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  • Articles  (42)
  • Latest Papers from Table of Contents or Articles in Press  (42)
  • Cells, Cultured
  • 1990-1994  (42)
  • 1935-1939
  • 1992  (42)
  • Natural Sciences in General  (42)
  • Geography
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  • Articles  (42)
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  • Latest Papers from Table of Contents or Articles in Press  (42)
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  • 1990-1994  (42)
  • 1935-1939
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  • 1
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    Increased osteoclast development after estrogen loss: mediation by interleukin-6 (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-07-03
    Description: Osteoclasts, the cells that resorb bone, develop from hematopoietic precursors of the bone marrow under the control of factors produced in their microenvironment. The cytokine interleukin-6 can promote hematopoiesis and osteoclastogenesis. Interleukin-6 production by bone and marrow stromal cells is suppressed by 17 beta-estradiol in vitro. In mice, estrogen loss (ovariectomy) increased the number of colony-forming units for granulocytes and macrophages, enhanced osteoclast development in ex vivo cultures of marrow, and increased the number of osteoclasts in trabecular bone. These changes were prevented by 17 beta-estradiol or an antibody to interleukin-6. Thus, estrogen loss results in an interleukin-6-mediated stimulation of osteoclastogenesis, which suggests a mechanism for the increased bone resorption in postmenopausal osteoporosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jilka, R L -- Hangoc, G -- Girasole, G -- Passeri, G -- Williams, D C -- Abrams, J S -- Boyce, B -- Broxmeyer, H -- Manolagas, S C -- AI21761/AI/NIAID NIH HHS/ -- AR41313/AR/NIAMS NIH HHS/ -- CA36464/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1992 Jul 3;257(5066):88-91.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Veterans Affairs Medical Center, Indiana University School of Medicine, Indianapolis 46202.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1621100" target="_blank"〉PubMed〈/a〉
    Keywords: Analysis of Variance ; Animals ; Antibodies, Monoclonal ; Bone Marrow Cells ; Cells, Cultured ; Estradiol/*pharmacology ; Female ; Granulocyte-Macrophage Colony-Stimulating Factor/pharmacology ; Immunoglobulin G ; Interleukin-6/immunology/*physiology ; Mice ; Osteoclasts/*cytology/drug effects ; *Ovariectomy ; Recombinant Proteins/pharmacology ; Spleen/cytology ; Stem Cells/cytology/drug effects
    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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    High probability opening of NMDA receptor channels by L-glutamate (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-01-24
    Description: Synaptic plasticity can be triggered by calcium flux into neurons through synaptically activated N-methyl-D-aspartate (NMDA) receptor channels. The amplitude and time course of the resulting intracellular calcium transient depend on the number of open NMDA receptor channels and the kinetics of their activation. Short applications of L-glutamate to outside-out patches from hippocampal neurons in the presence and absence of MK-801 revealed that about 30 percent of L-glutamate-bound channels are open at the peak of the current. This high probability of opening suggests that very few channels are required to guarantee a large, localized postsynaptic calcium transient.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jahr, C E -- NS21419/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1992 Jan 24;255(5043):470-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Vollum Institute L474, Oregon Health Sciences University, Portland 97201.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1346477" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Cells, Cultured ; Dizocilpine Maleate/pharmacology ; Glutamates/*physiology ; Glutamic Acid ; Hippocampus/physiology ; In Vitro Techniques ; *Ion Channel Gating ; Rats ; Receptors, N-Methyl-D-Aspartate/*physiology
    Print ISSN: 0036-8075
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  • 3
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    Chondroitin sulfate as a regulator of neuronal patterning in the retina (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-02-07
    Description: Highly sulfated proteoglycans are correlated with axon boundaries in the developing central nervous system which suggests that these molecules affect neural pattern formation. In the developing mammalian retina, gradual regression of chondroitin sulfate may help control the onset of ganglion cell differentiation and initial direction of their axons. Changes induced by the removal of chondroitin sulfate from intact retinas in culture confirm the function of chondroitin sulfate in retinal histogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brittis, P A -- Canning, D R -- Silver, J -- New York, N.Y. -- Science. 1992 Feb 7;255(5045):733-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurosciences, Case Western Reserve University, Cleveland, OH 44106.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1738848" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/physiology ; Cell Differentiation/drug effects ; Cells, Cultured ; Chondroitin Lyases/pharmacology ; Chondroitin Sulfate Proteoglycans/pharmacology ; Chondroitin Sulfates/analysis/*physiology ; Immunohistochemistry ; Rats ; Retina/chemistry/cytology/*embryology ; Retinal Ganglion Cells/chemistry/*cytology ; Tubulin/analysis
    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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    Interleukin-8 as a macrophage-derived mediator of angiogenesis (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-12-11
    Description: Angiogenic factors produced by monocytes-macrophages are involved in the pathogenesis of chronic inflammatory disorders characterized by persistent angiogenesis. The possibility was tested that interleukin-8 (IL-8), which is a cytokine that is chemotactic for lymphocytes and neutrophils, is also angiogenic. Human recombinant IL-8 was potently angiogenic when implanted in the rat cornea and induced proliferation and chemotaxis of human umbilical vein endothelial cells. Angiogenic activity present in the conditioned media of inflamed human rheumatoid synovial tissue macrophages or lipopolysaccharide-stimulated blood monocytes was equally blocked by antibodies to either IL-8 or tumor necrosis factor-alpha. An IL-8 antisense oligonucleotide specifically blocked the production of monocyte-induced angiogenic activity. These data suggest a function for macrophage-derived IL-8 in angiogenesis-dependent disorders such as rheumatoid arthritis, tumor growth, and wound repair.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koch, A E -- Polverini, P J -- Kunkel, S L -- Harlow, L A -- DiPietro, L A -- Elner, V M -- Elner, S G -- Strieter, R M -- AR30692/AR/NIAMS NIH HHS/ -- AR41492/AR/NIAMS NIH HHS/ -- HL39926/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1992 Dec 11;258(5089):1798-801.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Northwestern University Medical School, Chicago, IL 60611.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1281554" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arthritis, Rheumatoid/physiopathology ; Base Sequence ; Cell Division/drug effects ; Cells, Cultured ; Chemotaxis/*drug effects ; Cornea/*drug effects/physiology ; Dose-Response Relationship, Drug ; Endothelium, Vascular/drug effects/*physiology ; Fibroblast Growth Factor 2/pharmacology ; Humans ; Interleukin-8/genetics/*pharmacology ; Macrophages/*physiology ; Mice ; Molecular Sequence Data ; Monocytes/physiology ; *Neovascularization, Pathologic ; Oligonucleotides, Antisense/*pharmacology ; Rabbits ; Rats ; Recombinant Proteins/pharmacology ; Synovial Fluid/physiology ; Tumor Necrosis Factor-alpha/genetics ; Umbilical Veins
    Print ISSN: 0036-8075
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  • 5
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    Flow-dependent cytosolic acidification of vascular endothelial cells (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-10-23
    Description: Hemodynamic shear stress affects endothelial cell structure and function, but little is known about the signal transduction mechanisms involved in these processes. The effect of laminar shear stress on cytosolic pH (pHi) was examined in rat aortic endothelial cells cultured in glass capillary tubes. Shear stress forces led to a rapid decrease in pHi (maximal effect 0.09 pH unit at 13.4 dynes per square centimeter). Removal of specific ions or addition of exchange inhibitors suggests that in vascular endothelial cells shear stress forces activate both an alkali extruder, sodium ion-independent chloride-bicarbonate ion exchange, and an acid extruder, sodium-hydrogen ion exchange; the net effect in physiologic buffer with the bicarbonate ion is a decrease in pHi.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ziegelstein, R C -- Cheng, L -- Capogrossi, M C -- New York, N.Y. -- Science. 1992 Oct 23;258(5082):656-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Cardiovascular Science, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1329207" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bicarbonates/metabolism ; Carrier Proteins/physiology ; Cells, Cultured ; Chloride-Bicarbonate Antiporters ; Cytosol/*physiology ; Endothelium, Vascular/*physiology ; Hydrogen-Ion Concentration ; Membrane Proteins/physiology ; Rats ; Signal Transduction/physiology ; Sodium-Hydrogen Antiporter ; Stress, Mechanical
