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  • Cells, Cultured  (57)
  • American Association for the Advancement of Science (AAAS)  (57)
  • American Chemical Society
  • Periodicals Archive Online (PAO)
  • 1985-1989  (57)
  • 1980-1984
  • 1965-1969
  • 1988  (30)
  • 1986  (27)
Collection
Publisher
  • American Association for the Advancement of Science (AAAS)  (57)
  • American Chemical Society
  • Periodicals Archive Online (PAO)
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  • 1985-1989  (57)
  • 1980-1984
  • 1965-1969
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  • 1
    Publication Date: 1988-12-02
    Description: Human gamma-aminobutyric acid A (GABAA) receptor subunits were expressed transiently in cultured mammalian cells. This expression system allows the simultaneous characterization of ligand-gated ion channels by electrophysiology and by pharmacology. Thus, coexpression of the alpha and beta subunits of the GABAA receptor generated GABA-gated chloride channels and binding sites for GABAA receptor ligands. Channels consisting of only alpha or beta subunits could also be detected. These homomeric channels formed with reduced efficiencies compared to the heteromeric receptors. Both of these homomeric GABA-responsive channels were potentiated by barbiturate, indicating that sites for both ligand-gating and allosteric potentiation are present on receptors assembled from either subunit.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pritchett, D B -- Sontheimer, H -- Gorman, C M -- Kettenmann, H -- Seeburg, P H -- Schofield, P R -- New York, N.Y. -- Science. 1988 Dec 2;242(4883):1306-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Neuroendocrinology, ZMBH, University of Heidelberg, Federal Republic of Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2848320" target="_blank"〉PubMed〈/a〉
    Keywords: Allosteric Regulation ; Blotting, Northern ; Cells, Cultured ; Chloride Channels ; Chlorides/*physiology ; Cloning, Molecular ; Electric Conductivity ; Humans ; Macromolecular Substances ; Membrane Proteins/*physiology ; Muscimol/metabolism ; Receptors, GABA-A/*physiology/ultrastructure ; Structure-Activity Relationship ; Transfection
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  • 2
    Publication Date: 1988-06-17
    Description: Behavioral sensitization leads to both short- and long-term enhancement of synaptic transmission between the sensory and motor neurons of the gill-withdrawal reflex in Aplysia. Serotonin (5-HT), a transmitter important for short-term sensitization, can evoke long-term enhancement of synaptic strength detected 1 day later. Because 5-HT mediates short-term facilitation through adenosine 3',5'-monophosphate (cAMP)-dependent protein phosphorylation, the role of cAMP in the long-term modulation of this identified synapse was examined. Like 5-HT, cAMP can also evoke long-term facilitation lasting 24 hours. Unlike the short-term change, the long-lasting change is blocked by anisomycin, a reversible inhibitor of protein synthesis, and therefore must involve the synthesis of gene products not required for the short-term change.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schacher, S -- Castellucci, V F -- Kandel, E R -- GM 32099/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1988 Jun 17;240(4859):1667-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Neurobiology and Behavior, Howard Hughes Medical Institute, College of Physicians and Surgeons of Columbia University, New York State Psychiatric Institute, NY 10032.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2454509" target="_blank"〉PubMed〈/a〉
    Keywords: 1-Methyl-3-isobutylxanthine/pharmacology ; Animals ; Anisomycin/pharmacology ; Aplysia/*physiology ; Cells, Cultured ; Cyclic AMP/analogs & derivatives/*pharmacology ; Evoked Potentials/drug effects ; Motor Neurons/physiology ; Neurons, Afferent/drug effects/*physiology ; *Protein Biosynthesis ; Serotonin/pharmacology ; Synapses/drug effects/physiology
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  • 3
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-02-05
    Description: Identification of genes that function to protect cells from radiation damage is an essential step in understanding the molecular mechanisms by which mammalian cells cope with ionizing radiation. The intrinsic radiation resistance (D0) of NIH 3T3 cells was markedly and significantly increased by transformation with ras oncogenes activated by missense mutations. This radiobiologic activity appeared to be a specific consequence of the ras mutations rather than of transformation, since revertant cells that contained functional ras genes (but were no longer phenotypically transformed) retained their increased D0's.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sklar, M D -- CA 41166/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1988 Feb 5;239(4840):645-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Radiation Oncology, University of Michigan Medical School, Ann Arbor 48109.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3277276" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Survival/*radiation effects ; Cell Transformation, Neoplastic ; Cells, Cultured ; Clone Cells ; Dose-Response Relationship, Radiation ; *Genes, ras ; Mice ; Mice, Inbred Strains
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  • 4
    Publication Date: 1988-11-04
    Description: Studies in animals suggest that fetal neural grafts might restore lost neurological function in Parkinson's disease. In monkeys, such grafts survive for many months and reverse signs of parkinsonism, without attendant graft rejection. The successful and reliable application of a similar transplantation procedure to human patients, however, will require neural tissue obtained from human fetal cadavers, with demonstrated cellular identity, viability, and biological safety. In this report, human fetal neural tissue was successfully grafted into the brains of monkeys. Neural tissue was collected from human fetal cadavers after 9 to 12 weeks of gestation and cryopreserved in liquid nitrogen. Viability after up to 2 months of storage was demonstrated by cell culture and by transplantation into monkeys. Cryopreservation and storage of human fetal neural tissue would allow formation of a tissue bank. The stored cells could then be specifically tested to assure their cellular identity, viability, and bacteriological and virological safety before clinical use. The capacity to collect and maintain viable human fetal neural tissue would also facilitate research efforts to understand the development and function of the human brain and provide opportunities to study neurological diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Redmond, D E Jr -- Naftolin, F -- Collier, T J -- Leranth, C -- Robbins, R J -- Sladek, C D -- Roth, R H -- Sladek, J R Jr -- New York, N.Y. -- Science. 1988 Nov 4;242(4879):768-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychiatry, 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/2903552" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Survival ; Cells, Cultured ; Cercopithecus ; Fetus ; Freezing ; Humans ; Male ; Mesencephalon/cytology/embryology/enzymology/*transplantation ; Preservation, Biological ; Transplantation, Heterologous ; Tyrosine 3-Monooxygenase/metabolism
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  • 5
    Publication Date: 1988-01-29
    Description: Soluble products of either Epstein-Barr virus (EBV)-infected B cells or activated monocytes promote the proliferation of EBV-infected B cells and permit their growth at low cell densities. This suggests that growth factors are important for B-cell immortalization by EBV. In this study, a monocyte-derived factor that promotes the growth of EBV-infected b cells was purified and identified as interferon-beta 2 (IFN-beta 2), which is also known as 26-kilodalton protein, B-cell differentiation factor (BSF-2), and interleukin-6 (IL-6). The purified protein has a specific activity of approximately 4 X 10(7) units per milligram of protein in assays of B-cell growth. Thus, IFN-beta 2/BSF-2 is a B-cell growth factor that promotes the proliferation of human B cells infected with EBV.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tosato, G -- Seamon, K B -- Goldman, N D -- Sehgal, P B -- May, L T -- Washington, G C -- Jones, K D -- Pike, S E -- AI-16262/AI/NIAID NIH HHS/ -- CA-44365/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1988 Jan 29;239(4839):502-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biochemistry and Biophysics, Food and Drug Administration, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2829354" target="_blank"〉PubMed〈/a〉
    Keywords: B-Lymphocytes/*cytology/microbiology ; Cell Count ; Cell Division ; Cells, Cultured ; Electrophoresis, Polyacrylamide Gel ; Herpesvirus 4, Human/*physiology ; Humans ; Immunoassay ; Interleukin-6 ; Interleukins/isolation & purification/*pharmacology ; Monocytes/*metabolism
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  • 6
    Publication Date: 1988-03-18
