frogs independently evolved this class of alkaloids.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dumbacher, J P -- Beehler, B M -- Spande, T F -- Garraffo, H M -- Daly, J W -- New York, N.Y. -- Science. 1992 Oct 30;258(5083):799-801.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Ecology and Evolution, University of Chicago, IL 60637.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1439786" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anura ; Batrachotoxins/*analysis ; Biological Assay ; Biological Evolution ; *Birds ; Chromatography, Thin Layer ; Feathers/*chemistry ; Gas Chromatography-Mass Spectrometry ; Mass Spectrometry ; Mice ; Muscles/*chemistry ; Skin/*chemistry
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    Establishment of stable, cell-mediated immunity that makes "susceptible" mice resistant to Leishmania major (1992)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1992-07-24
    Description: Cell-mediated, but not antibody-mediated, immune responses protect humans against certain pathogens that produce chronic diseases such as leishmaniasis. Effective vaccination against such pathogens must therefore produce an immunological "imprint" so that stable, cell-mediated immunity is induced in all individuals after natural infection. BALB/c mice "innately susceptible" to Leishmania major produce antibodies after substantial infection. In the present study, "susceptible" mice injected with a small number of parasites mounted a cell-mediated response and acquired resistance to a larger, normally pathogenic, challenge. This vaccination strategy may be applicable in diseases in which protection is dependent on cell-mediated immunity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bretscher, P A -- Wei, G -- Menon, J N -- Bielefeldt-Ohmann, H -- New York, N.Y. -- Science. 1992 Jul 24;257(5069):539-42.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, University of Saskatchewan, Saskatoon, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1636090" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Protozoan/analysis ; Disease Susceptibility ; *Immunity, Cellular ; Immunity, Innate ; Immunoglobulin G/analysis/classification ; Leishmaniasis, Cutaneous/*immunology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred CBA ; T-Lymphocytes/immunology
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  • 95
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    Expression of intra-MHC transporter (Ham) genes and class I antigens in diabetes-susceptible NOD mice (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-07-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wicker, L S -- Podolin, P L -- Fischer, P -- Sirotina, A -- Boltz, R C Jr -- Peterson, L B -- New York, N.Y. -- Science. 1992 Jun 26;256(5065):1828-30; author reply 1830-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1319611" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD27 ; Antigens, Differentiation, T-Lymphocyte/*biosynthesis ; B-Lymphocytes/immunology ; Blotting, Northern ; Diabetes Mellitus, Type 1/*immunology ; Disease Models, Animal ; Flow Cytometry ; H-2 Antigens/*biosynthesis ; Mice ; Mice, Inbred BALB C ; Mice, Inbred NOD ; T-Lymphocytes/immunology
    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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  • 96
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    Acetylcholine receptor channel structure probed in cysteine-substitution mutants (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-10-09
    Description: In order to understand the structural bases of ion conduction, ion selectivity, and gating in the nicotinic acetylcholine receptor, mutagenesis and covalent modification were combined to identify the amino acid residues that line the channel. The side chains of alternate residues--Ser248, Leu250, Ser252, and Thr254--in M2, a membrane-spanning segment of the alpha subunit, are exposed in the closed channel. Thus alpha 248-254 probably forms a beta strand, and the gate is closer to the cytoplasmic end of the channel than any of these residues. On channel opening, Leu251 is also exposed. These results lead to a revised view of the closed and open channel structures.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Akabas, M H -- Stauffer, D A -- Xu, M -- Karlin, A -- NS07065/NS/NINDS NIH HHS/ -- NS07258/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1992 Oct 9;258(5080):307-10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, College of Physicians and Surgeons, Columbia University, New York, NY 10032.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1384130" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcholine/metabolism/pharmacology ; Amino Acid Sequence ; Animals ; Cysteine/*chemistry ; Gene Expression ; Ion Channel Gating ; Ion Channels/*chemistry/physiology ; Mice ; Molecular Sequence Data ; Muscles/chemistry ; *Mutagenesis ; Oocytes/metabolism ; Receptors, Cholinergic/*chemistry/genetics ; Structure-Activity Relationship ; Sulfhydryl Reagents/pharmacology ; Thermodynamics ; Transfection ; Xenopus
    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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  • 97
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    Genes, patents, and product development (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-08-14
    Description: In the past year, the National Institutes of Health (NIH) has filed patent applications on more than 2750 partial complementary DNA sequences of unknown function. The rationale for the filings--that patent protection may be necessary to ensure that private firms are willing to invest in developing related products--rests on two premises: first, that NIH may obtain patent rights that will offer effective product monopolies to licensee firms, and second, that unless NIH obtains these rights now, firms will be unable to obtain a comparable degree of exclusivity by other means, such as by obtaining patents on their own subsequent innovations. Neither premise is clearly wrong, although both are subject to doubt in view of statements from industry representatives that the NIH patenting strategy will deter rather than promote product development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Eisenberg, R S -- New York, N.Y. -- Science. 1992 Aug 14;257(5072):903-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of Michigan Law School, Ann Arbor 48109.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1502556" target="_blank"〉PubMed〈/a〉