    Print ISSN: 0036-8075
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  • 6
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    Potocytosis: sequestration and transport of small molecules by caveolae (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-01-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Anderson, R G -- Kamen, B A -- Rothberg, K G -- Lacey, S W -- New York, N.Y. -- Science. 1992 Jan 24;255(5043):410-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1310359" target="_blank"〉PubMed〈/a〉
    Keywords: Carrier Proteins/physiology ; Cell Membrane/*physiology/ultrastructure ; Cells, Cultured ; *Endocytosis ; Folate Receptors, GPI-Anchored ; Folic Acid/metabolism ; Glycolipids/physiology ; Glycosylphosphatidylinositols ; In Vitro Techniques ; Membrane Glycoproteins/physiology ; Phosphatidylinositols/physiology ; Receptors, Cell Surface/physiology
    Print ISSN: 0036-8075
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  • 7
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    The time course of glutamate in the synaptic cleft (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-11-27
    Description: The peak concentration and rate of clearance of neurotransmitter from the synaptic cleft are important determinants of synaptic function, yet the neurotransmitter concentration time course is unknown at synapses in the brain. The time course of free glutamate in the cleft was estimated by kinetic analysis of the displacement of a rapidly dissociating competitive antagonist from N-methyl-D-aspartate (NMDA) receptors during synaptic transmission. Glutamate peaked at 1.1 millimolar and decayed with a time constant of 1.2 milliseconds at cultured hippocampal synapses. This time course implies that transmitter saturates postsynaptic NMDA receptors. However, glutamate dissociates much more rapidly from alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors. Thus, the time course of free glutamate predicts that dissociation contributes to the decay of the AMPA receptor-mediated postsynaptic current.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Clements, J D -- Lester, R A -- Tong, G -- Jahr, C E -- Westbrook, G L -- MH46613/MH/NIMH NIH HHS/ -- NS21419/NS/NINDS NIH HHS/ -- NS26494/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1992 Nov 27;258(5087):1498-501.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Vollum Institute, Oregon Health Sciences University, Portland 97201.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1359647" target="_blank"〉PubMed〈/a〉
    Keywords: 2-Aminoadipic Acid/pharmacology ; Action Potentials/physiology ; Animals ; Cells, Cultured ; Glutamates/*metabolism ; Glutamic Acid ; Hippocampus/cytology/physiology ; Models, Neurological ; Neurons/physiology ; Neurotransmitter Agents/*metabolism ; Piperazines/pharmacology ; Rats ; Receptors, N-Methyl-D-Aspartate/drug effects/physiology ; Synapses/drug effects/*metabolism ; Time Factors
    Print ISSN: 0036-8075
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  • 8
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    Harpin, elicitor of the hypersensitive response produced by the plant pathogen Erwinia amylovora (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-07-03
    Description: A proteinaceous elicitor of the plant defense reaction known as the hypersensitive response was isolated from Erwinia amylovora, the bacterium that causes fire blight of pear, apple, and other rosaceous plants. The elicitor, named harpin, is an acidic, heat-stable, cell-envelope-associated protein with an apparent molecular weight of 44 kilodaltons. Harpin caused tobacco leaf lamina to collapse and caused an increase in the pH of bathing solutions of suspension-cultured tobacco cells. The gene encoding harpin (hrpN) was located in the 40-kilobase hrp gene cluster of E. amylovora, sequenced, and mutated with Tn5tac1. The hrpN mutants were not pathogenic to pear, did not elicit the hypersensitive response, and did not produce harpin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wei, Z M -- Laby, R J -- Zumoff, C H -- Bauer, D W -- He, S Y -- Collmer, A -- Beer, S V -- New York, N.Y. -- Science. 1992 Jul 3;257(5066):85-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Plant Pathology, Cornell University, Ithaca, NY 14853.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1621099" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; *Bacterial Outer Membrane Proteins ; Bacterial Proteins/*genetics/isolation & purification/metabolism ; Cells, Cultured ; Erwinia/genetics/pathogenicity/*physiology ; Escherichia coli/genetics ; *Genes, Bacterial ; Membrane Proteins/*genetics/isolation & purification/metabolism ; Molecular Sequence Data ; *Multigene Family ; Plants, Toxic ; Restriction Mapping ; Tobacco/microbiology
    Print ISSN: 0036-8075
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  • 9
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    GAP domains responsible for ras p21-dependent inhibition of muscarinic atrial K+ channel currents (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-01-10
    Description: The interaction between the low molecular weight G protein ras p21 and a guanosine triphosphatase activating protein (GAP) uncouples a heterotrimeric G protein (Gk) from muscarinic receptors. Through the use of isolated atrial cell membranes and genetically engineered GAP deletion mutants, the src homology regions (SH2-SH3) at the amino terminus of GAP have been identified as the domains responsible for this effect. Deletion of the domain required to stimulate the guanosine triphosphatase activity of ras p21 relieves the requirement for ras p21 in this system. A model is presented that suggests that ras p21 induces a conformational change in GAP, which allows the SH2-SH3 regions of GAP to function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Martin, G A -- Yatani, A -- Clark, R -- Conroy, L -- Polakis, P -- Brown, A M -- McCormick, F -- CA51992-01/CA/NCI NIH HHS/ -- HL36930/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1992 Jan 10;255(5041):192-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Cetus Corporation, Emeryville, CA 94608.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1553544" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Baculoviridae ; Cell Membrane/metabolism ; Cells, Cultured ; Cloning, Molecular ; GTP-Binding Proteins/*physiology ; GTPase-Activating Proteins ; Genetic Engineering ; Genetic Vectors ; Guanosine 5'-O-(3-Thiotriphosphate)/pharmacology ; Guanosine Triphosphate/pharmacology ; Guinea Pigs ; Heart/*physiology ; Heart Atria ; Models, Biological ; Polymerase Chain Reaction ; Potassium Channels/drug effects/*physiology ; Proteins/genetics/*physiology ; Proto-Oncogene Proteins p21(ras)/*metabolism ; Receptors, Muscarinic/drug effects/*physiology ; ras GTPase-Activating Proteins
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  • 10
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    Calcium-permeable AMPA-kainate receptors in fusiform cerebellar glial cells (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-06-12
    Description: Glutamate-operated ion channels (GluR channels) of the L-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)-kainate subtype are found in both neurons and glial cells of the central nervous system. These channels are assembled from the GluR-A, -B, -C, and -D subunits; channels containing a GluR-B subunit show an outwardly rectifying current-voltage relation and low calcium permeability, whereas channels lacking the GluR-B subunit are characterized by a doubly rectifying current-voltage relation and high calcium permeability. Most cell types in the central nervous system coexpress several subunits, including GluR-B. However, Bergmann glia in rat cerebellum do not express GluR-B subunit genes. In a subset of cultured cerebellar glial cells, likely derived from Bergmann glial cells. GluR channels exhibit doubly rectifying current-voltage relations and high calcium permeability, whereas GluR channels of cerebellar neurons have low calcium permeability. Thus, differential expression of the GluR-B subunit gene in neurons and glia is one mechanism by which functional properties of native GluR channels are regulated.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Burnashev, N -- Khodorova, A -- Jonas, P -- Helm, P J -- Wisden, W -- Monyer, H -- Seeburg, P H -- Sakmann, B -- New York, N.Y. -- Science. 1992 Jun 12;256(5063):1566-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max-Planck-Institut fur Medizinische Forschung, Abteilung Zellphysiologie, Heidelberg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1317970" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/*metabolism ; Cell Membrane Permeability ; Cells, Cultured ; Cerebellum/*physiology ; Gene Expression ; Glutamates/physiology ; In Vitro Techniques ; Ion Channel Gating ; Neuroglia/*physiology ; Nucleic Acid Hybridization ; RNA, Messenger/genetics ; Rats ; Receptors, Kainic Acid ; Receptors, Neurotransmitter/*physiology