    Description: A probe for the 5' end of the Duchenne muscular dystrophy (DMD) gene was used to study expression of the gene in normal human muscle, myogenic cell cultures, and muscle from patients with DMD. Expression was found in RNA from normal fetal muscle, adult cardiac and skeletal muscle, and cultured muscle after myoblast fusion. In DMD muscle, expression of this portion of the gene was also revealed by in situ RNA hybridization, particularly in regenerating muscle fibers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Scott, M O -- Sylvester, J E -- Heiman-Patterson, T -- Shi, Y J -- Fieles, W -- Stedman, H -- Burghes, A -- Ray, P -- Worton, R -- Fischbeck, K H -- GM32592/GM/NIGMS NIH HHS/ -- NS08075/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1988 Mar 18;239(4846):1418-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neurology Department, Hospital of the University of Pennsylvania, Philadelphia, 19104.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2450401" target="_blank"〉PubMed〈/a〉
    Keywords: Cells, Cultured ; DNA/genetics ; DNA, Recombinant ; *Gene Expression Regulation ; Humans ; Muscles/embryology/*metabolism ; Muscular Dystrophies/*genetics ; Myocardium/metabolism ; Nucleic Acid Hybridization ; RNA/metabolism ; RNA, Messenger/metabolism ; Regeneration ; Transcription, Genetic
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  • 7
    Publication Date: 1988-05-06
    Description: A point mutation in the human insulin receptor gene in a patient with type A insulin resistance alters the amino acid sequence within the tetrabasic processing site of the proreceptor molecule from Arg-Lys-Arg-Arg to Arg-Lys-Arg-Ser. Epstein-Barr virus-transformed lymphocytes from this patient synthesize an insulin receptor precursor that is normally glycosylated and inserted into the plasma membrane but is not cleaved to mature alpha and beta subunits. Insulin binding to these cells is severely reduced but can be increased about fivefold by gentle treatment with trypsin, accompanied by the appearance of normal alpha subunits. These results indicate that proteolysis of the proreceptor is necessary for its normal full insulin-binding sensitivity and signal-transducing activity and that a cellular protease that is more stringent in its specificity than trypsin is required to process the receptor precursor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yoshimasa, Y -- Seino, S -- Whittaker, J -- Kakehi, T -- Kosaki, A -- Kuzuya, H -- Imura, H -- Bell, G I -- Steiner, D F -- AM 13914/AM/NIADDK NIH HHS/ -- AM 20595/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1988 May 6;240(4853):784-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Biology, University of Chicago, IL 60637.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3283938" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Amino Acid Sequence ; Cell Membrane/metabolism ; Cells, Cultured ; DNA/genetics ; Diabetes Mellitus/*genetics/metabolism ; Female ; Glycosylation ; Humans ; Insulin/metabolism ; Insulin Resistance/*genetics ; Lymphocytes/metabolism ; Molecular Sequence Data ; Mutation ; Nucleic Acid Hybridization ; Protein Precursors/*genetics/metabolism ; RNA, Messenger/metabolism ; Receptor, Insulin/*genetics/metabolism ; Trypsin/metabolism
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  • 8
    Publication Date: 1988-04-08
    Description: The protein kinase inhibitor 2-aminopurine (2AP) blocks the induction of the human beta-interferon gene by virus or poly(I)-poly(C) at the level of transcription. This inhibition is specific, since 2AP does not inhibit induction of either the hsp70 heat-shock gene by high temperature or the metallothionein gene by cadmium or dexamethasone. However, 2AP does block the induction of the c-fos and c-myc proto-oncogenes by serum growth factors or virus, suggesting that a protein kinase may be involved in the regulation of these genes, as well as of the beta-interferon gene. However, different factors must be required for the induction of these three genes, since they are not coordinately regulated by the same inducers in most of the cell lines examined.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zinn, K -- Keller, A -- Whittemore, L A -- Maniatis, T -- AI20642/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1988 Apr 8;240(4849):210-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Biology, Harvard University, Cambridge, MA 02138.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3281258" target="_blank"〉PubMed〈/a〉
    Keywords: 2-Aminopurine/*pharmacology ; Adenine/*analogs & derivatives ; Animals ; Cells, Cultured ; Gene Expression Regulation/*drug effects ; Heat-Shock Proteins/genetics ; Humans ; Interferon Type I/*genetics ; Mice ; Protein Kinase Inhibitors ; Proto-Oncogene Proteins/*genetics ; *Proto-Oncogenes ; Regulatory Sequences, Nucleic Acid ; Transcription, Genetic/drug effects
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  • 9
    Publication Date: 1988-02-05
    Description: The turnover of phosphatidylinositol 4,5-bisphosphate (PIP2) is believed to constitute a crucial step in the signaling pathways for stimulation of cells by a variety of bioactive substances, including mitogens, but decisive evidence for the idea has not been obtained. In the present study, a monoclonal antibody to PIP2 was microinjected into the cytoplasm of NIH 3T3 cells before or after exposure to mitogens. The antibody completely abolished nuclear labeling with [3H]thymidine induced by platelet-derived growth factor and bombesin, but not by fibroblast growth factor, epidermal growth factor, insulin, or serum. The findings strongly suggest that PIP2 breakdown is crucial in the elicitation and sustaining of cell proliferation induced by some types of mitogens such as platelet-derived growth factor and bombesin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Matuoka, K -- Fukami, K -- Nakanishi, O -- Kawai, S -- Takenawa, T -- New York, N.Y. -- Science. 1988 Feb 5;239(4840):640-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, Tokyo Metropolitan Institute of Gerontology, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2829356" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antibodies, Monoclonal ; Antigen-Antibody Complex ; Bombesin/*pharmacology ; Cell Division/*drug effects ; Cells, Cultured ; Insulin/pharmacology ; Kinetics ; Mice ; Mice, Inbred Strains ; Phosphatidylinositol 4,5-Diphosphate ; Phosphatidylinositols/immunology/*physiology ; Platelet-Derived Growth Factor/*pharmacology
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  • 10
    Publication Date: 1988-10-21
    Description: Expression of a complementary DNA (cDNA) encoding the mouse MyoD1 protein in a variety of fibroblast and adipoblast cell lines converts them to myogenic cells. Polyclonal antisera to fusion proteins containing the MyoD1 sequence show that MyoD1 is a phosphoprotein present in the nuclei of proliferating myoblasts and differentiated myotubes but not expressed in 10T1/2 fibroblasts or other nonmuscle cell types. Functional domains of the MyoD1 protein were analyzed by site-directed deletional mutagenesis of the MyoD1 cDNA. Deletion of a highly basic region (residues 102 to 135) interferes with both nuclear localization and induction of myogenesis. Deletion of a short region (residues 143 to 162) that is similar to a conserved region in the c-Myc family of proteins eliminates the ability of the MyoD1 protein to initiate myogenesis but does not alter nuclear localization. Deletions of regions spanning the remainder of MyoD1 did not affect nuclear localization and did not inhibit myogenesis. Furthermore, expression of only 68 amino acids of MyoD1, containing the basic and the Myc similarity domains, is sufficient to activate myogenesis in stably transfected 10T1/2 cells. Genetic analysis maps the MyoD1 gene to mouse chromosome 7 and human chromosome 11.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tapscott, S J -- Davis, R L -- Thayer, M J -- Cheng, P F -- Weintraub, H -- Lassar, A B -- New York, N.Y. -- Science. 1988 Oct 21;242(4877):405-11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, 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/3175662" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cell Division ; Cells, Cultured ; Chromosome Mapping ; DNA/genetics ; Fibroblasts/cytology ; *Genes ; Humans ; Mice ; Muscles/cytology ; *MyoD Protein ; Nuclear Proteins/*genetics/physiology ; *Oncogenes ; Phosphoproteins/*genetics/physiology
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  • 11
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-07-01
    Description: Membrane microcarriers were used to determine the ability of regional extracellular matrices to direct neural crest cell differentiation in culture. Neural crest cells from the axolotl embryo responded to extracellular matrix material explanted from the subepidermal migratory pathway by dispersing and by differentiating into pigment cells. In contrast, matrix material from the presumptive site of dorsal root ganglia stimulated pronounced cell-cell association and neurotypic expression. Cell line segregation during ontogeny of the neural crest that leads to diversification into pigment cells of the skin or into elements of the peripheral nervous system appears to be controlled in part by local cell-matrix interactions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Perris, R -- von Boxberg, Y -- Lofberg, J -- New York, N.Y. -- Science. 1988 Jul 1;241(4861):86-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Zoology, Uppsala University, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3388022" target="_blank"〉PubMed〈/a〉
