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  • Mice  (1,066)
  • Cloning, Molecular  (293)
  • National Institutes of Health (U.S.)  (265)
  • American Association for the Advancement of Science (AAAS)  (1,565)
  • Annual Reviews
  • 1990-1994  (1,009)
  • 1980-1984  (556)
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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
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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
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    Induction of AIDS in rhesus monkeys by molecularly cloned simian immunodeficiency virus (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-06-01
    Description: Better understanding of the pathogenesis of acquired immunodeficiency syndrome (AIDS) would be greatly facilitated by a relevant animal model that uses molecularly cloned virus of defined sequence to induce the disease. Such a system would also be of great value for AIDS vaccine research. An infectious molecular clone of simian immunodeficiency virus (SIV) was identified that induces AIDS in common rhesus monkeys in a time frame suitable for laboratory investigation. These results provide another strong link in the chain of evidence for the viral etiology of AIDS. More importantly, they define a system for molecular dissection of the determinants of AIDS pathogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kestler, H -- Kodama, T -- Ringler, D -- Marthas, M -- Pedersen, N -- Lackner, A -- Regier, D -- Sehgal, P -- Daniel, M -- King, N -- AI25328/AI/NIAID NIH HHS/ -- RR00168/RR/NCRR NIH HHS/ -- RR00169/RR/NCRR NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1990 Jun 1;248(4959):1109-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉New England Regional Primate Research Center, Harvard Medical School, Southborough, MA 01772.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2160735" target="_blank"〉PubMed〈/a〉
    Keywords: *Acquired Immunodeficiency Syndrome ; Animals ; Antibodies, Viral/biosynthesis ; Cloning, Molecular ; *Disease Models, Animal ; Leukocytes, Mononuclear/microbiology ; Macaca mulatta ; Macrophages/microbiology ; Opportunistic Infections/etiology ; *Retroviridae Infections/complications/immunology ; *Simian Immunodeficiency Virus/genetics/immunology/isolation & ; purification/pathogenicity ; Transfection ; Virus Replication
    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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    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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  • 6
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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
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  • 7
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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
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  • 8
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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
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  • 9
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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
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
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    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
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  • 11
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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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  • 12
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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
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  • 13
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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
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  • 14
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    GT-1 binding site confers light responsive expression in transgenic tobacco (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-04-27
    Description: Light-dependent expression of rbcS, the gene encoding the small subunit of ribulose-1,5-bisphosphate carboxylase, which is the key enzyme involved in carbon fixation in higher plants, is regulated at the transcriptional level. Sequence analysis of the gene has uncovered a conserved GT motif in the -150 to -100 region of many rbcS promoters. This motif serves as the binding site of a nuclear factor, designated GT-1. Analysis of site-specific mutants of pea rbcS-3A promoter demonstrated that GT-1 binding in vitro is correlated with light-responsive expression of the rbcS promoter in transgenic plants. However, it is not known whether factors other than GT-1 might also be required for activation of transcription by light. A synthetic tetramer of box II (TGTGTGGTTAATATG), the GT-1 binding site located between -152 to -138 of the rbcS-3A promoter, inserted upstream of a truncated cauliflower mosaic virus 35S promoter is sufficient to confer expression in leaves of transgenic tobacco. This expression occurs principally in chloroplast-containing cells, is induced by light, and is correlated with the ability of box II to bind GT-1 in vitro. The data show that the binding site for GT-1 is likely to be a part of the molecular light switch for rbcS activation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lam, E -- Chua, N H -- New York, N.Y. -- Science. 1990 Apr 27;248(4954):471-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Plant Molecular Biology, Rockefeller University, New York, NY 10021.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2330508" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Binding Sites ; Chloramphenicol O-Acetyltransferase/genetics ; Cloning, Molecular ; DNA-Binding Proteins/*metabolism ; Gene Expression Regulation/*physiology ; Genetic Vectors ; *Light ; Molecular Sequence Data ; Mutation ; Nuclear Proteins/*metabolism ; Plant Proteins/*metabolism ; *Plants, Toxic ; Promoter Regions, Genetic/genetics ; Ribulose-Bisphosphate Carboxylase/*genetics ; Tobacco/enzymology/*genetics ; Transcription, Genetic/radiation effects ; Transformation, Genetic
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  • 15