    Print ISSN: 0036-8075
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  • 11
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    Cloning and characterization of inducible nitric oxide synthase from mouse macrophages (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-04-10
    Description: Nitric oxide (NO) conveys a variety of messages between cells, including signals for vasorelaxation, neurotransmission, and cytotoxicity. In some endothelial cells and neurons, a constitutive NO synthase is activated transiently by agonists that elevate intracellular calcium concentrations and promote the binding of calmodulin. In contrast, in macrophages, NO synthase activity appears slowly after exposure of the cells to cytokines and bacterial products, is sustained, and functions independently of calcium and calmodulin. A monospecific antibody was used to clone complementary DNA that encoded two isoforms of NO synthase from immunologically activated mouse macrophages. Liquid chromatography-mass spectrometry was used to confirm most of the amino acid sequence. Macrophage NO synthase differs extensively from cerebellar NO synthase. The macrophage enzyme is immunologically induced at the transcriptional level and closely resembles the enzyme in cytokine-treated tumor cells and inflammatory neutrophils.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Xie, Q W -- Cho, H J -- Calaycay, J -- Mumford, R A -- Swiderek, K M -- Lee, T D -- Ding, A -- Troso, T -- Nathan, C -- AI30165/AI/NIAID NIH HHS/ -- CA43610/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1992 Apr 10;256(5054):225-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Beatrice and Samuel A. Seaver Laboratory, Department of Medicine, Cornell University Medical College, New York, NY 10021.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1373522" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Oxidoreductases/biosynthesis/*genetics ; Amino Acid Sequence ; Animals ; Base Sequence ; Cell Line ; Cells, Cultured ; Cloning, Molecular ; Codon ; Enzyme Induction ; Interferon-gamma/pharmacology ; Isoenzymes/biosynthesis/*genetics ; Kinetics ; Lipopolysaccharides ; Macrophages/drug effects/*enzymology ; Mammary Neoplasms, Experimental ; Mice ; Molecular Sequence Data ; Molecular Weight ; Neutrophils/drug effects/enzymology ; Nitric Oxide Synthase ; Oligodeoxyribonucleotides ; Poly A/genetics ; RNA/genetics ; RNA, Messenger ; Rats ; Sequence Homology, Nucleic Acid ; Transcription, Genetic
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  • 12
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    IP3 receptor: localization to plasma membrane of T cells and cocapping with the T cell receptor (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-08-07
    Description: Immune responses in lymphocytes require cellular accumulation of large amounts of calcium (Ca2+) from extracellular sources. In the T cell tumor line Jurkat, receptors for the Ca(2+)-releasing messenger inositol 1,4,5-trisphosphate (IP3) were localized to the plasma membrane (PM). Capping of the T cell receptor-CD3 complex, which is associated with signal transduction, was accompanied by capping of IP3 receptors. The IP3 receptor on T cells appears to be responsible for the entry of Ca2+ that initiates proliferative responses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Khan, A A -- Steiner, J P -- Klein, M G -- Schneider, M F -- Snyder, S H -- DA-00074/DA/NIDA NIH HHS/ -- MH-18501/MH/NIMH NIH HHS/ -- P01-HL27867/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1992 Aug 7;257(5071):815-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Johns Hopkins University School of Medicine, Department of Neuroscience, Baltimore, MD 21205.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1323146" target="_blank"〉PubMed〈/a〉
    Keywords: Antigens, CD/metabolism ; Antigens, CD3 ; Antigens, Differentiation, T-Lymphocyte/analysis/*metabolism ; Burkitt Lymphoma ; Calcium/*metabolism ; *Calcium Channels ; Cell Line ; Cell Membrane/*metabolism ; Cells, Cultured ; Concanavalin A/pharmacology ; Fluorescent Antibody Technique ; Humans ; Inositol 1,4,5-Trisphosphate/*metabolism ; Inositol 1,4,5-Trisphosphate Receptors ; Kinetics ; Receptors, Antigen, T-Cell/analysis/*metabolism ; Receptors, Cell Surface/analysis/*metabolism ; *Receptors, Cytoplasmic and Nuclear ; Second Messenger Systems ; T-Lymphocytes/*immunology
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  • 13
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    Modulation of an NCAM-related adhesion molecule with long-term synaptic plasticity in Aplysia (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-05-01
    Description: A form of learning in the marine mollusk Aplysia, long-term sensitization of the gill- and siphon-withdrawal reflex, results in the formation of new synaptic connections between the presynaptic siphon sensory neurons and their target cells. These structural changes can be mimicked, when the cells are maintained in culture, by application of serotonin, an endogenous facilitating neurotransmitter in Aplysia. A group of cell surface proteins, designated Aplysia cell adhesion molecules (apCAM's) was down-regulated in the sensory neurons in response to serotonin. The deduced amino acid sequence obtained from complementary DNA clones indicated that the apCAM's are a family of proteins that seem to arise from a single gene. The apCAM's are members of the immunoglobulin class of cell adhesion molecules and resemble two neural cell adhesion molecules, NCAM and fasciclin II. In addition to regulating newly synthesized apCAM, serotonin also altered the amount of preexisting apCAM on the cell surface of the presynaptic sensory neurons. By contrast, the apCAM on the surface of the postsynaptic motor neuron was not modulated by serotonin. This rapid, transmitter-mediated down-regulation of a cell adhesion molecule in the sensory neurons may be one of the early molecular changes in long-term synaptic facilitation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mayford, M -- Barzilai, A -- Keller, F -- Schacher, S -- Kandel, E R -- New York, N.Y. -- Science. 1992 May 1;256(5057):638-44.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, College of Physicians and Surgeons of Columbia University, New York, NY 10032.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1585176" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Aplysia/*metabolism ; Blotting, Northern ; Cell Adhesion Molecules, Neuronal/chemistry/genetics/*metabolism ; Cells, Cultured ; Cloning, Molecular ; DNA/chemistry/genetics ; Fluorescent Antibody Technique ; Molecular Sequence Data ; Motor Neurons/drug effects/metabolism ; Neuronal Plasticity/*physiology ; Neurons, Afferent/drug effects/metabolism ; Protein Sorting Signals/chemistry ; Serotonin/pharmacology ; Synapses/*physiology
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  • 14
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    Cell biology. A new kind of organic gardening (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-11-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Amato, I -- New York, N.Y. -- Science. 1992 Nov 13;258(5085):1084.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1439816" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Adhesion ; Cell Division ; *Cell Physiological Phenomena ; Cells, Cultured ; Electronics
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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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    The cytosensor microphysiometer: biological applications of silicon technology (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-09-25
    Description: A silicon-based device, dubbed a microphysiometer, can be used to detect and monitor the response of cells to a variety of chemical substances, especially ligands for specific plasma membrane receptors. The microphysiometer measures the rate of proton excretion from 10(4) to 10(6) cells. This article gives an overview of experiments currently being carried out with this instrument with emphasis on receptors with seven transmembrane helices and tyrosine kinase receptors. As a scientific instrument, the microphysiometer can be thought of as serving two distinct functions. In terms of detecting specific molecules, selected biological cells in this instrument serve as detectors and amplifiers. The microphysiometer can also investigate cell function and biochemistry. A major application of this instrument may prove to be screening for new receptor ligands. In this respect, the microphysiometer appears to offer significant advantages over other techniques.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McConnell, H M -- Owicki, J C -- Parce, J W -- Miller, D L -- Baxter, G T -- Wada, H G -- Pitchford, S -- New York, N.Y. -- Science. 1992 Sep 25;257(5078):1906-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry, Stanford University, CA 94305.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1329199" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biotechnology ; *Cell Physiological Phenomena ; Cells, Cultured ; Culture Media ; HIV Infections/physiopathology ; Humans ; *Hydrogen-Ion Concentration ; In Vitro Techniques ; Potentiometry/*instrumentation ; Receptors, Cell Surface/physiology ; Silicon
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  • 16