    Keywords: Ambystoma mexicanum/embryology ; Animals ; Antigens, Surface/analysis ; Cell Adhesion ; Cell Adhesion Molecules ; Cell Aggregation ; Cell Differentiation ; Cells, Cultured ; Epidermis/physiology ; Epithelial Cells ; Extracellular Matrix/*physiology ; Ganglia, Spinal/embryology/physiology ; Melanocytes/cytology ; Neural Crest/*cytology ; Neurons/cytology ; *Phenotype ; Pigments, Biological/metabolism
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  • 12
    Publication Date: 1988-08-12
    Description: Calcium channels are inactivated by voltage and intracellular calcium. To study the kinetics and the mechanism of calcium-induced inactivation of calcium channels, a "caged" calcium compound, dimethoxy-nitrophen was used to photo-release about 50 microM calcium ion within 0.2 millisecond in dorsal root ganglion neurons. When divalent cations were the charge carriers, intracellular photo-release of calcium inactivated the calcium channel with an invariant rate [time constant (tau) approximately equal to 7 milliseconds]. When the monovalent cation sodium was the charge carrier, photorelease of calcium inside or outside of the cell blocked the channel rapidly (tau approximately equal to 0.4 millisecond), but the block was greater from the external side. Thus the kinetics of calcium-induced calcium channel inactivation depends on the valency of the permeant cation. The data imply that calcium channels exist in either of two conformational states, the calcium- and sodium-permeant forms, or, alternatively, calcium-induced inactivation occurs at a site closely associated with the internal permeating site.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Morad, M -- Davies, N W -- Kaplan, J H -- Lux, H D -- R01 HL-16152/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1988 Aug 12;241(4867):842-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of Pennsylvania, Department of Physiology, Philadelphia 19104-6085.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2457253" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/*physiology/radiation effects ; Cells, Cultured ; Chickens ; Ganglia, Spinal/*physiology/radiation effects ; Ion Channels/*physiology ; Kinetics ; Neurons/*physiology/radiation effects ; Photolysis ; Sodium/metabolism ; *Ultraviolet Rays
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  • 13
    Publication Date: 1988-04-08
    Description: Genetically transformed maize plants were obtained from protoplasts treated with recombinant DNA. Protoplasts that were digested from embryogenic cell suspension cultures of maize inbred A188 were combined with plasmid DNA containing a gene coding for neomycin phosphotransferase (NPT II) next to the 35S promoter region of cauliflower mosaic virus. A high voltage electrical pulse was applied to the protoplasts, which were then grown on filters placed over feeder layers of maize suspension cells (Black Mexican Sweet) and selected for growth in the presence of kanamycin. Selected cell lines showed NPT II activity. Plants were regenerated from transformed cell lines and grown to maturity. Southern analysis of DNA extracted from callus and plants indicated the presence of the NPT II gene.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rhodes, C A -- Pierce, D A -- Mettler, I J -- Mascarenhas, D -- Detmer, J J -- New York, N.Y. -- Science. 1988 Apr 8;240(4849):204-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Sandoz Crop Protection Corporation, Palo Alto, CA 94304-1104.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2832947" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Membrane Permeability ; Cells, Cultured ; DNA/analysis ; DNA, Recombinant ; Electricity ; Genetic Engineering/*methods ; Kanamycin Kinase ; Phosphotransferases/metabolism ; Plasmids ; Transformation, Genetic ; Zea mays/*genetics
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  • 14
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-08-19
    Description: Ingestion of the excitotoxic cycad seed amino acid beta-N-methylamino-L-alanine may be responsible for the neuronal degeneration associated with Guam amyotrophic lateral sclerosis-parkinsonism-dementia in man. However, the basis for the central neurotoxicity of beta-N-methylamino-L-alanine has been unclear, as it lacks the omega acidic (or equivalent electronegative) moiety characteristic of other excitatory amino acids. beta-N-methylamino-L-alanine produced neurotoxic and neuroexcitatory effects in murine cortical cell cultures only when physiological concentrations of bicarbonate were available in the extracellular bathing medium. Bicarbonate may interact noncovalently with beta-N-methylamino-L-alanine to produce, in combination, a molecular configuration that activates glutamate receptors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weiss, J H -- Choi, D W -- NS12151/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1988 Aug 19;241(4868):973-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, Stanford University Medical Center, Stanford 94305.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3136549" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acids, Diamino/*toxicity ; Animals ; Bicarbonates/*metabolism ; Cells, Cultured ; Cerebral Cortex/*drug effects ; Electrophysiology ; Hydrogen-Ion Concentration ; Mice ; Microelectrodes ; Neurons/*drug effects ; Oxadiazoles/toxicity ; Quisqualic Acid ; beta-Alanine/analogs & derivatives/toxicity
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  • 15
    Publication Date: 1986-05-23
    Description: Infection of the central nervous system by mouse hepatitis virus strain A59, a murine neurotropic coronavirus, induces class I major histocompatibility complex antigens on mouse oligodendrocytes and astrocytes, cells that do not normally express these antigens on their surfaces. This induction, which occurs through soluble factors elaborated by infected glial cells, potentially allows immunocytes to interact with the glial cells and may play a critical role in the pathogenesis of virus-induced, immune-mediated demyelination in the central nervous system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Suzumura, A -- Lavi, E -- Weiss, S R -- Silberberg, D H -- NS11037/NS/NINDS NIH HHS/ -- NS21954/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1986 May 23;232(4753):991-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3010460" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Astrocytes/*immunology ; Cells, Cultured ; Fluorescent Antibody Technique ; H-2 Antigens/*immunology ; Hepatitis, Viral, Animal/*immunology ; Macrophages/immunology ; Mice ; Murine hepatitis virus/immunology ; Neuroglia/*immunology ; Oligodendroglia/*immunology
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  • 16
    Publication Date: 1988-12-09
    Description: The rapid induction of the proto-oncogene c-fos by growth factors and other bioactive agents, and the recent evidence that the c-fos protein (Fos) is associated with transcriptional complexes, suggests that Fos may represent an integral part of an intracellular messenger pathway that triggers changes in gene expression and ultimately phenotypic alterations. This report examines the role of c-fos in growth factor stimulation of transin, a matrix-degrading secreted metalloproteinase. Platelet-derived growth factor (PDGF) stimulation of transin RNA was blocked by a selective reduction in Fos synthesis with antisense c-fos mRNA, whereas epidermal growth factor (EGF) stimulation of transin occurred despite an equivalent inhibition of Fos levels. The stimulatory effect of both PDGF and EGF on transin transcription involved factors recognizing the sequence TGAGTCA, which is found in the transin promoter and is reported to be a binding site for the transcriptional factor Jun/AP-1 and for associated Fos and Fos-related complexes. Thus both Fos-dependent and Fos-independent pathways exist for growth factor regulation of gene expression, and both effects may be mediated through the same cis-acting transcription element.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kerr, L D -- Holt, J T -- Matrisian, L M -- New York, N.Y. -- Science. 1988 Dec 9;242(4884):1424-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Vanderbilt University, Nashville, TN 37232.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2462278" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; *Gene Expression Regulation ; Genes/*drug effects ; Growth Substances/*pharmacology ; Humans ; Matrix Metalloproteinase 3 ; Metalloendopeptidases/*genetics ; Mice ; Neoplasm Proteins/*genetics ; Proto-Oncogenes/*drug effects ; RNA/genetics ; RNA, Antisense ; RNA, Messenger/antagonists & inhibitors ; Tetradecanoylphorbol Acetate/pharmacology ; Transcription, Genetic/*drug effects ; Transfection
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  • 17
    Publication Date: 1988-03-11