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    A cDNA for a protein that interacts with the human immunodeficiency virus Tat transactivator (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-06-29
    Description: The human immunodeficiency virus (HIV) tat protein (Tat) is a positive regulator of virus gene expression and replication. Biotinylated Tat was used as a probe to screen a lambda gt11 fusion protein library, and a complementary DNA encoding a protein that interacts with Tat was cloned. Expression of this protein, designated TBP-1 (for Tat binding protein-1), was observed in a variety of cell lines, with expression being highest in human cells. TBP-1 was localized predominantly in the nucleus, which is consistent with the nuclear localization of Tat. In cotransfection experiments, expression of TBP-1 was able to specifically suppress Tat-mediated transactivation. The strategy described may be useful for direct identification and cloning of genes encoding proteins that associate with other proteins to modulate their activity in a positive or negative fashion.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nelbock, P -- Dillon, P J -- Perkins, A -- Rosen, C A -- New York, N.Y. -- Science. 1990 Jun 29;248(4963):1650-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Oncology and Virology, Roche Institute of Molecular Biology, Hoffmann-La Roche Inc., Nutley, NJ 07110.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2194290" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cell Line ; Cloning, Molecular ; DNA, Neoplasm/genetics ; DNA-Binding Proteins/*genetics/metabolism ; Escherichia coli/genetics ; Gene Expression ; Gene Library ; Gene Products, tat/*metabolism ; HIV/genetics ; Humans ; Molecular Sequence Data ; Plasmids ; Polymerase Chain Reaction ; *Proteasome Endopeptidase Complex ; Recombinant Fusion Proteins/metabolism ; Trans-Activators/*metabolism ; Transcriptional Activation ; Transfection ; tat Gene Products, Human Immunodeficiency Virus
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  • 16
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    Common modifications of trimeric G proteins and ras protein: involvement of polyisoprenylation (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-07-13
    Description: The heterotrimeric guanine nucleotide-binding regulatory proteins act at the inner surface of the plasma membrane to relay information from cell surface receptors to effectors inside the cell. These G proteins are not integral membrane proteins, yet are membrane associated. The processing and function of the gamma subunit of the yeast G protein involved in mating-pheromone signal transduction was found to be affected by the same mutations that block ras processing. The nature of these mutations implied that the gamma subunit was polyisoprenylated and that this modification was necessary for membrane association and biological activity. A microbial screen was developed for pharmacological agents that inhibit polyisoprenylation and that have potential application in cancer therapy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Finegold, A A -- Schafer, W R -- Rine, J -- Whiteway, M -- Tamanoi, F -- CA 41996/CA/NCI NIH HHS/ -- GM 07183/GM/NIGMS NIH HHS/ -- GM 35827/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1990 Jul 13;249(4965):165-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Biology, University of Chicago, IL 60637.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1695391" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Cell Membrane/metabolism ; Cloning, Molecular ; Epitopes/genetics ; GTP-Binding Proteins/genetics/*metabolism ; Hemagglutinins, Viral/immunology ; Lovastatin/pharmacology ; Mevalonic Acid/pharmacology ; Molecular Sequence Data ; Mutation ; Oncogene Protein p21(ras)/genetics/*metabolism ; Orthomyxoviridae/immunology ; Protein Processing, Post-Translational ; Saccharomyces cerevisiae/*genetics/metabolism ; Signal Transduction ; Suppression, Genetic
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  • 17
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    A potent GAL4 derivative activates transcription at a distance in vitro (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-02-09
    Description: Transcription of a typical eukaryotic gene by RNA polymerase II is activated by proteins bound to sites found near the beginning of the gene as well as to sites, called enhancers, located a great distance from the gene. According to one view, the primary difference between an activator that can work at a large distance and one that cannot is that the former bears a particularly strong activating region; the stronger the activating region, the more readily the activator interacts with its target bound near the transcriptional start site, with the intervening DNA looping out to accommodate the reaction. One alternative view is that the effect of proteins bound to enhancers might require some special aspect of cellular or chromosome structure. Consistent with the first view, an activator bearing an unusually potent activating region can stimulate transcription of a mammalian gene in a HeLa nuclear extract when bound as far as 1.3 kilobase pairs upstream or 320 base pairs downstream of the transcriptional start site.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Carey, M -- Leatherwood, J -- Ptashne, M -- New York, N.Y. -- Science. 1990 Feb 9;247(4943):710-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Biology, Harvard University, Cambridge, MA 02138.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2405489" target="_blank"〉PubMed〈/a〉
    Keywords: Activating Transcription Factors ; Binding Sites ; Blood Proteins/pharmacology ; Cloning, Molecular ; DNA/metabolism ; DNA-Binding Proteins ; Fungal Proteins/metabolism/*pharmacology ; HeLa Cells ; Phosphoproteins/pharmacology ; Promoter Regions, Genetic ; RNA Polymerase II/metabolism ; Recombinant Fusion Proteins/pharmacology ; *Saccharomyces cerevisiae Proteins ; Templates, Genetic ; Trans-Activators/pharmacology ; Transcription Factors/pharmacology ; Transcription, Genetic/*drug effects
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  • 18
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    Autophosphorylation of protein kinase C at three separated regions of its primary sequence (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-07-27
