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  • Articles  (188)
  • Cells, Cultured  (175)
  • Chemistry
  • 1990-1994  (188)
  • Science. 247(4939): 189-92.  (1)
  • Science. 247(4939): 209-12.  (1)
  • Science. 247(4941): 456-9.  (1)
  • Science. 247(4941): 470-3.  (1)
  • Science. 247(4942): 559-61.  (1)
  • Science. 247(4944): 836-8.  (1)
  • Science. 247(4945): 925-9.  (1)
  • Science. 247(4946): 1067-9.  (1)
  • Science. 247(4948): 1328-30.  (1)
  • Science. 247(4949 Pt 1): 1385-6.  (1)
  • Science. 247(4949 Pt 1): 1446-51.  (1)
  • Science. 247(4949 Pt 1): 1454-7.  (1)
  • Science. 247(4950): 1578-81.  (1)
  • Science. 248(4952): 217-20.  (1)
  • Science. 248(4953): 364-7.  (1)
  • Science. 248(4954): 492-5.  (1)
  • Science. 248(4955): 607-10.  (1)
  • Science. 248(4957): 863-6.  (1)
  • Science. 248(4960): 1234-7.  (1)
  • Science. 248(4961): 1349-56.  (1)
  • 25
Collection
  • Articles  (188)
Years
Year
Journal
  • 1
    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
    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
    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
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
    Publication Date: 1990-09-28
    Description: Methodology has been developed that enables virtually complete purification and abundant recovery of early hematopoietic progenitors from normal human adult peripheral blood. A fraction of the pure progenitors is multipotent (generates mixed colonies) and exhibits self-renewal capacity (gives rise to blast cell colonies). This methodology provides a fundamental tool for basic and clinical studies on hematopoiesis. Optimal in vitro cloning of virtually pure progenitors requires not only the stimulatory effect of interleukin-3, granulocyte-macrophage colony-stimulating factor, and erythropoietin, but also the permissive action of basic fibroblast growth factor. These findings suggest a regulatory role for this growth factor in early hematopoiesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gabbianelli, M -- Sargiacomo, M -- Pelosi, E -- Testa, U -- Isacchi, G -- Peschle, C -- New York, N.Y. -- Science. 1990 Sep 28;249(4976):1561-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Hematology and Oncology, Istituto Superiore di Sanita, Rome, Italy.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2218497" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Antibodies, Monoclonal/immunology ; Cell Separation ; Cells, Cultured ; Clone Cells ; Erythropoietin/pharmacology ; Fibroblast Growth Factor 2/*pharmacology ; Granulocyte-Macrophage Colony-Stimulating Factor/pharmacology ; Hematopoietic Stem Cells/*cytology/drug effects ; Humans ; Interleukin-3/pharmacology ; Monocytes/*cytology/drug effects ; Recombinant Proteins/pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1990-08-03
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Waldrop, M M -- New York, N.Y. -- Science. 1990 Aug 3;249(4968):472-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2382127" target="_blank"〉PubMed〈/a〉
    Keywords: Chemical Phenomena ; Chemistry ; *Information Systems ; Jurisprudence ; Societies, Scientific ; United States
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
    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
    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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  • 6
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1990-11-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gibbons, A -- New York, N.Y. -- Science. 1990 Nov 2;250(4981):622-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2237413" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/*physiology ; Animals ; Cells, Cultured ; DNA Damage ; Free Radicals ; Humans ; Life Expectancy
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
    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
    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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  • 8
    Publication Date: 1990-03-16
    Description: Many proteins are initially synthesized as part of a large precursor. The role of the pro-region in the biosynthesis of transforming growth factor--beta 1 (TGF-beta 1) and activin A, two structurally related disulfide-linked homodimers synthesized as large precursors, was studied. Vectors that expressed either the pro-region or the mature regions of these molecules were used in complementation experiments, only when the pro-region was coexpressed with the mature region did intracellular dimerization and secretion of biologically active homodimers occur. The pro-regions of activin A and TGF-beta 1, therefore, aid the folding, disulfide bond formation, and export of their respective homodimers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gray, A M -- Mason, A J -- New York, N.Y. -- Science. 1990 Mar 16;247(4948):1328-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Developmental Biology, Genentech, Inc., South San Francisco, CA 94080.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2315700" target="_blank"〉PubMed〈/a〉
    Keywords: Activins ; Amino Acid Sequence ; Cells, Cultured ; Genetic Complementation Test ; Humans ; Inhibins/*biosynthesis/ultrastructure ; Macromolecular Substances ; Molecular Sequence Data ; Protein Processing, Post-Translational ; Protein Sorting Signals/physiology ; Transfection ; Transforming Growth Factors/*biosynthesis
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
    Publication Date: 1991-10-25
    Description: The presence of clathrate hydrates in cometary ice has been suggested to account for anomalous gas release at large radial distances from the sun as well as the retention of volatiles in comets to elevated temperatures. However, how clathrate hydrates can form in low-pressure environments, such as in cold interstellar molecular clouds, in the outer reaches of the early solar nebula, or in cometary ices, has been poorly understood. Experiments performed with the use of a modified electron microscope demonstrate that during the warming of vapor-deposited amorphous ices in vacuo, clathrate hydrates can form by rearrangements in the solid state. Phase separations and microporous textures that are the result of these rearrangements may account for a variety of anomalous cometary phenomena.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Blake, D -- Allamandola, L -- Sandford, S -- Hudgins, D -- Freund, F -- New York, N.Y. -- Science. 1991 Oct 25;254:548-51.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Planetary Biology Branch, Ames Research Center, Moffett Field, CA 94035, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11538372" target="_blank"〉PubMed〈/a〉
    Keywords: Chemical Phenomena ; Chemistry ; Crystallography ; Earth (Planet) ; Hydrocarbons/chemistry ; Ice/*analysis ; *Meteoroids ; Microscopy, Electron ; *Solar System
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
    Publication Date: 1991-11-08
    Description: Voltage-gated sodium channels are responsible for generation of action potentials in excitable cells. Activation of protein kinase C slows inactivation of sodium channels and reduces peak sodium currents. Phosphorylation of a single residue, serine 1506, that is located in the conserved intracellular loop between domains III and IV and is involved in inactivation of the sodium channel, is required for both modulatory effects. Mutant sodium channels lacking this phosphorylation site have normal functional properties in unstimulated cells but do not respond to activation of protein kinase C. Phosphorylation of this conserved site in sodium channel alpha subunits may regulate electrical activity in a wide range of excitable cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉West, J W -- Numann, R -- Murphy, B J -- Scheuer, T -- Catterall, W A -- GM07270/GM/NIGMS NIH HHS/ -- NS15751/NS/NINDS NIH HHS/ -- NS25704/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1991 Nov 8;254(5033):866-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of Washington, Seattle 98195.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1658937" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cell Membrane/physiology ; Cells, Cultured ; Membrane Potentials ; Models, Structural ; Molecular Sequence Data ; Phosphorylation ; Protein Conformation ; Protein Kinase C/*metabolism ; Sodium Channels/metabolism/*physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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