    Description: Functional nicotinic cholinergic receptors are found on mammalian retinal ganglion cell neurons in culture. The neurotransmitter acetylcholine (ACh) can be detected in the medium of many of these retinal cultures, after release presumably from the choline acetyltransferase-positive amacrine cells. The postsynaptic effect of endogenous or applied ACh on the ganglion cells can be blocked with specific nicotinic antagonists. Here it is shown that within 24 hours of producing such a pharmacologic blockade, the retinal ganglion cells begin to sprout or regenerate neuronal processes. Thus, the growth-enhancing effect of nicotinic antagonists may be due to the removal of inhibition to growth by tonic levels of ACh present in the culture medium. Since there is a spontaneous leak of ACh in the intact retina, the effects of nicotinic cholinergic drugs on process outgrowth in culture may reflect a normal control mechanism for growth or regeneration of retinal ganglion cell processes that is exerted by ACh in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lipton, S A -- Frosch, M P -- Phillips, M D -- Tauck, D L -- Aizenman, E -- EY05477/EY/NEI NIH HHS/ -- EY06087/EY/NEI NIH HHS/ -- NS00879/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1988 Mar 11;239(4845):1293-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Neuroscience, Children's Hospital, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3344435" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Atropine/*pharmacology ; Cells, Cultured ; Mecamylamine/*pharmacology ; Picrotoxin/pharmacology ; Rats ; Receptors, Nicotinic/drug effects/*physiology ; Retina/*cytology ; Retinal Ganglion Cells/*cytology/drug effects ; Tubocurarine/*pharmacology
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  • 18
    Publication Date: 1988-07-29
    Description: The ionic currents of carotid body type I cells and their possible involvement in the detection of oxygen tension (Po2) in arterial blood are unknown. The electrical properties of these cells were studied with the whole-cell patch clamp technique, and the hypothesis that ionic conductances can be altered by changes in PO2 was tested. The results show that type I cells have voltage-dependent sodium, calcium, and potassium channels. Sodium and calcium currents were unaffected by a decrease in PO2 from 150 to 10 millimeters of mercury, whereas, with the same experimental protocol, potassium currents were reversibly reduced by 25 to 50 percent. The effect of hypoxia was independent of internal adenosine triphosphate and calcium. Thus, ionic conductances, and particularly the O2-sensitive potassium current, play a key role in the transduction mechanism of arterial chemoreceptors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lopez-Barneo, J -- Lopez-Lopez, J R -- Urena, J -- Gonzalez, C -- New York, N.Y. -- Science. 1988 Jul 29;241(4865):580-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departmento de Fisiologia, Facultad de Medicina, Universidad de Sevilla, Spain.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2456613" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/physiology ; Carotid Body/*physiology ; Cells, Cultured ; Chemoreceptor Cells/*physiology ; Electric Conductivity ; In Vitro Techniques ; Ion Channels/*physiology ; Membrane Potentials ; Oxygen/*blood ; Potassium/*physiology ; Rabbits ; Sodium/physiology
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  • 19
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-09-02
    Description: Two groups of mediators, the neuropeptides substance P and K and the monocyte-derived cytokines, interact in the neural regulation of immunological and inflammatory responses. Substance P, substance K, and the carboxyl-terminal peptide SP(4-11) induce the release of interleukin-1, tumor necrosis factor-alpha, and interleukin-6 from human blood monocytes. The neuropeptide effects occur at low doses, are specific as shown by inhibition studies with a substance P antagonist, and require de novo protein synthesis. Since monocyte-derived cytokines regulate multiple cellular functions in inflammation and immunity and since neuropeptides can be released from peripheral nerve endings into surrounding tissues, these findings identify a potent mechanism for nervous system regulation of host defense responses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lotz, M -- Vaughan, J H -- Carson, D A -- AI10386/AI/NIAID NIH HHS/ -- AR21175/AR/NIAMS NIH HHS/ -- AR25443/AR/NIAMS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1988 Sep 2;241(4870):1218-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Basic and Clinical Research, Research Institute of Scripps Clinic, La Jolla, CA 92037.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2457950" target="_blank"〉PubMed〈/a〉
    Keywords: Cells, Cultured ; Humans ; Interleukin-1/biosynthesis ; Interleukin-6 ; Interleukins/*biosynthesis ; Kinetics ; Monocytes/drug effects/immunology/*metabolism ; Neurokinin A ; Neuropeptides/*pharmacology ; Protein Biosynthesis ; Substance P/pharmacology ; Tumor Necrosis Factor-alpha/*biosynthesis
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  • 20
    Publication Date: 1986-08-15
    Description: Y-chromosomal DNA is present in the genomes of most human XX males. In these cases, maleness is probably due to the presence of the Y-encoded testis-determining factor (TDF). By means of in situ hybridization of a probe (pDP105) detecting Y-specific DNA to metaphases from three XX males, it was demonstrated that the Y DNA is located on the tip of the short arm of an X chromosome. This finding supports the hypothesis that XX maleness is frequently the result of transfer of Y DNA, including TDF, to a paternally derived X chromosome.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Andersson, M -- Page, D C -- de la Chapelle, A -- New York, N.Y. -- Science. 1986 Aug 15;233(4765):786-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3738510" target="_blank"〉PubMed〈/a〉
    Keywords: Cells, Cultured ; Chromosome Mapping ; DNA/*genetics ; Humans ; Lymphocyte Activation ; Lymphocytes/cytology ; Male ; Metaphase ; Nucleic Acid Hybridization ; *Sex Chromosome Aberrations ; Sex Determination Analysis ; *X Chromosome ; *Y Chromosome
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  • 21
    Publication Date: 1986-09-05
    Description: Expression of the ras oncogene is thought to be one of the contributing events in the initiation of certain types of human cancer. To determine the cellular activities that are directly triggered by ras proteins, the early consequences of microinjection of the human H-ras proteins into quiescent rat embryo fibroblasts were investigated. Within 30 minutes to 1 hour after injection, cells show a marked increase in surface ruffles and fluid-phase pinocytosis. The rapid enhancement of membrane ruffling and pinocytosis is induced by both the proto-oncogenic and the oncogenic forms of the H-ras protein. The effects produced by the oncogenic protein persist for more than 15 hours after injection, whereas the effects of the proto-oncogenic protein are short-lived, being restricted to a 3-hour interval after injection. The stimulatory effect of the ras oncogene protein on ruffling and pinocytosis is dependent on the amount of injected protein and is accompanied by an apparent stimulation of phospholipase A2 activity. These rapid changes in cell membrane activities induced by ras proteins may represent primary events in the mechanism of action of ras proteins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bar-Sagi, D -- Feramisco, J R -- CA07896/CA/NCI NIH HHS/ -- CA39811/CA/NCI NIH HHS/ -- GM28277/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1986 Sep 5;233(4768):1061-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3090687" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Cycle/drug effects ; Cell Membrane/*drug effects/ultrastructure ; Cells, Cultured ; Culture Media ; DNA/biosynthesis ; GTP-Binding Proteins/*pharmacology ; Humans ; Microinjections ; Oncogene Proteins, Viral/*pharmacology ; Phospholipases A/metabolism ; Phospholipases A2 ; Phospholipids/metabolism ; Pinocytosis/*drug effects ; Rats ; Time Factors
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  • 22
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1986-12-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barnes, D M -- New York, N.Y. -- Science. 1986 Dec 12;234(4782):1324-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2431480" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/*diagnosis/pathology ; Animals ; Brain/pathology ; Cells, Cultured ; Glutamates/pharmacology ; Glutamic Acid ; Humans ; Ion Channels/*physiology ; Mollusca ; Neurons/drug effects ; Neurotransmitter Agents/*physiology ; Time Factors
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  • 23
    Publication Date: 1986-07-25
    Description: Rat thyroid cells in culture, rendered quiescent by hormone deprivation, can be stimulated to undergo DNA synthesis in the absence of serum by the addition of purified thyrotropin. The primary effect in response to thyrotropin action in thyroid cells is the induction of the c-fos oncogene, followed by c-myc expression. This suggests that thyrotropin acts as a competence growth factor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Colletta, G -- Cirafici, A M -- Vecchio, G -- New York, N.Y. -- Science. 1986 Jul 25;233(4762):458-60.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3726540" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cattle ; Cell Division/drug effects ; Cells, Cultured ; Cycloheximide/pharmacology ; DNA/biosynthesis ; Oncogenes/*drug effects ; Rats ; Thyroid Gland/*cytology/drug effects/metabolism ; Thyrotropin/*pharmacology