    Description: The major autophosphorylation sites of the rat beta II isozyme of protein kinase C were identified. The modified threonine and serine residues were found in the amino-terminal peptide, the carboxyl-terminal tail, and the hinge region between the regulatory lipid-binding domain and the catalytic kinase domain. Because this autophosphorylation follows an intrapeptide mechanism, extraordinary flexibility of the protein is necessary to phosphorylate the three regions. Comparison of the sequences surrounding the modified residues showed no obvious recognition motif nor any similarity to substrate phosphorylation sites, suggesting that proximity to the active site may be the primary criterion for their phosphorylation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Flint, A J -- Paladini, R D -- Koshland, D E Jr -- DK09765/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1990 Jul 27;249(4967):408-11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Biology, University of California, Berkeley 94720.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2377895" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Binding Sites ; Brain/enzymology ; Cloning, Molecular ; Isoenzymes/genetics/*metabolism ; Molecular Sequence Data ; Peptide Fragments/isolation & purification/metabolism ; Phosphorylation ; Protein Conformation ; Protein Kinase C/genetics/*metabolism ; Rats ; Recombinant Proteins/metabolism ; Signal Transduction ; Trypsin
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  • 19
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    Pinning down sequencing costs (1990)
    American Association for the Advancement of Science (AAAS)
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    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
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  • 20
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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
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  • 21
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    Cloning of a 67-kD neutrophil oxidase factor with similarity to a noncatalytic region of p60c-src (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-05-11
    Description: Chronic granulomatous diseases (CGDs) are characterized by recurrent infections resulting from impaired superoxide production by a phagocytic cell, nicotinamide adenine dinucleotide phosphate (reduced) (NADPH) oxidase. Complementary DNAs were cloned that encode the 67-kilodalton (kD) cytosolic oxidase factor (p67), which is deficient in 5% of CGD patients. Recombinant p67 (r-p67) partially restored NADPH oxidase activity to p67-deficient neutrophil cytosol from these patients. The p67 cDNA encodes a 526-amino acid protein with acidic middle and carboxyl-terminal domains that are similar to a sequence motif found in the noncatalytic domain of src-related tyrosine kinases. This motif was recently noted in phospholipase C-gamma, nonerythroid alpha-spectrin (fodrin), p21ras-guanosine triphophatase-activating protein (GAP), myosin-1 isoforms, yeast proteins cdc-25 and fus-1, and the 47-kD phagocyte oxidase factor (p47), which suggests the possibility of common regulatory features.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Leto, T L -- Lomax, K J -- Volpp, B D -- Nunoi, H -- Sechler, J M -- Nauseef, W M -- Clark, R A -- Gallin, J I -- Malech, H L -- I01 BX000513/BX/BLRD VA/ -- New York, N.Y. -- Science. 1990 May 11;248(4956):727-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Clinical Investigation, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1692159" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cloning, Molecular ; Granulomatous Disease, Chronic/blood/enzymology/genetics ; Humans ; Molecular Sequence Data ; NADH, NADPH Oxidoreductases/blood/*genetics ; NADPH Oxidase ; Neutrophils/*enzymology ; Protein-Tyrosine Kinases/genetics ; Proto-Oncogene Proteins/*genetics ; Proto-Oncogene Proteins pp60(c-src) ; Sequence Homology, Nucleic Acid
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  • 22
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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)
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    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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  • 23
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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
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  • 24
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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)
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    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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  • 25
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    High-resolution mapping of human chromosome 11 by in situ hybridization with cosmid clones (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-01-05
    Description: Cosmid clones containing human DNA inserts have been mapped on chromosome 11 by fluorescence in situ hybridization under conditions that suppress signal from repetitive DNA sequences. Thirteen known genes, one chromosome 11-specific DNA repeat, and 36 random clones were analyzed. High-resolution mapping was facilitated by using digital imaging microscopy and by analyzing extended (prometaphase) chromosomes. The map coordinates established by in situ hybridization showed a one to one correspondence with those determined by Southern (DNA) blot analysis of hybrid cell lines containing fragments of chromosome 11. Furthermore, by hybridizing three or more cosmids simultaneously, gene order on the chromosome could be established unequivocally. These results demonstrate the feasibility of rapidly producing high-resolution maps of human chromosomes by in situ hybridization.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lichter, P -- Tang, C J -- Call, K -- Hermanson, G -- Evans, G A -- Housman, D -- Ward, D C -- GM-27882/GM/NIGMS NIH HHS/ -- GM-33868/GM/NIGMS NIH HHS/ -- HD-18012/HD/NICHD NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1990 Jan 5;247(4938):64-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Human Genetics, 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/2294592" target="_blank"〉PubMed〈/a〉