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    Programmed death of T cells in HIV-1 infection (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-07-10
    Description: In human immunodeficiency virus (HIV) infection, functional defects and deletion of antigen-reactive T cells are more frequent than can be explained by direct viral infection. On culturing, both CD4+ and CD8+ T cells from asymptomatic HIV-infected individuals died as a result of programmed cell death (apoptosis). Apoptosis was enhanced by activation with CD3 antibodies. Programmed cell death, associated with impaired T cell reactivity, may thus be responsible for the deletion of reactive T cells that contributes to HIV-induced immunodeficiency.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Meyaard, L -- Otto, S A -- Jonker, R R -- Mijnster, M J -- Keet, R P -- Miedema, F -- New York, N.Y. -- Science. 1992 Jul 10;257(5067):217-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Clinical Viro-Immunology, Central Laboratory of The Netherlands Red Cross Blood Transfusion Service, Amsterdam.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1352911" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/*pathology ; Antigens, CD/physiology ; Antigens, CD8/immunology ; CD4-Positive T-Lymphocytes/pathology ; Cell Death/physiology ; Cell Division/immunology ; Cells, Cultured ; HIV Envelope Protein gp120/physiology ; *Hiv-1 ; Humans ; Male ; Microscopy, Electron ; T-Lymphocytes/*pathology ; Zinc/pharmacology
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  • 17
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    Generation of neurons and astrocytes from isolated cells of the adult mammalian central nervous system (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-03-27
    Description: Neurogenesis in the mammalian central nervous system is believed to end in the period just after birth; in the mouse striatum no new neurons are produced after the first few days after birth. In this study, cells isolated from the striatum of the adult mouse brain were induced to proliferate in vitro by epidermal growth factor. The proliferating cells initially expressed nestin, an intermediate filament found in neuroepithelial stem cells, and subsequently developed the morphology and antigenic properties of neurons and astrocytes. Newly generated cells with neuronal morphology were immunoreactive for gamma-aminobutyric acid and substance P, two neurotransmitters of the adult striatum in vivo. Thus, cells of the adult mouse striatum have the capacity to divide and differentiate into neurons and astrocytes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Reynolds, B A -- Weiss, S -- New York, N.Y. -- Science. 1992 Mar 27;255(5052):1707-10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, University of Calgary Faculty of Medicine, Alberta, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1553558" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Astrocytes/*cytology ; Cell Division/drug effects ; Cell Survival/drug effects ; Cells, Cultured ; Corpus Striatum/*cytology ; Culture Media, Serum-Free ; Epidermal Growth Factor/pharmacology ; Fluorescent Antibody Technique ; Glial Fibrillary Acidic Protein/metabolism ; In Vitro Techniques ; Intermediate Filament Proteins/metabolism ; Intermediate Filaments/metabolism ; Mice ; *Nerve Tissue Proteins ; Nestin ; Neurons/*cytology ; Phosphopyruvate Hydratase/metabolism
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  • 18
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    Selective role of N-type calcium channels in neuronal migration (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-08-07
    Description: Analysis of neuronal migration in mouse cerebellar slice preparations by a laser scanning confocal microscope revealed that postmitotic granule cells initiate their migration only after the expression of N-type calcium channels on their plasmalemmal surface. Furthermore, selective blockade of these channels by addition of omega-conotoxin to the incubation medium curtailed cell movement. In contrast, inhibitors of L- and T-type calcium channels, as well as those of sodium and potassium channels, had no effect on the rate of granule cell migration. These results suggest that N-type calcium channels, which have been predominantly associated with neurotransmitter release in adult brain, also play a transient but specific developmental role in directed migration of immature neurons before the establishment of their synaptic circuits.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Komuro, H -- Rakic, P -- New York, N.Y. -- Science. 1992 Aug 7;257(5071):806-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Neurobiology, 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/1323145" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/pharmacology ; Calcium Channels/drug effects/*physiology ; Cell Movement/drug effects ; Cells, Cultured ; Cerebellum/cytology/*physiology ; In Vitro Techniques ; Kinetics ; Mice ; Mollusk Venoms/pharmacology ; Neurons/cytology/drug effects/*physiology ; Peptides, Cyclic/pharmacology ; Time Factors ; *omega-Conotoxins
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  • 19
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    Defective epithelial chloride transport in a gene-targeted mouse model of cystic fibrosis (1992)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1992-08-21
    Description: The cystic fibrosis transmembrane conductance regulator (CFTR) gene encodes an adenosine 3',5'-monophosphate (cyclic AMP)-activated chloride channel. In cystic fibrosis (CF) patients, loss of CFTR function because of a genetic mutation results in defective cyclic AMP-mediated chloride secretion across epithelia. Because of their potential role as an animal model for CF, mice with targeted disruption of the murine CFTR gene [CFTR(-/-)] were tested for abnormalities in epithelial chloride transport. In both freshly excised tissue from the intestine and in cultured epithelia from the proximal airways, the cyclic AMP-activated chloride secretory response was absent in CFTR(-/-) mice as compared to littermate controls. Thus, disruption of the murine CFTR gene results in the chloride transport abnormalities predicted from studies of human CF epithelia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Clarke, L L -- Grubb, B R -- Gabriel, S E -- Smithies, O -- Koller, B H -- Boucher, R C -- GM20069/GM/NIGMS NIH HHS/ -- HL 42384/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1992 Aug 21;257(5073):1125-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of North Carolina, Chapel Hill 27514.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1380724" target="_blank"〉PubMed〈/a〉
    Keywords: Amiloride/pharmacology ; Animals ; Biological Transport ; Cells, Cultured ; Chlorides/*metabolism ; Colforsin/pharmacology ; Cyclic AMP/pharmacology ; Cystic Fibrosis/genetics/*metabolism ; Cystic Fibrosis Transmembrane Conductance Regulator ; *Disease Models, Animal ; Epithelium/metabolism ; Intestines/metabolism ; Membrane Proteins/genetics/*physiology ; Mice ; Mutation ; Nose/metabolism ; Trachea/metabolism
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  • 20
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    Hebbian depression of isolated neuromuscular synapses in vitro (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-06-12
    Description: Modulation of synaptic efficacy may depend on the temporal correlation between pre- and postsynaptic activities. At isolated neuromuscular synapses in culture, repetitive postsynaptic application of acetylcholine pulses alone or in the presence of asynchronous presynaptic activity resulted in immediate and persistent synaptic depression, whereas synchronous pre- and postsynaptic coactivation had no effect. This synaptic depression was a result of a reduction of evoked transmitter release, but induction of the depression requires a rise in postsynaptic cytosolic calcium concentration. Thus, Hebbian modulation operates at isolated peripheral synapses in vitro, and transsynaptic retrograde interaction appears to be an underlying mechanism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dan, Y -- Poo, M M -- NS 22764/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1992 Jun 12;256(5063):1570-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, Columbia University, New York, NY 10027.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1317971" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; In Vitro Techniques ; Neural Inhibition ; Neuromuscular Junction/*physiology ; *Synaptic Transmission ; Xenopus laevis
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  • 21
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    Sporogonic development of a malaria parasite in vitro (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-01-24