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  • 24
    Publication Date: 1986-09-05
    Description: Damage to the vessel wall is a signal for endothelial migration and replication and for platelet release at the site of injury. Addition of transforming growth factor-beta (TGF-beta) purified from platelets to growing aortic endothelial cells inhibited [3H]thymidine incorporation in a concentration-dependent manner. A transient inhibition of DNA synthesis was also observed in response to wounding; cell migration and replication are inhibited during the first 24 hours after wounding. By 48 hours after wounding both TGF-beta-treated and -untreated cultures showed similar responses. Flow microfluorimetric analysis of cell cycle distribution indicated that after 24 hours of exposure to TGF-beta the cells were blocked from entering S phase, and the fraction of cells in G1 was increased. The inhibition of the initiation of regeneration by TGF-beta could allow time for recruitment of smooth muscle cells into the site of injury by other platelet components.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Heimark, R L -- Twardzik, D R -- Schwartz, S M -- HL-18645/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1986 Sep 5;233(4768):1078-80.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3461562" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Platelets/*physiology ; Cell Cycle/drug effects ; Cell Movement/drug effects ; Cells, Cultured ; Endothelium/cytology/*physiology ; Flow Cytometry ; *Growth Inhibitors ; Humans ; In Vitro Techniques ; Peptides/*pharmacology ; Rats ; Regeneration ; Transforming Growth Factors
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  • 25
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1986-10-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kolata, G -- New York, N.Y. -- Science. 1986 Oct 10;234(4773):151-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3018927" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acids/*metabolism ; Cells, Cultured ; Half-Life ; Proteins/*metabolism ; Ubiquitins/metabolism ; beta-Galactosidase/metabolism
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  • 26
    Publication Date: 1986-04-04
    Description: The human gonadotropin-releasing hormone (GnRH) precursor comprises the GnRH sequence followed by an extension of 59 amino acids. Basic amino acid residues in the carboxyl terminal extension may represent sites of processing to biologically active peptides. A synthetic peptide comprising the first 13 amino acids (H X Asp-Ala-Glu-Asn-Leu-Ile-Asp-Ser-Phe-Gln-Glu-Ile-Val X OH) of the 59-amino acid peptide was found to stimulate the release of gonadotropic hormones from human and baboon anterior pituitary cells in culture. The peptide did not affect thyrotropin or prolactin secretion. A GnRH antagonist did not inhibit gonadotropin stimulation by the peptide, and the peptide did not compete with GnRH for GnRH pituitary receptors, indicating that the action of the peptide is independent of the GnRH receptor. The GnRH precursor contains two distinct peptide sequences capable of stimulating gonadotropin release from human and baboon pituitary cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Millar, R P -- Wormald, P J -- Milton, R C -- New York, N.Y. -- Science. 1986 Apr 4;232(4746):68-70.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3082009" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Follicle Stimulating Hormone/*secretion ; Gonadotropin-Releasing Hormone/*analogs & derivatives/*pharmacology ; Humans ; Kinetics ; Luteinizing Hormone/*secretion ; Papio ; Peptide Fragments/*pharmacology ; Peptides/*pharmacology ; Pituitary Gland, Anterior/drug effects/*secretion ; Protein Precursors/*pharmacology ; Structure-Activity Relationship
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  • 27
    Publication Date: 1986-11-28
    Description: The bombesin-like peptides are potent mitogens for Swiss 3T3 fibroblasts, human bronchial epithelial cells, and cells isolated from small cell carcinoma of the lung. The mechanism of signal transduction in the proliferative response to bombesin was investigated by studying the effect of Bordetella pertussis toxin on bombesin-stimulated mitogenesis. At nanomolar concentrations, bombesin increased levels of c-myc messenger RNA and stimulated DNA synthesis in Swiss 3T3 cells. Treatment of the cells with pertussis toxin (5 nanograms per milliliter) completely blocked bombesin-enhanced c-myc expression and eliminated bombesin-stimulated DNA synthesis. This treatment had essentially no effect on the mitogenic responses to either platelet-derived growth factor or phorbol 12,13-dibutyrate. These results suggest that the mitogenic actions of bombesin-like growth factors are mediated through a pertussis toxin-sensitive guanine nucleotide-binding protein. Furthermore they indicate that bombesin-like growth factors act through pathways that are different from those activated by platelet-derived growth factor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Letterio, J J -- Coughlin, S R -- Williams, L T -- R01 HL 32898/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1986 Nov 28;234(4780):1117-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3465038" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bombesin/*pharmacology ; Cells, Cultured ; DNA, Neoplasm/*biosynthesis ; Humans ; Mice ; Oncogenes/*drug effects ; *Pertussis Toxin ; Phorbol 12,13-Dibutyrate ; Phorbol Esters/pharmacology ; Platelet-Derived Growth Factor/pharmacology ; Virulence Factors, Bordetella/*pharmacology
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  • 28
    Publication Date: 1986-10-24
    Description: Rhinosporidium seeberi, a fungus that is associated with polyp-like tumors in animals and man, was successfully cultivated. This organism stimulated proliferation of epithelial cells in vitro, producing polyp-like structures. Spores produced in culture required a period of aging or development, or both, before they were capable of reinitiating the growth cycle.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Levy, M G -- Meuten, D J -- Breitschwerdt, E B -- New York, N.Y. -- Science. 1986 Oct 24;234(4775):474-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3764422" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Cycle ; Cells, Cultured ; Dogs ; Epithelium/microbiology ; Humans ; Polyps/microbiology ; Rhinosporidium/*growth & development
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  • 29
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1986-08-22
    Description: The B19 parvovirus is responsible for at least three human diseases. The virus was successfully propagated in suspension cultures of human erythroid bone marrow from patients with hemolytic anemias; release of newly synthesized virus into the supernatants of infected cultures was observed. This culture system allowed study at a molecular level of events associated with the B19 life cycle. The B19 parvovirus replicated through high molecular weight intermediate forms, linked through a terminal hairpin structure. B19 replication in vitro was highly dependent on the erythropoietic content of cultures and on addition of the hormone erythropoietin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ozawa, K -- Kurtzman, G -- Young, N -- New York, N.Y. -- Science. 1986 Aug 22;233(4766):883-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3738514" target="_blank"〉PubMed〈/a〉
    Keywords: Anemia, Hemolytic/*microbiology ; Bone Marrow/*microbiology ; Cells, Cultured ; Culture Media ; DNA, Viral/analysis ; Erythropoietin/metabolism ; Humans ; Parvoviridae/*growth & development ; Virus Replication
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  • 30
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1986-01-24
    Description: A model of a blood vessel was constructed in vitro. Its multilayered structure resembled that of an artery and it withstood physiological pressures. Electron microscopy showed that the endothelial cells lining the lumen and the smooth muscle cells in the wall were healthy and well differentiated. The lining of endothelial cells functioned physically, as a permeability barrier, and biosynthetically, producing von Willebrand's factor and prostacyclin. The strength of the model depended on its multiple layers of collagen integrated with a Dacron mesh.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weinberg, C B -- Bell, E -- New York, N.Y. -- Science. 1986 Jan 24;231(4736):397-400.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2934816" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aorta/anatomy & histology/cytology ; Blood Vessels/*anatomy & histology/physiology ; Cattle ; Cells, Cultured ; Collagen/*physiology ; Endothelium/anatomy & histology/cytology ; Microscopy, Electron, Scanning ; *Models, Cardiovascular ; Muscle, Smooth, Vascular/anatomy & histology/cytology ; Polyethylene Terephthalates
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  • 31
    Publication Date: 1988-09-23