    Keywords: Blotting, Southern ; Cell Line ; *Chromosome Mapping ; *Chromosomes, Human, Pair 11 ; Cloning, Molecular ; Cosmids/*genetics ; DNA/*genetics ; DNA Probes ; Fluorescent Dyes ; Humans ; Hybrid Cells ; Microscopy, Fluorescence ; *Nucleic Acid Hybridization ; Repetitive Sequences, Nucleic Acid
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  • 26
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    What's holding up "aversives" report? (1990)
    American Association for the Advancement of Science (AAAS)
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    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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  • 27
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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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  • 28
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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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  • 29
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    beta-Arrestin: a protein that regulates beta-adrenergic receptor function (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-06-22
    Description: Homologous or agonist-specific desensitization of beta-adrenergic receptors is thought to be mediated by a specific kinase, the beta-adrenergic receptor kinase (beta ARK). However, recent data suggest that a cofactor is required for this kinase to inhibit receptor function. The complementary DNA for such a cofactor was cloned and found to encode a 418-amino acid protein homologous to the retinal protein arrestin. The protein, termed beta-arrestin, was expressed and partially purified. It inhibited the signaling function of beta ARK-phosphorylated beta-adrenergic receptors by more than 75 percent, but not that of rhodopsin. It is proposed that beta-arrestin in concert with beta ARK effects homologous desensitization of beta-adrenergic receptors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lohse, M J -- Benovic, J L -- Codina, J -- Caron, M G -- Lefkowitz, R J -- DK19318/DK/NIDDK NIH HHS/ -- HL16037/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1990 Jun 22;248(4962):1547-50.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Medicine, Biochemistry and Cell Biology, Durham, NC 27710.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2163110" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antigens/*genetics/isolation & purification/pharmacology ; Arrestin ; Blotting, Northern ; Chromatography, Ion Exchange ; Cloning, Molecular ; *Cyclic AMP-Dependent Protein Kinases ; DNA/genetics ; Eye Proteins/*genetics/isolation & purification/pharmacology ; Gene Expression Regulation ; Molecular Sequence Data ; Phosphodiesterase Inhibitors/*pharmacology ; Phosphorylation ; Protein Kinases/*pharmacology ; RNA, Messenger/analysis ; Receptors, Adrenergic, beta/*drug effects/physiology ; Transfection ; beta-Adrenergic Receptor Kinases
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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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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    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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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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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    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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    Reversal of creatine kinase translational repression by 3' untranslated sequences (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-05-25
    Description: A subline of U937 cells (U937D) was obtained in which creatine kinase B (CK-B) messenger RNA was present and bound to ribosomes, but CK activity was undetectable. Transformation of U937D cells with retrovirus vectors that contain the 3' untranslated region (3' UTR) of CK-B messenger RNA exhibited CK activity with no change in abundance of CK-B mRNA. The 3' UTR formed a complex in vitro with a component of S100 extracts from wild-type cells. This binding activity was not detectable in S100 extracts from cells that expressed CK activity after transformation with the 3' UTR-containing vector. These results suggest that translation of CK-B is repressed by binding of a soluble factor or factors to the 3' UTR.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ch'ng, J L -- Shoemaker, D L -- Schimmel, P -- Holmes, E W -- GM34366/GM/NIGMS NIH HHS/ -- R01-CA 47631-02/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1990 May 25;248(4958):1003-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Duke University, Durham, NC 27710.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2343304" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Cloning, Molecular ; Creatine Kinase/*genetics ; *Gene Expression Regulation ; Humans ; Hypoxanthine Phosphoribosyltransferase/genetics ; Polyribosomes/metabolism ; *Protein Biosynthesis ; RNA, Messenger/*genetics
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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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    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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    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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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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)
    Details
    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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    HSP104 required for induced thermotolerance (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-06-01
    Description: A heat shock protein gene, HSP104, was isolated from Saccharomyces cerevisiae and a deletion mutation was introduced into yeast cells. Mutant cells grew at the same rate as wild-type cells and died at the same rate when exposed directly to high temperatures. However, when given a mild pre-heat treatment, the mutant cells did not acquire tolerance to heat, as did wild-type cells. Transformation with the wild-type gene rescued the defect of mutant cells. The results demonstrate that a particular heat shock protein plays a critical role in cell survival at extreme temperatures.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sanchez, Y -- Lindquist, S L -- GM 35483/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1990 Jun 1;248(4959):1112-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Molecular Genetics and Cell Biology, University of Chicago, Illinois 60637.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2188365" target="_blank"〉PubMed〈/a〉