    Keywords: Biomedical Research ; Biotechnology ; DNA/*genetics ; *Federal Government ; *Genes ; Human Genome Project ; Humans ; National Institutes of Health (U.S.) ; *Patents 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
    Published by American Association for the Advancement of Science (AAAS)
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  • 98
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    Gallo wins one--and loses one (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-06-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉New York, N.Y. -- Science. 1992 Jun 5;256(5062):1391.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1604312" target="_blank"〉PubMed〈/a〉
    Keywords: *Acquired Immunodeficiency Syndrome ; Ethics, Professional ; History, 20th Century ; Humans ; Jurisprudence ; National Institutes of Health (U.S.) ; Newspapers as Topic ; Paris ; Research/*standards ; Scientific Misconduct ; *Societies, Scientific ; 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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  • 99
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    Overlapping but nonidentical binding sites on CD2 for CD58 and a second ligand CD59 (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-06-26
    Description: The interaction of the T cell glycoprotein CD2 with one ligand, CD58, contributes to T cell function. We have identified CD59, a glycoprotein with complement-inhibitory function, as a second physiological ligand for CD2. Antibodies to CD59 inhibit CD2-dependent T cell activation in murine T cell hybridomas expressing human CD2. In an in vitro binding assay with purified CD58 and CD59, CD2+ cells bind not only immobilized CD58 but also CD59. With two complementary approaches, it was demonstrated that the binding sites on CD2 for CD58 and CD59 are overlapping but nonidentical. These observations suggest that direct interactions between CD2 and both CD58 and CD59 contribute to T cell activation and adhesion.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hahn, W C -- Menu, E -- Bothwell, A L -- Sims, P J -- Bierer, B E -- AI28554/AI/NIAID NIH HHS/ -- HL36061/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1992 Jun 26;256(5065):1805-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Pediatric Oncology, Dana-Farber Cancer Institute, and Harvard Medical School, Boston, MA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1377404" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD/*metabolism ; Antigens, CD2 ; Antigens, CD58 ; Antigens, CD59 ; Antigens, Differentiation, T-Lymphocyte/*metabolism ; Binding Sites ; Dose-Response Relationship, Drug ; Humans ; Hybridomas ; Immunity, Cellular ; In Vitro Techniques ; Membrane Glycoproteins/*metabolism ; Mice ; Receptors, Antigen, T-Cell/*physiology ; Receptors, Immunologic/*metabolism ; T-Lymphocytes/immunology
    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
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    Interleukin-8 as a macrophage-derived mediator of angiogenesis (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-12-11
    Description: Angiogenic factors produced by monocytes-macrophages are involved in the pathogenesis of chronic inflammatory disorders characterized by persistent angiogenesis. The possibility was tested that interleukin-8 (IL-8), which is a cytokine that is chemotactic for lymphocytes and neutrophils, is also angiogenic. Human recombinant IL-8 was potently angiogenic when implanted in the rat cornea and induced proliferation and chemotaxis of human umbilical vein endothelial cells. Angiogenic activity present in the conditioned media of inflamed human rheumatoid synovial tissue macrophages or lipopolysaccharide-stimulated blood monocytes was equally blocked by antibodies to either IL-8 or tumor necrosis factor-alpha. An IL-8 antisense oligonucleotide specifically blocked the production of monocyte-induced angiogenic activity. These data suggest a function for macrophage-derived IL-8 in angiogenesis-dependent disorders such as rheumatoid arthritis, tumor growth, and wound repair.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koch, A E -- Polverini, P J -- Kunkel, S L -- Harlow, L A -- DiPietro, L A -- Elner, V M -- Elner, S G -- Strieter, R M -- AR30692/AR/NIAMS NIH HHS/ -- AR41492/AR/NIAMS NIH HHS/ -- HL39926/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1992 Dec 11;258(5089):1798-801.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Northwestern University Medical School, Chicago, IL 60611.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1281554" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arthritis, Rheumatoid/physiopathology ; Base Sequence ; Cell Division/drug effects ; Cells, Cultured ; Chemotaxis/*drug effects ; Cornea/*drug effects/physiology ; Dose-Response Relationship, Drug ; Endothelium, Vascular/drug effects/*physiology ; Fibroblast Growth Factor 2/pharmacology ; Humans ; Interleukin-8/genetics/*pharmacology ; Macrophages/*physiology ; Mice ; Molecular Sequence Data ; Monocytes/physiology ; *Neovascularization, Pathologic ; Oligonucleotides, Antisense/*pharmacology ; Rabbits ; Rats ; Recombinant Proteins/pharmacology ; Synovial Fluid/physiology ; Tumor Necrosis Factor-alpha/genetics ; Umbilical Veins
    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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