    Description: A defective herpes simplex virus 1 (HSV-1) vector, pHSVlac, has been developed that contains a transcription unit that places the Escherichia coli lacZ gene under the control of the HSV-1 immediate early 4/5 promoter. The vector pHSVlac was propagated with the HSV-1 temperature-sensitive mutant ts K as helper virus. Infection of neurons from rat superior cervical ganglia and dorsal root ganglia in primary culture resulted in stable expression of high levels of beta-galactosidase without cell death. These HSV-1 vectors should be useful for introducing genes into postmitotic cells, such as neurons, in vitro and in vivo.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2581874/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2581874/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Geller, A I -- Breakefield, X O -- DK39836/DK/NIDDK NIH HHS/ -- NS24279/NS/NINDS NIH HHS/ -- R01 NS034025/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1988 Sep 23;241(4873):1667-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, Massachusetts General Hospital, Boston 02114.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2843986" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; DNA, Viral/metabolism ; Defective Viruses/*genetics ; Escherichia coli/enzymology/*genetics ; Fluorescent Antibody Technique ; Galactosidases/*genetics ; *Genetic Vectors ; Helper Viruses ; Neurons/*microbiology ; Rats ; Recombinant Fusion Proteins/biosynthesis ; Simplexvirus/genetics ; Transfection ; beta-Galactosidase/biosynthesis/*genetics
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  • 32
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-07-22
    Description: Diets rich in fish and fish oils are associated with a reduced risk of cardiovascular disease and atherosclerosis. The interaction of a commercial fish oil extract (MaxEPA) with vascular endothelial cells (ECs) was studied as a possible mechanism for this protective effect. MaxEPA almost completely inhibited EC production of platelet-derived growth factor-like protein (PDGFc) while other lipids had a lesser effect or no effect. Overall protein synthesis was not reduced, nor was the inhibition due to defective secretion or increased degradation of the growth factor. Antioxidants suppressed the inhibitory activity of MaxEPA indicating that free radical oxidative processes were required for the inhibition. These results suggest that fish oils may suppress intimal smooth muscle cell proliferation by decreasing the production of EC-derived paracrine growth factors. This inhibitory process represents a possible molecular mechanism for the antiatherosclerotic action of marine lipids.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fox, P L -- DiCorleto, P E -- HL1561/HL/NHLBI NIH HHS/ -- HL29582/HL/NHLBI NIH HHS/ -- HL40352/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1988 Jul 22;241(4864):453-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Brain and Vascular Research, Cleveland Clinic Research Institute, OH 44195.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3393911" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cattle ; Cells, Cultured ; Endothelium, Vascular/*physiology ; Fatty Acids, Unsaturated/pharmacology ; Fish Oils/*pharmacology ; In Vitro Techniques ; Oxidation-Reduction ; Platelet-Derived Growth Factor/*biosynthesis ; Structure-Activity Relationship
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  • 33
    Publication Date: 1986-01-24
    Description: Parathyroid hormone-like factors have been found in extracts of tumors associated with humoral hypercalcemia of malignancy, many of which are of squamous epithelial origin. Cultured, nonmalignant human keratinocytes were examined for the production of similar factors. Keratinocyte-conditioned medium from ten cultures stimulated the production of cyclic adenosine monophosphate in clonally derived rat osteosarcoma cells sensitive to parathyroid hormone. Bovine [Nle8,18, Tyr34]PTH-(3-34)NH2, a competitive inhibitor of parathyroid hormone, stopped the adenylate cyclase production stimulated by keratinocyte-conditioned medium, but antisera to parathyroid hormone had no effect on such adenylate cyclase activity. The active component of keratinocyte-conditioned medium has a molecular weight exceeding that of native parathyroid hormone. These characteristics are shared by the parathyroid hormone receptor agonists associated with humoral hypercalcemia of malignancy, which suggests that normal human keratinocytes may produce a factor related to that produced by malignant tumors associated with humoral hypercalcemia of malignancy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Merendino, J J Jr -- Insogna, K L -- Milstone, L M -- Broadus, A E -- Stewart, A F -- AM 30102/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1986 Jan 24;231(4736):388-90.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2417317" target="_blank"〉PubMed〈/a〉
    Keywords: Adenylyl Cyclases/metabolism ; Animals ; Cattle ; Cells, Cultured ; Cyclic AMP/metabolism ; Epidermis/*cytology/metabolism/physiology ; Humans ; Isoproterenol/pharmacology ; Keratins/*metabolism ; Mice ; Osteosarcoma/metabolism ; Parathyroid Hormone/pharmacology/*physiology ; Peptide Fragments/pharmacology ; Rats ; Teriparatide
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  • 34
    Publication Date: 1986-12-05
    Description: Both long-term and short-term sensitization of the gill and siphon withdrawal reflex in Aplysia involve facilitation of the monosynaptic connections between the sensory and motor neurons. To analyze the relationship between these two forms of synaptic facilitation at the cellular and molecular level, this monosynaptic sensorimotor component of the gill-withdrawal reflex of Aplysia can be reconstituted in dissociated cell culture. Whereas one brief application of 1 microM serotonin produced short-term facilitation in the sensorimotor connection that lasted minutes, five applications over 1.5 hours resulted in long-term facilitation that lasted more than 24 hours. Inhibitors of protein synthesis or RNA synthesis selectively blocked long-term facilitation, but not short-term facilitation, indicating that long-term facilitation requires the expression of gene products not essential for short-term facilitation. Moreover, the inhibitors only blocked long-term facilitation when given during the serotonin applications; the inhibitors did not block the facilitation when given either before or after serotonin application. These results parallel those for behavioral performance in vertebrates and indicate that the critical time window characteristic of the requirement for macromolecular synthesis in long-term heterosynaptic facilitation is not a property of complex circuitry, but an intrinsic characteristic of specific nerve cells and synaptic connections involved in the long-term storage of information.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Montarolo, P G -- Goelet, P -- Castellucci, V F -- Morgan, J -- Kandel, E R -- Schacher, S -- NS 19595/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1986 Dec 5;234(4781):1249-54.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3775383" target="_blank"〉PubMed〈/a〉
    Keywords: Amanitins/pharmacology ; Anisomycin/pharmacology ; Aplysia/*physiology ; Cells, Cultured ; Memory/*physiology ; Memory, Short-Term/physiology ; Motor Neurons/drug effects ; Neurons, Afferent/drug effects ; Protein Biosynthesis ; RNA, Messenger/biosynthesis ; Reflex/drug effects ; Serotonin/pharmacology
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  • 35
    Publication Date: 1986-02-21
    Description: Long-term cultures were established of HTLV-III-infected T4 cells from patients with the acquired immune deficiency syndrome (AIDS) and of T4 cells from normal donors after infection of the cells in vitro. By initially reducing the number of cells per milliliter of culture medium it was possible to grow the infected cells for 50 to 60 days. As with uninfected T cells, immunologic activation of the HTLV-III-infected cells with phytohemagglutinin led to patterns of gene expression typical of T-cell differentiation, such as production of interleukin-2 and expression of interleukin-2 receptors, but in the infected cells immunologic activation also led to expression of HTLV-III, which was followed by cell death. The results revealed a cytopathogenic mechanism that may account for T4 cell depletion in AIDS patients and suggest how repeated antigenic stimulation by infectious agents, such as malaria in Africa, or by allogeneic blood or semen, may be important determinants of the latency period in AIDS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zagury, D -- Bernard, J -- Leonard, R -- Cheynier, R -- Feldman, M -- Sarin, P S -- Gallo, R C -- New York, N.Y. -- Science. 1986 Feb 21;231(4740):850-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2418502" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/immunology/microbiology/*pathology ; Antigens, Differentiation, T-Lymphocyte ; Antigens, Surface/analysis ; Cell Differentiation ; Cells, Cultured ; Cytopathogenic Effect, Viral ; Deltaretrovirus/*growth & development ; Gene Expression Regulation ; Humans ; Interleukin-2/biosynthesis ; RNA-Directed DNA Polymerase/metabolism ; Receptors, Immunologic/biosynthesis ; Receptors, Interleukin-2 ; T-Lymphocytes/immunology/*microbiology