    Keywords: Cloning, Molecular ; Fungal Proteins/biosynthesis/*genetics ; Genes, Fungal ; Heat-Shock Proteins/biosynthesis/genetics/*physiology ; *Hot Temperature ; Mutation ; Restriction Mapping ; Saccharomyces cerevisiae/genetics/growth & development/*physiology
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    Identification of a specialized adenylyl cyclase that may mediate odorant detection (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-12-07
    Description: The mammalian olfactory system may transduce odorant information via a G protein-mediated adenosine 3',5'-monophosphate (cAMP) cascade. A newly discovered adenylyl cyclase, termed type III, has been cloned, and its expression was localized to olfactory neurons. The type III protein resides in the sensory neuronal cilia, which project into the nasal lumen and are accessible to airborne odorants. The enzymatic activity of the type III adenylyl cyclase appears to differ from nonsensory cyclases. The large difference seen between basal and stimulated activity for the type III enzyme could allow considerable modulation of the intracellular cAMP concentration. This property may represent one mechanism of achieving sensitivity in odorant perception.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bakalyar, H A -- Reed, R R -- 5T32CA09339/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1990 Dec 7;250(4986):1403-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology and Genetics, Howard Hughes Medical Institute, 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/2255909" target="_blank"〉PubMed〈/a〉
    Keywords: Adenylyl Cyclases/genetics/*physiology ; Amino Acid Sequence ; Animals ; Brain/enzymology/physiology ; Cell Line ; Clone Cells ; Cloning, Molecular ; Gene Library ; Glycosylation ; Isoenzymes/genetics/*physiology ; Macromolecular Substances ; Molecular Sequence Data ; Molecular Weight ; Neurons, Afferent/enzymology/physiology ; Nose/enzymology/physiology ; *Odors ; Protein Conformation ; Rats ; *Signal Transduction
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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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    Peptide processing and targeting in the neuronal secretory pathway (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-03-15
    Description: The abdominal ganglion of the marine mollusk Aplysia contains a pair of identified neuronal clusters, the bag cells, which control egg laying by means of a number of unique regulatory mechanisms. Each neuron in the bag cell clusters synthesizes several peptides derived from a single prohormone and packages them into separate vesicles. These vesicles are then differentially localized in specific neuronal processes, thus segregating peptides destined for autocrine and hormonal release sites. Therefore in this system, protein trafficking through the secretory pathway organizes multiple peptide neurochemical messengers to efficiently regulate simple behaviors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jung, L J -- Scheller, R H -- New York, N.Y. -- Science. 1991 Mar 15;251(4999):1330-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Molecular and Cellular Physiology, Beckman Center, Stanford University, CA 94305.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2003219" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aplysia/genetics/*physiology ; Cell Compartmentation ; Cloning, Molecular ; DNA/genetics ; Invertebrate Hormones/genetics/*metabolism ; Neuropeptides/*physiology ; Neurosecretory Systems/*physiology ; Protein Precursors/metabolism ; Protein Processing, Post-Translational ; Sexual Behavior, Animal/physiology ; Transfection
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    Identification of the DNA binding site for NGFI-B by genetic selection in yeast (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-05-31
    Description: An in vivo selection system for isolating targets of DNA binding proteins in yeast was developed and used to identify the DNA binding site for the NGFI-B protein, a member of the steroid-thyroid hormone receptor superfamily. The feasibility of the technique was verified by selecting DNA fragments that contained binding sites for GCN4, a well-characterized yeast transcriptional activator. The DNA binding domain of NGFI-B, expressed as part of a LexA-NGFI-B-GAL4 chimeric activator, was then used to isolate a rat genomic DNA fragment that contained an NGFI-B binding site. The NGFI-B response element (NBRE) is similar to but functionally distinct from elements recognized by the estrogen and thyroid hormone receptors and the hormone receptor-like proteins COUP-TF, CF1, and H-2RIIBP. Cotransfection experiments in mammalian cells demonstrated that NGFI-B can activate transcription from the NBRE with or without its putative ligand binding domain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wilson, T E -- Fahrner, T J -- Johnston, M -- Milbrandt, J -- NS01018/NS/NINDS NIH HHS/ -- P01 CA49712/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1991 May 31;252(5010):1296-300.〈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/1925541" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacterial Proteins/metabolism ; Base Sequence ; Binding Sites ; Cloning, Molecular ; DNA, Fungal/*metabolism ; DNA-Binding Proteins/genetics/*metabolism/pharmacology ; Fungal Proteins/metabolism ; Molecular Sequence Data ; Nuclear Receptor Subfamily 4, Group A, Member 1 ; Plasmids ; *Protein Kinases ; Rats ; Receptors, Cytoplasmic and Nuclear ; Receptors, Steroid ; Repressor Proteins ; Saccharomyces cerevisiae/*genetics ; *Saccharomyces cerevisiae Proteins ; *Serine Endopeptidases ; Transcription Factors/genetics/*metabolism/pharmacology ; Transcription, Genetic ; Transfection
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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)
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    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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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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)