    Description: The sporogonic cycle of the avian malaria parasite Plasmodium gallinaceum was completed in vitro. Ookinetes (motile zygotes) were seeded onto a murine basement membrane-like gel (Matrigel) in coculture with Drosophila melanogaster cells (Schneider's L2). Transformation into oocysts as well as subsequent growth and differentiation were observed in parasites attached to Matrigel and depended on the presence of L2 cells. Sporozoites were first observed on day 10 in culture. Specific circumsporozoite protein antigenicity was identified in mature oocysts and in sporozoites. It is now possible to follow the entire life cycle of Plasmodium in vitro.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Warburg, A -- Miller, L H -- New York, N.Y. -- Science. 1992 Jan 24;255(5043):448-50.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Malaria 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/1734521" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Protozoan/metabolism ; Cells, Cultured ; Drosophila melanogaster/cytology ; Extracellular Matrix ; In Vitro Techniques ; Microscopy, Electron ; Plasmodium/*growth & development/ultrastructure ; *Protozoan Proteins
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    Initiation of deregulated growth of multipotent progenitor cells by bcr-abl in vitro (1992)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1992-05-08
    Description: Expression of the bcr-abl oncogene in multipotent progenitor cells (MPPCs) is implicated as a key event in the development of chronic myelogenous leukemia. Bone marrow enriched for MPPCs was infected with a retrovirus that carried bcr-abl. The mixed-lineage colonies that resulted were responsive to growth factors and could differentiate. These cells later became growth factor-independent but, when injected into severe combined immunodeficient mice, were not leukemogenic. Thus, the presence of bcr-abl alone does not cause growth factor independence, although it initiates a stepwise process. This system may prove useful in the study of other oncogenes that cause leukemia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gishizky, M L -- Witte, O N -- New York, N.Y. -- Science. 1992 May 8;256(5058):836-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Molecular Genetics, University of California, Los Angeles 90024.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1375394" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bone Marrow/drug effects ; Bone Marrow Cells ; Cell Differentiation/drug effects ; Cell Division/drug effects ; Cells, Cultured ; Clone Cells ; Drug Resistance, Microbial/genetics ; Fluorouracil/pharmacology ; Fusion Proteins, bcr-abl/*genetics ; Hematopoietic Cell Growth Factors/pharmacology ; Hematopoietic Stem Cells/*cytology/drug effects/physiology ; Humans ; Interleukin-3/pharmacology ; Macrophages/cytology/drug effects ; Mast Cells/cytology/drug effects ; Mice ; Rats ; Retroviridae/genetics ; Stem Cell Factor ; Transfection
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  • 23
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    Identification of the Ah receptor nuclear translocator protein (Arnt) as a component of the DNA binding form of the Ah receptor (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-05-22
    Description: The Ah (dioxin) receptor binds a number of widely disseminated environmental pollutants, including 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and polycyclic aromatic hydrocarbons, and mediates their carcinogenic effects. The ligand-bound receptor activates Cyp 1a1 gene transcription through interaction with specific DNA sequences, termed xenobiotic responsive elements (XREs). The Ah receptor nuclear translocator protein (Arnt) is required for Ah receptor function. Arnt is now shown to be a structural component of the XRE binding form of the Ah receptor. Furthermore, Arnt and the ligand-binding subunit of the receptor were extracted as a complex from the nuclei of cells treated with ligand. Arnt contains a basic helix-loop-helix motif, which may be responsible for interacting with both the XRE and the ligand-binding subunit.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Reyes, H -- Reisz-Porszasz, S -- Hankinson, O -- CA 28868/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1992 May 22;256(5060):1193-5.〈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/1317062" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies ; Aryl Hydrocarbon Receptor Nuclear Translocator ; Base Sequence ; Cell Line ; Cells, Cultured ; Cytochrome P-450 Enzyme System/genetics ; DNA/genetics/metabolism ; DNA-Binding Proteins/genetics/isolation & purification/*metabolism ; Humans ; Hydrocarbons/metabolism ; Mice ; Molecular Sequence Data ; Oligodeoxyribonucleotides ; Proteins/genetics/isolation & purification/*metabolism ; Receptors, Aryl Hydrocarbon ; Receptors, Drug/genetics/isolation & purification/*metabolism ; Recombinant Proteins/isolation & purification/metabolism ; Tetrachlorodibenzodioxin/metabolism ; *Transcription Factors ; Transcription, Genetic ; Transfection
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  • 24
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    Actin filament dynamics in living glial cells imaged by atomic force microscopy (1992)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1992-09-25
    Description: Observation of filamentous actin (F-actin) in living cells is currently limited to the resolution of the light microscope. Higher resolution procedures require sample fixation and preclude dynamic studies. The atomic force microscope (AFM) can image and manipulate samples at very high, sometimes atomic resolution by scanning a fine tip over the surface of interest and detecting physical interactions between the tip and sample. This study demonstrates that F-actin can be readily resolved in living cells with the AFM and that the dynamic properties of F-actin are easily observed.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Henderson, E -- Haydon, P G -- Sakaguchi, D S -- New York, N.Y. -- Science. 1992 Sep 25;257(5078):1944-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Zoology and Genetics, Iowa State University, Ames 50011.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1411511" target="_blank"〉PubMed〈/a〉
    Keywords: Actin Cytoskeleton/*ultrastructure ; Actins/*physiology ; Animals ; *Cell Movement ; Cells, Cultured ; In Vitro Techniques ; Membrane Fluidity ; Microscopy/*methods ; Neuroglia/*ultrastructure ; Xenopus laevis
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  • 25
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    Burst firing in dopamine neurons induced by N-methyl-D-aspartate: role of electrogenic sodium pump (1992)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1992-10-23
    Description: Dopamine-containing neurons of the mammalian midbrain are required for normal behavior and movements. In vivo they fire action potentials in bursts, but in vitro they discharge regularly spaced action potentials. Burst firing in vitro has now been shown to be robustly induced by the glutamate agonist N-methyl-D-aspartate (NMDA) although not by the non-NMDA agonists kainate or quisqualate. The hyperpolarization between bursts of action potentials results from electrogenic sodium ion extrusion by a ouabain-sensitive pump. This mechanism of burst generation in mammalian neurons may be important in the pathophysiology of schizophrenia and Parkinson's disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Johnson, S W -- Seutin, V -- North, R A -- New York, N.Y. -- Science. 1992 Oct 23;258(5082):665-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Vollum Institute, Oregon Health Sciences University, Portland 97201.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1329209" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials/physiology ; Animals ; Cells, Cultured ; Dopamine/*physiology ; Kainic Acid/pharmacology ; N-Methylaspartate/*pharmacology ; Neurons/*drug effects/physiology ; Quisqualic Acid/pharmacology ; Rats ; Sodium/physiology ; Sodium-Potassium-Exchanging ATPase/*physiology ; Synaptic Transmission/*physiology
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  • 26
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    Intercellular propagation of calcium waves mediated by inositol trisphosphate (1992)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1992-10-09
    Description: Two types of calcium (Ca2+) signaling-propagating intercellular Ca2+ waves of increasing intracellular Ca2+ concentration ([Ca2+]i) and nonpropagating oscillations in [Ca2+]i-co-exist in a variety of cell types. To investigate this difference in Ca2+ signaling, airway epithelial cells were loaded with heparin, an inositol 1,4,5-triphosphate (IP3) receptor antagonist, by pulsed, high-frequency electroporation. Heparin inhibited propagation of intercellular Ca2+ waves but not oscillations of [Ca2+]i. In heparin-free cells, Ca2+ waves propagated through cells displaying [Ca2+]i oscillations. Depletion of intracellular Ca2+ pools with the Ca2+-pump inhibitor thapsigargin also inhibited the propagation of Ca2+ waves. These studies demonstrate that the release of Ca2+ by IP3 is necessary for the propagation of intercellular Ca2+ waves and suggest that IP3 moves through gap junctions to communicate intercellular Ca2+ waves.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Boitano, S -- Dirksen, E R -- Sanderson, M J -- New York, N.Y. -- Science. 1992 Oct 9;258(5080):292-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy, UCLA School of Medicine, CA 90024.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1411526" target="_blank"〉PubMed〈/a〉