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  • 36
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-10-07
    Description: Adhesion of blood cells to endothelial cells is an essential component of all inflammatory responses. The capacity of the endothelium to support adhesion of neutrophils is increased by cytokines such as tumor necrosis factor-alpha, interleukin-1, and endotoxin. Another cytokine, transforming growth factor-beta (TGF-beta), was a strong inhibitor of basalneutrophil adhesion and also decreased the adhesive response of endothelial cells to tumor necrosis factor-alpha (TNF-alpha). The ability of cells to respond to TGF-beta was related to the duration of culture of endothelial cells after explantation from umbilical veins. TGF-beta is likely to serve an anti-inflammatory role at sites of blood vessel injury undergoing active endothelial regeneration.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gamble, J R -- Vadas, M A -- New York, N.Y. -- Science. 1988 Oct 7;242(4875):97-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Human Immunology, Institute of Medical and Veterinary Science, Adelaide, South Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3175638" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Adhesion/drug effects ; Cells, Cultured ; Endothelium, Vascular/cytology/drug effects/*physiology ; Humans ; Kinetics ; Neutrophils/cytology/drug effects/*physiology ; Transforming Growth Factors/*pharmacology ; Umbilical Veins
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  • 37
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-01-15
    Description: In a variety of vertebrates and invertebrates, long-lasting enhancement of synaptic transmission contributes to the storage of memory lasting one or more days. However, it has not been demonstrated directly whether this increase in synaptic transmission is caused by an enhancement of transmitter release or an increase in the sensitivity of the postsynaptic receptors. These possibilities can be distinguished by a quantal analysis in which the size of the miniature excitatory postsynaptic potential released spontaneously from the presynaptic terminal is used as a reference. By means of microcultures, in which single sensory and motor neurons of Aplysia were plated together, miniature excitatory postsynaptic potentials attributable to the spontaneous release of single transmitter quanta from individual presynaptic neurons were recorded and used to analyze long-term facilitation induced by repeated applications of 5-hydroxytryptamine. The results indicate that the facilitation is caused by an increase in the number of transmitter quanta released by the presynaptic neuron.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dale, N -- Schacher, S -- Kandel, E R -- GM32099/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1988 Jan 15;239(4837):282-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, College of Physicians and Surgeons of Columbia University, New York State Psychiatric Institute, NY 10032.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2892269" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aplysia/*physiology ; Cells, Cultured ; Evoked Potentials/drug effects ; Membrane Potentials ; Motor Neurons/drug effects/*physiology ; Neurons, Afferent/drug effects/*physiology ; Neurotransmitter Agents/*metabolism ; Serotonin/pharmacology ; Synapses/drug effects/*physiology
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  • 38
    Publication Date: 1988-07-01
    Description: In seven strains of cultured normal human osteoblast-like cells, a mean of 1615 molecules of tritium-labeled 17 beta-estradiol per cell nucleus could be bound to specific nuclear sites. The nuclear binding of the labeled steroid was temperature-dependent, steroid-specific, saturable, and cell type-specific. These are characteristics of biologically active estrogen receptors. Pretreatment with 10 nanomolar estradiol in vitro increased the specific nuclear binding of progesterone in four of six cell strains, indicating an induction of functional progesterone receptors. RNA blot analysis demonstrated the presence of messenger RNA for the human estrogen receptor. The data suggest that estrogen acts directly on human bone cells through a classical estrogen receptor-mediated mechanism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Eriksen, E F -- Colvard, D S -- Berg, N J -- Graham, M L -- Mann, K G -- Spelsberg, T C -- Riggs, B L -- AG-04875/AG/NIA NIH HHS/ -- CA-90441/CA/NCI NIH HHS/ -- HD-9140/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1988 Jul 1;241(4861):84-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Endocrine Research Unit, Mayo Clinic, Rochester, MN 55905.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3388021" target="_blank"〉PubMed〈/a〉
    Keywords: Binding, Competitive ; Cell Nucleus/metabolism ; Cells, Cultured ; DNA/genetics ; Dexamethasone/metabolism ; Diethylstilbestrol/metabolism ; Estradiol/metabolism/pharmacology ; Humans ; Nucleic Acid Hybridization ; Osteoblasts/drug effects/*metabolism ; Progesterone/metabolism ; Promegestone/metabolism ; RNA, Messenger/metabolism ; Receptors, Estrogen/drug effects/genetics/*metabolism ; Receptors, Progesterone/drug effects/metabolism ; Tritium
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  • 39
    Publication Date: 1988-06-10
    Description: The proliferating cell nuclear antigen (PCNA or cyclin) is a nuclear protein recently identified as a cofactor of DNA polymerase delta. When exponentially growing Balb/c3T3 cells are exposed to antisense oligodeoxynucleotides to PCNA, both DNA synthesis and mitosis are completely suppressed. A corresponding sense oligodeoxynucleotide has no inhibitory effects. These experiments indicate that PCNA (cyclin) is important in cellular DNA synthesis and in cell cycle progression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jaskulski, D -- deRiel, J K -- Mercer, W E -- Calabretta, B -- Baserga, R -- CA 42866/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1988 Jun 10;240(4858):1544-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Temple University Medical School, Philadelphia, PA 19140.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2897717" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autoantigens/*genetics ; Base Sequence ; Cell Division/drug effects ; Cells, Cultured ; Codon ; DNA Replication/*drug effects ; Kinetics ; Mice ; Mice, Inbred BALB C ; Mitosis/*drug effects ; Molecular Sequence Data ; Nuclear Proteins/*genetics ; Oligodeoxyribonucleotides/*pharmacology ; Proliferating Cell Nuclear Antigen
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  • 40
    Publication Date: 1988-09-30
    Description: Resistance to antineoplastic agents is the major obstacle to curative therapy of cancer. Tumor cell lines with acquired resistance to the antineoplastic agent cis-diamminedichloroplatinum(II) overexpressed metallothionein and demonstrated cross-resistance to alkylating agents such as chlorambucil and melphalan. Human carcinoma cells that maintained high levels of metallothionein because of chronic exposure to heavy metals were resistant to cis-diamminedichloroplatinum(II), melphalan, and chlorambucil. Furthermore, cells transfected with bovine papilloma virus expression vectors containing DNA encoding human metallothionein-IIA were resistant to cis-diamminedichloroplatinum(II), melphalan, and chlorambucil but not to 5-fluorouracil or vincristine. Thus, overexpression of metallothionein represents one mechanism of resistance to a subset of clinically important anticancer drugs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kelley, S L -- Basu, A -- Teicher, B A -- Hacker, M P -- Hamer, D H -- Lazo, J S -- CA-01012/CA/NCI NIH HHS/ -- CA-38497/CA/NCI NIH HHS/ -- CA-43917/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1988 Sep 30;241(4874):1813-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Pharmaceutical Research and Development Division, Bristol Myers Co., Wallingford, CT 06492.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3175622" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antineoplastic Agents ; Blotting, Northern ; Cells, Cultured ; *Drug Resistance ; In Vitro Techniques ; Metallothionein/*physiology ; Mice
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  • 41
    Publication Date: 1988-09-02