    Details
    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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    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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    Cloning and expression of a cocaine-sensitive rat dopamine transporter (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-10-25
    Description: The action of dopamine and other monoamine neurotransmitters at synapses is terminated predominantly by high-affinity reuptake into presynaptic terminals by specific sodium-dependent neurotransmitter transport proteins. A complementary DNA encoding a rat dopamine transporter has been isolated that exhibits high sequence similarity with the previously cloned norepinephrine and gamma-aminobutyric acid transporters. Transient expression of the complementary DNA in HeLa cells confirms the cocaine sensitivity of this transporter.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kilty, J E -- Lorang, D -- Amara, S G -- New York, N.Y. -- Science. 1991 Oct 25;254(5031):578-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Yale University, New Haven, CT 06510.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1948035" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Carrier Proteins/drug effects/*genetics/metabolism ; Cloning, Molecular ; Cocaine/*pharmacology ; Dopamine/*metabolism ; Dopamine Plasma Membrane Transport Proteins ; Gene Expression ; HeLa Cells ; Humans ; Kinetics ; *Membrane Glycoproteins ; *Membrane Transport Proteins ; Molecular Sequence Data ; *Nerve Tissue Proteins ; Oligodeoxyribonucleotides ; Polymerase Chain Reaction/methods ; Rats ; Sequence Homology, Nucleic Acid ; 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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    Mutation identified as a possible cause of Alzheimer's disease (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-02-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J -- New York, N.Y. -- Science. 1991 Feb 22;251(4996):876-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1900373" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/*genetics ; Amyloid beta-Peptides/*genetics ; Amyloid beta-Protein Precursor ; Chromosomes, Human, Pair 21 ; Cloning, Molecular ; Humans ; *Mutation ; Protein Precursors/*genetics
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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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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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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    Exchange of conduction pathways between two related K+ channels (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-02-22
    Description: The structure of the ion conduction pathway or pore of voltage-gated ion channels is unknown, although the linker between the membrane spanning segments S5 and S6 has been suggested to form part of the pore in potassium channels. To test whether this region controls potassium channel conduction, a 21-amino acid segment of the S5-S6 linker was transplanted from the voltage-activated potassium channel NGK2 to another potassium channel DRK1, which has very different pore properties. In the resulting chimeric channel, the single channel conductance and blockade by external and internal tetraethylammonium (TEA) ion were characteristic of the donor NGK2 channel. Thus, this 21-amino acid segment controls the essential biophysical properties of the pore and may form the conduction pathway of these potassium channels.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hartmann, H A -- Kirsch, G E -- Drewe, J A -- Taglialatela, M -- Joho, R H -- Brown, A M -- NS08805/NS/NINDS NIH HHS/ -- NS23877/NS/NINDS NIH HHS/ -- NS28407/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1991 Feb 22;251(4996):942-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Physiology and Biophysics, Baylor College of Medicine, Houston, TX 77030.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2000495" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Brain/physiology ; Chimera ; Cloning, Molecular ; Female ; Ion Channel Gating ; Membrane Potentials ; Molecular Sequence Data ; Oligonucleotide Probes ; Oocytes/physiology ; Polymerase Chain Reaction ; Potassium Channels/drug effects/genetics/*physiology ; Rats ; Restriction Mapping ; Sequence Homology, Nucleic Acid ; Tetraethylammonium ; Tetraethylammonium Compounds/pharmacology ; Xenopus
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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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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  • 75
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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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Selective activation of the B natriuretic peptide receptor by C-type natriuretic peptide (CNP) (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-04-05
    Description: The natriuretic peptides are hormones that can stimulate natriuretic, diuretic, and vasorelaxant activity in vivo, presumably through the activation of two known cell surface receptor guanylyl cyclases (ANPR-A and ANPR-B). Although atrial natriuretic peptide (ANP) and, to a lesser extent, brain natriuretic peptide (BNP) are efficient activators of the ANPR-A guanylyl cyclase, neither hormone can significantly stimulate ANPR-B. A member of this hormone family, C-type natriuretic peptide (CNP), potently and selectively activated the human ANPR-B guanylyl cyclase. CNP does not increase guanosine 3',5'-monophosphate accumulation in cells expressing human ANPR-A. The affinity of CNP for ANPR-B is 50- or 500-fold higher than ANP or BNP, respectively. This ligand-receptor pair may be involved in the regulation of fluid homeostasis by the central nervous system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koller, K J -- Lowe, D G -- Bennett, G L -- Minamino, N -- Kangawa, K -- Matsuo, H -- Goeddel, D V -- New York, N.Y. -- Science. 1991 Apr 5;252(5002):120-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Genentech, Inc., South San Francisco 94080.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1672777" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Atrial Natriuretic Factor/*physiology ; Cells, Cultured ; Cercopithecus aethiops ; Cloning, Molecular ; Dose-Response Relationship, Drug ; Guanylate Cyclase/metabolism ; Humans ; Natriuretic Peptide, Brain ; Natriuretic Peptide, C-Type ; Nerve Tissue Proteins/*pharmacology ; Receptors, Atrial Natriuretic Factor ; Receptors, Cell Surface/*physiology ; Recombinant Proteins ; Signal Transduction
