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  • Articles  (3,446)
  • Animals  (2,269)
  • Physical Chemistry  (1,177)
  • 1990-1994  (3,390)
  • 1965-1969  (56)
  • Chemistry and Pharmacology  (3,446)
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  • Articles  (3,446)
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  • 11
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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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  • 12
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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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 13
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    Antibody-mediated activation of Drosophila heat shock factor in vitro (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-08-03
    Description: Eukaryotic cells respond to elevated temperatures by rapidly activating the expression of heat shock genes. Central to this activation is heat shock-inducible binding of the transcriptional activator, termed heat shock factor (HSF), to common regulatory elements, which are located upstream of all heat shock genes. The DNA binding activity of the inactive form of Drosophila HSF was induced in vitro by treatment with polyclonal antibodies to the purified, in vivo-activated factor. This finding, together with observations that high temperature and low pH activate HSF binding in vitro, suggests that the inactive form of HSF can directly recognize and transduce the heat shock signal without undergoing a covalent modification of protein structure.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zimarino, V -- Wilson, S -- Wu, C -- New York, N.Y. -- Science. 1990 Aug 3;249(4968):546-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Biochemistry, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2200124" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies ; Drosophila/*genetics ; *Gene Expression Regulation ; HeLa Cells/metabolism ; Heat-Shock Proteins/*genetics/immunology/isolation & purification/metabolism ; Humans ; Saccharomyces cerevisiae/genetics ; Transcription Factors/*metabolism ; *Transcription, Genetic
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 14
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    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
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 15
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    Contributions of two types of calcium channels to synaptic transmission and plasticity (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-11-23
    Description: In Aplysia sensory and motor neurons in culture, the contributions of the major classes of calcium current can be selectively examined while transmitter release and its modulation are examined. A slowly inactivating, dihydropyridine-sensitive calcium current does not contribute either to normal synaptic transmission or to any of three different forms of plasticity: presynaptic inhibition, homosynaptic depression, and presynaptic facilitation. This current does contribute, however, to a fourth form of plasticity--modulation of transmitter release by tonic depolarization of the sensory neuron. By contrast, a second calcium current, which is rapidly inactivating and dihydropyridine-insensitive, contributes to release elicited by the transient depolarization of an action potential and to the other three forms of plasticity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Edmonds, B -- Klein, M -- Dale, N -- Kandel, E R -- New York, N.Y. -- Science. 1990 Nov 23;250(4984):1142-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University College of London, United Kingdom.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2174573" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Aplysia/*physiology ; Cadmium/pharmacology ; Calcium Channels/drug effects/*physiology ; Cells, Cultured ; Dihydropyridines/antagonists & inhibitors/pharmacology ; Electric Conductivity ; FMRFamide ; Motor Neurons/physiology ; Neuronal Plasticity/*physiology ; Neurons, Afferent/physiology ; Neuropeptides/pharmacology ; Nifedipine/pharmacology ; Serotonin/pharmacology ; Synapses/*physiology ; Synaptic Transmission/*physiology
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  • 16
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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
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  • 17
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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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  • 18
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    A structural basis for Hering's law: projections to extraocular motoneurons (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-06-01
    Description: Conjugate eye movements are executed through the concurrent activation of several muscles in both eyes. The neural mechanisms that underlie such synergistic muscle activations have been a matter of considerable experimentation and debate. In order to investigate this issue, the projections of a class of primate premotoneuronal cells were studied, namely, the vertical medium-lead burst neurons (VMLBs), which drive vertical rapid eye movements. Axons of upward VMLBs ramify bilaterally within motoneuron pools that supply the superior rectus and inferior oblique muscles of both eyes. Axons of downward VMLBs ramify ipsilaterally in the inferior rectus portion of the oculomotor nucleus and in the trochlear nucleus. Thus, VMLBs can drive vertical motoneuron pools of both eyes during conjugate vertical rapid eye movements; these data support Hering's law.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Moschovakis, A K -- Scudder, C A -- Highstein, S M -- EY-05433/EY/NEI NIH HHS/ -- EY-05954/EY/NEI NIH HHS/ -- NS-17763/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1990 Jun 1;248(4959):1118-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Neural Control, National Institute of Neurological Diseases and Stroke, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2343316" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Axons/ultrastructure ; Eye Movements/*physiology ; *Models, Neurological ; Motor Neurons/cytology/*physiology/ultrastructure ; Neural Pathways/anatomy & histology/cytology ; Oculomotor Muscles/*innervation ; Saimiri
    Print ISSN: 0036-8075
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  • 19
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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
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  • 20
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    Cell interactions in the sea urchin embryo studied by fluorescence photoablation (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-06-01
    Description: In many organisms, interactions between cells play a critical role in the specification of cell fates. In the sea urchin embryo, primary mesenchyme cells (PMCs) regulate the developmental program of a subpopulation of secondary mesenchyme cells (SMCs). The timing of this cell interaction was analyzed by means of a fluorescence photoablation technique, which was used to specifically ablate PMCs at various stages of development. In addition, the PMCs were microinjected into PMC-depleted recipient embryos at different developmental stages and their effect on SMC fate was examined. The critical interaction between PMCs and SMCs was brief and took place late in gastrulation. Before that time, SMCs were insensitive to the suppressive signals transmitted by the PMCs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ettensohn, C A -- HD24690/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1990 Jun 1;248(4959):1115-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, Carnegie Mellon University, Pittsburgh, PA 15213.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2188366" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Communication/*physiology ; Cell Survival/radiation effects ; Fluorescent Antibody Technique ; Fluorescent Dyes ; Light ; Mesoderm/*cytology/radiation effects ; Microinjections ; Rhodamines ; Sea Urchins/embryology
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