    Keywords: Calcium/*metabolism ; Cells, Cultured ; Chondroitin Sulfates/pharmacology ; Electric Stimulation ; Epithelium/drug effects/metabolism ; Fluorescent Dyes ; Heparin/pharmacology ; Inositol 1,4,5-Trisphosphate/pharmacology/*physiology ; Intercellular Junctions/physiology ; Respiratory System/drug effects/metabolism ; Signal Transduction/*physiology ; Terpenes/pharmacology ; Thapsigargin
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 27
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    CD19: lowering the threshold for antigen receptor stimulation of B lymphocytes (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-04-03
    Description: Lymphocytes must proliferate and differentiate in response to low concentrations of a vast array of antigens. The requirements of broad specificity and sensitivity conflict because the former is met by low-affinity antigen receptors, which precludes achieving the latter with high-affinity receptors. Coligation of the membrane protein CD19 with the antigen receptor of B lymphocytes decreased the threshold for antigen receptor-dependent stimulation by two orders of magnitude. B lymphocytes proliferated when approximately 100 antigen receptors per cell, 0.03 percent of the total, were coligated with CD19. The B cell resolves its dilemma by having an accessory protein that enables activation when few antigen receptors are occupied.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Carter, R H -- Fearon, D T -- AI-22833/AI/NIAID NIH HHS/ -- AI-28191/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1992 Apr 3;256(5053):105-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1373518" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/immunology ; Antigens, CD/genetics/*immunology ; Antigens, CD19 ; Antigens, Differentiation, B-Lymphocyte/genetics/*immunology ; B-Lymphocytes/*immunology ; Cell Line ; Cells, Cultured ; DNA Replication ; Humans ; Kinetics ; L Cells (Cell Line) ; *Lymphocyte Activation ; Mice ; Receptors, Antigen, B-Cell/*immunology ; Recombinant Proteins/immunology ; Thymidine/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 28
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    Negative inotropic effects of cytokines on the heart mediated by nitric oxide (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-07-17
    Description: The direct effects of pro-inflammatory cytokines on the contractility of mammalian heart were studied. Tumor necrosis factor alpha, interleukin-6, and interleukin-2 inhibited contractility of isolated hamster papillary muscles in a concentration-dependent, reversible manner. The nitric oxide synthase inhibitor NG-monomethyl-L-arginine (L-NMMA) blocked these negative inotropic effects. L-Arginine reversed the inhibition by L-NMMA. Removal of the endocardial endothelium did not alter these responses. These findings demonstrate that the direct negative inotropic effect of cytokines is mediated through a myocardial nitric oxide synthase. The regulation of pro-inflammatory cytokines and myocardial nitric oxide synthase may provide new therapeutic strategies for the treatment of cardiac disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Finkel, M S -- Oddis, C V -- Jacob, T D -- Watkins, S C -- Hattler, B G -- Simmons, R L -- GM-37753/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1992 Jul 17;257(5068):387-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of Pittsburgh School of Medicine, PA 15213.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1631560" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arginine/analogs & derivatives/pharmacology ; Cells, Cultured ; Cricetinae ; Cytokines/*pharmacology ; Dose-Response Relationship, Drug ; Drug Interactions ; Endocardium/cytology ; Epithelium/physiology ; Interleukin-2/pharmacology ; Interleukin-6/pharmacology ; Microscopy, Electron ; Myocardial Contraction/*drug effects ; Nitric Oxide/*pharmacology ; Tumor Necrosis Factor-alpha/pharmacology ; omega-N-Methylarginine
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  • 29
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    Restoration of viral immunity in immunodeficient humans by the adoptive transfer of T cell clones (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-07-10
    Description: The adoptive transfer of antigen-specific T cells to establish immunity is an effective therapy for viral infections and tumors in animal models. The application of this approach to human disease would require the isolation and in vitro expansion of human antigen-specific T cells and evidence that such T cells persist and function in vivo after transfer. Cytomegalovirus-specific CD8+ cytotoxic T cell (CTL) clones could be isolated from bone marrow donors, propagated in vitro, and adoptively transferred to immunodeficient bone marrow transplant recipients. No toxicity developed and the clones provided persistent reconstitution of CD8+ cytomegalovirus-specific CTL responses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Riddell, S R -- Watanabe, K S -- Goodrich, J M -- Li, C R -- Agha, M E -- Greenberg, P D -- CA18029/CA/NCI NIH HHS/ -- P01 CA018029/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1992 Jul 10;257(5067):238-41.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Fred Hutchinson Cancer Research Center, Seattle, WA 98104.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1352912" target="_blank"〉PubMed〈/a〉
    Keywords: Antigens, CD3 ; Antigens, CD8/immunology ; Antigens, Differentiation, T-Lymphocyte/immunology ; Bone Marrow Transplantation/immunology ; CD4-Positive T-Lymphocytes/immunology ; Cells, Cultured ; Cytomegalovirus Infections/*prevention & control ; Humans ; Receptors, Antigen, T-Cell/immunology ; T-Lymphocytes, Cytotoxic/*immunology ; Vaccination/*methods
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 30
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    Activation-induced ubiquitination of the T cell antigen receptor (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-08-07
    Description: The zeta subunit of the T cell antigen receptor (TCR) exists primarily as a disulfide-linked homodimer. This receptor subunit is important in TCR-mediated signal transduction and is a substrate for a TCR-activated protein tyrosine kinase. The zeta chain was found to undergo ubiquitination in response to receptor engagement. This posttranslational modification occurred in normal T cells and tumor lines. Both nonphosphorylated and phosphorylated zeta molecules were modified, and at least one other TCR subunit, CD3 delta, was also ubiquitinated after activation of the receptor. These findings suggest an expanded role for ubiquitination in transmembrane receptor function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cenciarelli, C -- Hou, D -- Hsu, K C -- Rellahan, B L -- Wiest, D L -- Smith, H T -- Fried, V A -- Weissman, A M -- New York, N.Y. -- Science. 1992 Aug 7;257(5071):795-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Experimental Immunology Branch, 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/1323144" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD3 ; Antigens, Differentiation, T-Lymphocyte/immunology/metabolism ; Cells, Cultured ; Hybridomas/immunology ; Lymphocyte Activation/*physiology ; Macromolecular Substances ; Mice ; Mice, Inbred C57BL ; Molecular Weight ; *Protein Processing, Post-Translational ; Receptors, Antigen, T-Cell/immunology/isolation & purification/*metabolism ; Spleen/immunology ; T-Lymphocytes/*immunology ; Ubiquitins/isolation & purification/*metabolism
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  • 31
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    Inhibition of myeloid differentiation by the helix-loop-helix protein Id (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-03-27
    Description: Id is a helix-loop-helix (HLH) protein that represses activity of several basic helix-loop-helix (bHLH) proteins involved in cell type--specific transcription and cell lineage commitment. The myeloid precursor cell line 32DC13(G) expressed Id messenger RNA, which was transiently decreased when cells were induced to terminally differentiate with granulocyte--colony-stimulating factor. Concomitant with the decrease of Id messenger RNA was the appearance in nuclear extracts of DNA binding proteins that recognized a canonical E-box motif, a DNA binding site for some bHLH proteins. Constitutive expression of an Id complementary DNA in 32DC13(G) cells blocked their ability to differentiate and to induce E-box-binding activity. These results suggest that Id and, hence, bHLH proteins function in the process of myeloid differentiation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kreider, B L -- Benezra, R -- Rovera, G -- Kadesch, T -- CA 10815/CA/NCI NIH HHS/ -- CA 21124/CA/NCI NIH HHS/ -- CA 25875/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1992 Mar 27;255(5052):1700-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wistar Institute of Anatomy and Biology, Philadelphia, PA 19104.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1372755" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Differentiation/*drug effects ; Cells, Cultured ; DNA-Binding Proteins/*physiology ; Gene Expression ; Granulocyte Colony-Stimulating Factor/pharmacology ; Hematopoiesis/*drug effects ; In Vitro Techniques ; Inhibitor of Differentiation Protein 1 ; Interleukin-3/pharmacology ; Macromolecular Substances ; RNA, Messenger/genetics ; *Repressor Proteins ; *Transcription Factors
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  • 32