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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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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    Targets for dioxin: genes for plasminogen activator inhibitor-2 and interleukin-1 beta (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-10-18
    Description: Dioxin (2,3,7,8-tetrachlorodibenzo-p-dioxin, TCDD), a widespread environmental contaminant, may elicit its effects by altering gene expression in susceptible cells. Five TCDD-responsive complementary DNA clones were isolated from a human keratinocyte cell line. One of these clones encodes plasminogen activator inhibitor-2, a factor that influences growth and differentiation by regulating proteolysis of the extracellular matrix. Another encodes the cytokine interleukin-1 beta. Thus, TCDD alters the expression of growth regulatory genes and has effects similar to those of other tumor-promoting agents that affect both inflammation and differentiation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sutter, T R -- Guzman, K -- Dold, K M -- Greenlee, W F -- New York, N.Y. -- Science. 1991 Oct 18;254(5030):415-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Chemical Industry Institute of Toxicology, Research Triangle Park, NC 27709.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1925598" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Blood Physiological Phenomena ; Blotting, Northern ; Calcium/pharmacology ; Cell Line ; Cloning, Molecular ; Cycloheximide/pharmacology ; Gene Expression Regulation/drug effects ; Humans ; Interleukin-1/*genetics ; *Plasminogen Inactivators ; RNA, Messenger/drug effects ; Tetrachlorodibenzodioxin/*pharmacology ; Transcription, Genetic/drug effects
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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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    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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  • 83
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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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  • 84
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    Cloning of a factor required for activity of the Ah (dioxin) receptor (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-05-17
    Description: The aryl hydrocarbon (Ah) receptor binds various environmental pollutants, such as polycyclic aromatic hydrocarbons, heterocyclic amines, and polychlorinated aromatic compounds (dioxins, dibenzofurans, and biphenyls), and mediates the carcinogenic effects of these agents. The complementary DNA and part of the gene for an 87-kilodalton human protein that is necessary for Ah receptor function have been cloned. The protein is not the ligand-binding subunit of the receptor but is a factor that is required for the ligand-binding subunit to translocate from the cytosol to the nucleus after binding ligand. The requirement for this factor distinguishes the Ah receptor from the glucocorticoid receptor, to which the Ah receptor has been presumed to be similar. Two portions of the 87-kilodalton protein share sequence similarities with two Drosophila proteins, Per and Sim. Another segment of the protein shows conformity to the consensus sequence for the basic helix-loop-helix motif found in proteins that bind DNA as homodimers or heterodimers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hoffman, E C -- Reyes, H -- Chu, F F -- Sander, F -- Conley, L H -- Brooks, B A -- Hankinson, O -- CA 16048/CA/NCI NIH HHS/ -- CA 28868/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1991 May 17;252(5008):954-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, University of California, Los Angeles 90024.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1852076" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Aryl Hydrocarbon Receptor Nuclear Translocator ; Base Sequence ; Cell Line ; Cell Nucleus/metabolism ; Cloning, Molecular ; Cytosol/metabolism ; *DNA-Binding Proteins ; Humans ; Macromolecular Substances ; Molecular Sequence Data ; Molecular Weight ; Oligonucleotide Probes ; Proteins/*genetics/metabolism ; RNA, Messenger/genetics ; Receptors, Aryl Hydrocarbon ; Receptors, Drug/genetics/*metabolism ; Sequence Homology, Nucleic Acid ; Tetrachlorodibenzodioxin/*metabolism ; *Transcription Factors ; Transfection
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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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  • 86
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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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  • 88
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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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  • 89
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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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  • 90
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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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 91
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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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  • 92
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    Regulation of the apolipoprotein AI gene by ARP-1, a novel member of the steroid receptor superfamily (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-02-01