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    Yeast biology enters a surprising new phase (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-03-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hoffman, M -- New York, N.Y. -- Science. 1992 Mar 20;255(5051):1510-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1549780" target="_blank"〉PubMed〈/a〉
    Keywords: Cells, Cultured ; Nitrogen/metabolism ; Saccharomyces cerevisiae/*physiology
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  • 33
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    Functional modulation of GABAA receptors by cAMP-dependent protein phosphorylation (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-07-31
    Description: gamma-Aminobutyric acidA (GABAA) receptors are ligand-gated ion channels that mediate inhibitory synaptic transmission in the central nervous system. The role of protein phosphorylation in the modulation of GABAA receptor function was examined with cells transiently transfected with GABAA receptor subunits. GABAA receptors consisting of the alpha 1 and beta 1 or the alpha 1, beta 1, and gamma 2 subunits were directly phosphorylated on the beta 1 subunit by adenosine 3',5'-monophosphate (cAMP)-dependent protein kinase (PKA). The phosphorylation decreased the amplitude of the GABA response of both receptor types and the extent of rapid desensitization of the GABAA receptor that consisted of the alpha 1 and beta 1 subunits. Site-specific mutagenesis of the serine residue phosphorylated by PKA completely eliminated the PKA phosphorylation and modulation of the GABAA receptor. In primary embryonic rat neuronal cell cultures, a similar regulation of GABAA receptors by PKA was observed. These results demonstrate that the GABAA receptor is directly modulated by protein phosphorylation and suggest that neurotransmitters or neuropeptides that regulate intracellular cAMP levels may modulate the responses of neurons to GABA and consequently have profound effects on synaptic excitability.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Moss, S J -- Smart, T G -- Blackstone, C D -- Huganir, R L -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 1992 Jul 31;257(5070):661-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, 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/1323140" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cells, Cultured ; Colforsin/pharmacology ; Cyclic AMP/*pharmacology ; Electric Conductivity ; Immunosorbent Techniques ; Kinetics ; Mice ; Mutagenesis, Site-Directed ; Neurons/drug effects/physiology ; Peptide Mapping ; Phosphorylation ; Protein Kinases/*metabolism ; Rats ; Receptors, GABA-A/genetics/*physiology ; Recombinant Proteins/physiology ; Transfection ; Zinc/pharmacology ; gamma-Aminobutyric Acid/pharmacology
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  • 34
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    Prevention of programmed cell death of sympathetic neurons by the bcl-2 proto-oncogene (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-10-09
    Description: Approximately half of the neurons produced during embryogenesis normally die before adulthood. Although target-derived neurotrophic factors are known to be major determinants of programmed cell death--apoptosis--the molecular mechanisms by which trophic factors interfere with cell death regulation are largely unknown. Overexpression of the bcl-2 proto-oncogene in cultured sympathetic neurons has now been shown to prevent apoptosis normally induced by deprivation of nerve growth factor. This finding, together with the previous demonstration of bcl-2 expression in the nervous system, suggests that the Bcl-2 protein may be a major mediator of the effects of neurotrophic factors on neuronal survival.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Garcia, I -- Martinou, I -- Tsujimoto, Y -- Martinou, J C -- CA-50551/CA/NCI NIH HHS/ -- CA-51864/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1992 Oct 9;258(5080):302-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Centre Medical Universitaire, Geneva, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1411528" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis/*genetics ; Cell Death/*genetics ; Cells, Cultured ; Ganglia, Sympathetic/cytology ; Gene Expression ; Humans ; Nerve Growth Factors/physiology ; Neurons/*physiology ; Proto-Oncogene Proteins/*genetics ; Proto-Oncogene Proteins c-bcl-2 ; Rats ; Sympathetic Nervous System/*cytology ; Transfection
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  • 35
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    Post-transcriptional regulation of early T cell development by T cell receptor signals (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-11-27
    Description: During differentiation in the thymus, immature T cells progress through an ordered sequence of developmental stages that are best characterized by variable expression of the co-receptor molecules CD4 and CD8. Crosslinking of T cell receptor (TCR) molecules on precursor thymocytes was found to block their differentiation into CD4+CD8+ cells by eliminating messenger RNA's encoding two families of developmentally important molecules: the co-receptor molecules CD4 and CD8 and the recombination activating genes 1 and 2. TCR-induced post-transcriptional regulation in early thymocytes was specific for selective messenger RNA's, required protein synthesis, and was itself developmentally regulated. These data identify a post-transcriptional mechanism that is influenced by TCR signals and that regulates early thymocyte development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Takahama, Y -- Singer, A -- New York, N.Y. -- Science. 1992 Nov 27;258(5087):1456-62.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Experimental Immunology Branch, 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/1439838" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD4/genetics ; Antigens, CD8/genetics ; Cell Differentiation/physiology ; Cells, Cultured ; Fetus/cytology ; Gene Rearrangement, T-Lymphocyte/genetics ; Genes, RAG-1/genetics ; Mice ; Protein Synthesis Inhibitors/pharmacology ; Protein-Tyrosine Kinases/genetics ; RNA Processing, Post-Transcriptional/physiology ; RNA, Messenger/metabolism ; Receptors, Antigen, T-Cell, alpha-beta/genetics/*physiology ; Signal Transduction/physiology ; T-Lymphocytes/*cytology/drug effects ; Tetradecanoylphorbol Acetate/pharmacology ; Thymus Gland/cytology/embryology
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  • 36
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    Serotonin-mediated endocytosis of apCAM: an early step of learning-related synaptic growth in Aplysia (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-05-01
    Description: The long-term facilitation of synaptic efficacy that is induced by serotonin in dissociated cell cultures of sensory and motor neurons of Aplysia is accompanied by the growth of new synaptic connections. This growth is associated with a down-regulation in the sensory neuron of Aplysia cell adhesion molecules (apCAMs). To examine the mechanisms of this down-regulation, thin-section electron microscopy was combined with immunolabeling by gold-conjugated monoclonal antibodies specific to apCAM. Within 1 hour, serotonin led to a 50% decrease in the density of gold-labeled complexes at the surface membrane of the sensory neuron. This down-regulation was achieved by a heterologous, protein synthesis-dependent activation of the endosomal pathway, which leads to internalization and apparent degradation of apCAM. The internalization is particularly prominent at sites where the processes of the sensory neurons contact one another and may act there to destabilize process-to-process contacts that normally inhibit growth. In turn, the endocytic activation may lead to a redistribution of membrane components to sites where new synapses form.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bailey, C H -- Chen, M -- Keller, F -- Kandel, E R -- GM32099/GM/NIGMS NIH HHS/ -- MH37134/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1992 May 1;256(5057):645-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Neurobiology and Behavior, College of Physicians and Surgeons of Columbia University, New York, NY.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1585177" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anisomycin/pharmacology ; Antibodies, Monoclonal ; Aplysia/*physiology ; Cell Adhesion Molecules/*metabolism ; Cell Membrane/metabolism/ultrastructure ; Cells, Cultured ; Coated Pits, Cell-Membrane/metabolism/ultrastructure ; Endocytosis/*drug effects ; Immunohistochemistry ; Microscopy, Electron ; Motor Neurons/physiology/ultrastructure ; Neurons, Afferent/physiology/ultrastructure ; Serotonin/*pharmacology ; Synapses/*physiology/ultrastructure ; Wheat Germ Agglutinins/metabolism
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  • 37
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    Polyamine depletion and drug-induced chromosomal damage: new results (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-11-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tofilon, P J -- Deen, D F -- Marton, L J -- New York, N.Y. -- Science. 1992 Nov 20;258(5086):1378.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1455236" target="_blank"〉PubMed〈/a〉