    Description: Apolipoprotein AI (apoAI) is a lipid-binding protein that participates in the transport of cholesterol and other lipids in the plasma. A complementary DNA clone for a protein that bound to regulatory elements of the apoAI gene was isolated. This protein, designated apoAI regulatory protein-1 (ARP-1), is a novel member of the steroid hormone receptor superfamily. ARP-1 bound to DNA as a dimer, and its dimerization domain was localized to the COOH-terminal region. ARP-1 also bound to a thyroid hormone-responsive element and to regulatory regions of the apoB, apoCIII, insulin, and ovalbumin genes. In cotransfection experiments, ARP-1 downregulated the apoAI gene. The involvement of ARP-1 in the regulation of apoAI gene expression suggests that it may participate in lipid metabolism and cholesterol homeostasis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ladias, J A -- Karathanasis, S K -- New York, N.Y. -- Science. 1991 Feb 1;251(4993):561-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cardiology, Children's Hospital, Boston, MA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1899293" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Apolipoprotein A-I ; Apolipoproteins A/*genetics ; Base Sequence ; COUP Transcription Factor II ; COUP Transcription Factors ; Cloning, Molecular ; DNA/metabolism ; DNA-Binding Proteins/*metabolism ; Gene Expression Regulation ; Humans ; Lipoproteins, HDL/*genetics ; Molecular Sequence Data ; Oligonucleotide Probes ; Receptors, Steroid/*metabolism ; Regulatory Sequences, Nucleic Acid ; *Transcription Factors
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  • 93
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    Identification of Ets- and notch-related subunits in GA binding protein (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-08-16
    Description: Recombinant cDNA clones that encode two distinct subunits of the transcription factor GA binding protein (GABP) have been isolated. The predicted amino acid sequence of one subunit, GABP alpha, exhibits similarity to the sequence of the product of the ets-1 protooncogene in a region known to encompass the Ets DNA binding domain. The sequence of the second subunit, GABP beta, contains four 33-amino acid repeats located close to the NH2-terminus of the subunit. The sequences of these repeats are similar to repeats in several transmembrane proteins, including Notch from Drosophila melanogaster and Glp-1 and Lin-12 from Caenorhabditis elegans. Avid, sequence-specific binding to DNA required the presence of both polypeptides, revealing a conceptual convergence of nuclear transforming proteins and membrane-anchored proteins implicated in developmentally regulated signal transduction processes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉LaMarco, K -- Thompson, C C -- Byers, B P -- Walton, E M -- McKnight, S L -- New York, N.Y. -- Science. 1991 Aug 16;253(5021):789-92.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Research Laboratories, Carnegie Institution of Washington, Department of Embryology, Baltimore, MD 21210.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1876836" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Blotting, Northern ; Cloning, Molecular ; DNA-Binding Proteins/*chemistry/genetics ; GA-Binding Protein Transcription Factor ; Gene Expression ; Molecular Sequence Data ; Nuclear Proteins/chemistry/genetics ; Peptides/chemistry ; Proto-Oncogene Protein c-ets-1 ; Proto-Oncogene Proteins/chemistry ; Proto-Oncogene Proteins c-ets ; RNA, Messenger/genetics ; Rats ; Recombinant Proteins ; Transcription Factors/*chemistry/genetics
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  • 94
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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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  • 95
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    A component of calcium-activated potassium channels encoded by the Drosophila slo locus (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-08-02
    Description: Calcium-activated potassium channels mediate many biologically important functions in electrically excitable cells. Despite recent progress in the molecular analysis of voltage-activated K+ channels, Ca(2+)-activated K+ channels have not been similarly characterized. The Drosophila slowpoke (slo) locus, mutations of which specifically abolish a Ca(2+)-activated K+ current in muscles and neurons, provides an opportunity for molecular characterization of these channels. Genomic and complementary DNA clones from the slo locus were isolated and sequenced. The polypeptide predicted by slo is similar to voltage-activated K+ channel polypeptides in discrete domains known to be essential for function. Thus, these results indicate that slo encodes a structural component of Ca(2+)-activated K+ channels.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Atkinson, N S -- Robertson, G A -- Ganetzky, B -- NS15390/NS/NINDS NIH HHS/ -- T32 GM07131/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1991 Aug 2;253(5019):551-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Genetics, University of Wisconsin, Madison 53706.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1857984" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Calcium/pharmacology ; Chromosome Aberrations ; Chromosome Deletion ; Cloning, Molecular ; DNA/genetics/isolation & purification ; Drosophila/*genetics/physiology ; Exons ; Molecular Sequence Data ; Nucleic Acid Hybridization ; Phenotype ; Potassium Channels/drug effects/*genetics/physiology ; Protein Conformation ; Sequence Homology, Nucleic Acid ; Transcription, Genetic ; Translocation, Genetic
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  • 96
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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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  • 97
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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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  • 98
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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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  • 99
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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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 100
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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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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