    Keywords: Carmustine/toxicity ; Cell Death ; Cells, Cultured ; *DNA Damage ; In Vitro Techniques ; Polyamines/*metabolism ; Sister Chromatid Exchange/drug effects
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  • 38
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    Inhibition of development of Kaposi's sarcoma-related lesions by a bacterial cell wall complex (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-03-13
    Description: In vitro and in vivo model systems for the study of human immunodeficiency virus (HIV)-associated Kaposi's sarcoma (KS) were used to evaluate compounds for their potential as therapeutic agents. A sulfated polysaccharide-peptidoglycan compound (SP-PG) produced by bacteria controlled the in vitro growth of acquired immunodeficiency syndrome (AIDS)-associated, KS-derived spindle-shaped cells (AIDS-KS cells) at noncytotoxic concentrations. Angiogenesis induced by AIDS-KS cells in the chicken chorioallantoic membrane assay was blocked by SP-PG, which also inhibited the vascular hyperpermeability response and the angiogenesis associated with the induction of KS-like lesions that develop after subcutaneous inoculation of AIDS-KS cells into nude mice. Suramin, pentosan polysulfate, and interferon alpha, which are currently in use for therapy of KS, were either less effective than SP-PG or much more cytotoxic, or both.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nakamura, S -- Sakurada, S -- Salahuddin, S Z -- Osada, Y -- Tanaka, N G -- Sakamoto, N -- Sekiguchi, M -- Gallo, R C -- New York, N.Y. -- Science. 1992 Mar 13;255(5050):1437-40.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Internal Medicine, University of Southern California, Los Angeles 90033.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1371891" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/complications ; Animals ; Arthrobacter ; Arylsulfatases ; Capillary Permeability/drug effects ; Cell Division/drug effects ; Cells, Cultured ; Endothelium, Vascular/cytology/drug effects ; Fibroblasts/drug effects ; Humans ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Neoplasm Transplantation ; Neovascularization, Pathologic/*prevention & control ; *Peptidoglycan ; Polysaccharides/*pharmacology ; Sarcoma, Kaposi/etiology/*pathology ; Tumor Cells, Cultured
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  • 39
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    No requirement for p56lck in the antigen-stimulated clonal deletion of thymocytes (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-07-03
    Description: Activation of protein-tyrosine kinases (PTKs) is required for signal transduction during T cell activation, although the pathway used during thymic selection is unknown. An in vitro system was established in which T cell receptor transgenic thymocytes underwent clonal deletion in response to peptide antigen. The effects of two PTK-specific inhibitors, herbimycin A and genistein, on the clonal deletion of immature thymocytes and the activation of mature thymocytes were examined. Clonal deletion occurred while T cell activation was inhibited and when no p56lck activity was evident. Thus, p56lck is not required for the antigen-stimulated step of clonal deletion of immature thymocytes, and negative selection proceeds via a distinct pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nakayama, K -- Loh, D Y -- New York, N.Y. -- Science. 1992 Jul 3;257(5066):94-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Medicine, 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/1621101" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Benzoquinones ; Cells, Cultured ; Chickens ; DNA Replication ; Genistein ; Isoflavones/pharmacology ; L Cells (Cell Line) ; Lactams, Macrocyclic ; *Lymphocyte Activation/drug effects ; Lymphocyte Specific Protein Tyrosine Kinase p56(lck) ; Mice ; Mice, Transgenic ; Ovalbumin/immunology ; Protein-Tyrosine Kinases/antagonists & inhibitors/*metabolism ; Quinones/pharmacology ; Receptors, Antigen, T-Cell/*genetics/immunology ; Rifabutin/analogs & derivatives ; *Signal Transduction ; T-Lymphocyte Subsets/immunology ; T-Lymphocytes/drug effects/*immunology ; Transfection
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  • 40
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    GnRH-induced Ca2+ oscillations and rhythmic hyperpolarizations of pituitary gonadotropes (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-01-24
    Description: Secretion of gonadotropic hormones from pituitary gonadotropes in response to gonadotropin-releasing hormone (GnRH) is essential for regulation of reproductive potential. Gonadotropes from male rats exhibited an unusual form of cellular excitation that resulted from periodic membrane hyperpolarization. GnRH induced an oscillatory release of intracellular Ca2+ via a guanosine triphosphate (GTP) binding protein-coupled phosphoinositide pathway and hyperpolarized the gonadotrope periodically by opening apamin-sensitive Ca(2+)-activated K+ (SK) channels. Each hyperpolarization was terminated by firing of a few action potentials that may result from removal of inactivation from voltage-gated Na+ and Ca2+ channels.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tse, A -- Hille, B -- New York, N.Y. -- Science. 1992 Jan 24;255(5043):462-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology and Biophysics, University of Washington School of Medicine, Seattle 98195.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1734523" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apamin/pharmacology ; Calcium/*metabolism ; Cells, Cultured ; GTP-Binding Proteins/physiology ; Gonadotropin-Releasing Hormone/*physiology ; In Vitro Techniques ; Inositol 1,4,5-Trisphosphate/physiology ; Membrane Potentials ; Periodicity ; Pituitary Gland, Anterior/cytology/*physiology ; Potassium Channels/physiology ; Rats
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 41
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    Identification of envelope V3 loop as the major determinant of CD4 neutralization sensitivity of HIV-1 (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-07-24
    Description: Laboratory isolates of human immunodeficiency virus type-1 (HIV-1) such as HTLV-IIIB are generally T cell line-tropic and highly sensitive to neutralization by soluble CD4 (sCD4), a potential antiviral agent that is undergoing clinical trial. However, many primary HIV-1 isolates are macrophage-tropic and sCD4-resistant. Envelope V3 loop sequences derived from primary HIV-1 isolates were sufficient to confer on HTLV-IIIB not only the tissue tropism but also the degree of sCD4 neutralization resistance characteristic of their HIV-1 strains of origin. Single amino acid changes in the V3 loop enhanced sCD4 resistance by up to tenfold. These observations suggest that the tissue tropism and sCD4 neutralization sensitivity of HIV-1 isolates are regulated by similar mechanisms.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hwang, S S -- Boyle, T J -- Lyerly, H K -- Cullen, B R -- AI28233/AI/NIAID NIH HHS/ -- AI28662/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1992 Jul 24;257(5069):535-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, Duke University Medical Center, Durham, NC 27710.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1636088" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antigens, CD4/*immunology ; Cell Line ; Cells, Cultured ; Gene Products, gag/*immunology ; HIV Envelope Protein gp120/*immunology ; HIV-1/*immunology/isolation & purification ; Humans ; Kinetics ; Molecular Sequence Data ; Neutralization Tests ; Proviruses/immunology ; T-Lymphocyte Subsets/*immunology ; Transfection ; Virion/immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 42
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    Encoding of a homolog of the IFN-gamma receptor by myxoma virus (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-11-20
    Description: Many poxvirus-encoded virulence factors have been identified as proteins that are secreted from infected cells. The major secreted protein (37 kilodaltons) from cells infected with myxoma virus is encoded by the M-T7 open reading frame. This protein has significant sequence similarity to the human and mouse receptors for interferon-gamma (IFN-gamma). Furthermore, the myxoma M-T7 protein specifically binds rabbit IFN-gamma and inhibits the biological activity of extracellular IFN-gamma, one of the key regulatory cytokines in the host immune response against viral infections.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Upton, C -- Mossman, K -- McFadden, G -- New York, N.Y. -- Science. 1992 Nov 20;258(5086):1369-72.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, University of Alberta, Edmonton, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1455233" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cells, Cultured ; Cloning, Molecular ; *Genes, Viral ; In Vitro Techniques ; Interferon-gamma/metabolism ; Molecular Sequence Data ; Myxoma virus/*genetics/pathogenicity ; Protein Binding ; Rabbits ; Receptors, Interferon/*genetics ; Restriction Mapping ; Sequence Alignment ; Sequence Homology, Amino Acid ; Viral Interference ; Viral Proteins/*genetics ; Viral Structural Proteins/*genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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