    Description: Peripheral blood lymphocytes (PBLs) isolated from woodchucks chronically infected with the woodchuck hepatitis virus (WHV) carry low levels of nonreplicating WHV DNA. When PBLs from chronic carrier woodchucks were activated in culture with the generalized mitogen lipopolysaccharide (LPS), WHV DNA replication was initiated in cells obtained from one of three animals examined. Intracellular WHV core particles, containing WHV DNA replication intermediates, RNA/DNA hybrid molecules, and an active endogenous DNA polymerase, appeared 3 days after the start of LPS stimulation. After 5 to 7 days of LPS stimulation, WHV DNA-containing particles, which displayed the properties of intact, mature virions, were released into the culture medium. These studies provide evidence for reactivation of a latent WHV infection of circulating lymphoid cells and indicate that the presence of nonreplicating hepadnaviral DNA in lymphoid cells represents a potentially active infection following cellular activation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Korba, B E -- Cote, P J -- Gerin, J L -- N01-AI-02651/AI/NIAID NIH HHS/ -- N01-AI-72623/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1988 Sep 2;241(4870):1213-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Molecular Virology and Immunology, Georgetown University Medical Center, Rockville, MD 20852.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3261887" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Centrifugation, Density Gradient ; Concanavalin A/pharmacology ; *DNA Replication ; Ducks/microbiology ; Hepatitis B virus/physiology ; Hepatitis Viruses/*physiology ; Hepatitis, Viral, Animal/*microbiology ; Interleukin-2/pharmacology ; Lipopolysaccharides/pharmacology ; Lymphocyte Activation ; Lymphocytes/*microbiology ; Marmota/*microbiology ; Mitogens/*pharmacology ; Nucleic Acid Hybridization ; Phytohemagglutinins/pharmacology ; Sciuridae/*microbiology ; *Virus Replication/*drug effects
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  • 42
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1986-06-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J L -- New York, N.Y. -- Science. 1986 Jun 20;232(4757):1500-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2872725" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/physiology ; Cells, Cultured ; Neurons/cytology/*metabolism ; Neurotransmitter Agents/*biosynthesis ; Peripheral Nerves/physiology
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  • 43
    Publication Date: 1986-06-06
    Description: Caffeine was shown to induce mitotic events in mammalian cells before DNA replication (S phase) was completed. Synchronized BHK cells that were arrested in early S phase underwent premature chromosome condensation, nuclear envelope breakdown, morphological "rounding up," and mitosis-specific phosphoprotein synthesis when they were exposed to caffeine. These mitotic responses occurred only after the cells had entered S phase and only while DNA synthesis was inhibited by more than 70 percent. Inhibitors of protein synthesis blocked these caffeine-induced events, while inhibitors of RNA synthesis had little effect. These results suggest that caffeine induces the translation or stabilizes the protein product (or products) of mitosis-related RNA that accumulates in S-phase cells when DNA replication is suppressed. The ability to chemically manipulate the onset of mitosis should be useful for studying the regulation of this event in mammalian cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schlegel, R -- Pardee, A B -- CA 22427/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1986 Jun 6;232(4755):1264-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2422760" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caffeine/*pharmacology ; Cells, Cultured ; Cricetinae ; Cycloheximide/pharmacology ; *DNA Replication ; Dactinomycin/pharmacology ; Interphase ; Mitosis/*drug effects ; RNA/metabolism
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  • 44
    Publication Date: 1986-05-23
    Description: Two metabolites of the steroid hormones progesterone and deoxycorticosterone, 3 alpha-hydroxy-5 alpha-dihydroprogesterone and 3 alpha, 5 alpha-tetrahydrodeoxycorticosterone, are potent barbiturate-like ligands of the gamma-aminobutyric acid (GABA) receptor-chloride ion channel complex. At concentrations between 10(-7) and 10(-5)M both steroids inhibited binding of the convulsant t-butylbicyclophosphorothionate to the GABA-receptor complex and increased the binding of the benzodiazepine flunitrazepam; they also stimulated chloride uptake (as measured by uptake of 36Cl-) into isolated brain vesicles, and potentiated the inhibitory actions of GABA in cultured rat hippocampal and spinal cord neurons. These data may explain the ability of certain steroid hormones to rapidly alter neuronal excitability and may provide a mechanism for the anesthetic and hypnotic actions of naturally occurring and synthetic anesthetic steroids.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Majewska, M D -- Harrison, N L -- Schwartz, R D -- Barker, J L -- Paul, S M -- New York, N.Y. -- Science. 1986 May 23;232(4753):1004-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2422758" target="_blank"〉PubMed〈/a〉
    Keywords: 20-alpha-Dihydroprogesterone/*analogs & derivatives/metabolism/pharmacology ; Animals ; Bicyclo Compounds/metabolism ; *Bicyclo Compounds, Heterocyclic ; Binding, Competitive ; Brain/metabolism ; Cells, Cultured ; Chlorides/metabolism ; Desoxycorticosterone/*analogs & derivatives/metabolism/pharmacology ; Drug Synergism ; Flunitrazepam/metabolism ; Hippocampus/metabolism ; In Vitro Techniques ; Ion Channels/metabolism ; Progesterone/*analogs & derivatives/metabolism/pharmacology ; Rats ; Receptors, GABA-A/*drug effects/metabolism ; Spinal Cord/metabolism
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  • 45
    Publication Date: 1986-12-19
    Description: Lymphocytes bearing the CD8 marker were shown to suppress replication of human immunodeficiency virus (HIV) in peripheral blood mononuclear cells. The effect was dose-dependent and most apparent with autologous lymphocytes; it did not appear to be mediated by a cytotoxic response. This suppression of HIV replication could be demonstrated by the addition of CD8+ cells at the initiation of virus production as well as after several weeks of virus replication by cultured cells. The observations suggest a potential approach to therapy in which autologous CD8 lymphocytes could be administered to individuals to inhibit HIV replication and perhaps progression of disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Walker, C M -- Moody, D J -- Stites, D P -- Levy, J A -- New York, N.Y. -- Science. 1986 Dec 19;234(4783):1563-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2431484" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/*immunology/therapy ; Antigens, Surface ; Cells, Cultured ; HIV/immunology/*physiology ; Humans ; Male ; RNA-Directed DNA Polymerase/metabolism ; T-Lymphocytes/*immunology ; *Virus Replication
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 46
    Publication Date: 1988-09-23
    Description: Lipoprotein lipase (LPL) plays a critical role in the metabolism of plasma lipoproteins. In 3T3-L1 adipocytes, insulin elicits the rapid release of LPL through mechanisms that are independent of energy metabolism and protein synthesis. Some of the metabolic actions of insulin may be mediated by the activation of a specific phospholipase that hydrolyzes a glycosyl phosphatidylinositol (PI) molecule. The insulin-sensitive glycosyl-PI is structurally similar to the glycolipid membrane anchor of a number of proteins. LPL appears to be anchored to the 3T3-L1 cell surface by glycosyl-PI, and its rapid release by insulin may be due to activation of a glycosyl-PI-specific phospholipase C.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chan, B L -- Lisanti, M P -- Rodriguez-Boulan, E -- Saltiel, A R -- DK33804/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1988 Sep 23;241(4873):1670-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Biochemical Endocrinology, Rockefeller University, New York, NY 10021.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2843987" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue/cytology/enzymology ; Animals ; Cell Membrane/metabolism ; Cells, Cultured ; Glycolipids/metabolism ; Heparitin Sulfate/metabolism ; Insulin/*physiology ; Lipoprotein Lipase/*metabolism ; Membrane Lipids/metabolism ; Phosphatidylinositol Diacylglycerol-Lyase ; Phosphatidylinositols/*metabolism ; Phosphoric Diester Hydrolases/metabolism ; Protein Binding
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  • 47
    Publication Date: 1988-06-10
    Description: The human platelet-derived growth factor (PDGF) receptor complementary DNA was cloned and expressed by transfection of Chinese hamster ovary (CHO) fibroblasts. The ability of CHO cells expressing the human receptor complementary DNA (CHO-HR5) to interact with different recombinant forms of PDGF (AA and BB homodimers) was tested. Both forms of PDGF bind to the transfected receptor, stimulate the receptor tyrosine kinase activity, and elicit a mitogenic response in a manner that was indistinguishable from the responses of Balb/c 3T3 cells to AA and BB forms of PDGF can be attributed to a single type of receptor and show that the AA form, like the BB form, is a true mitogen.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Escobedo, J A -- Navankasatussas, S -- Cousens, L S -- Coughlin, S R -- Bell, G I -- Williams, L T -- HL-32898/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1988 Jun 10;240(4858):1532-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of California, San Francisco.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2836953" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Division/drug effects ; Cell Line ; Cells, Cultured ; DNA Replication/drug effects ; Enzyme Activation ; Humans ; Kinetics ; Macromolecular Substances ; Mice ; Phosphorylation ; Platelet-Derived Growth Factor/genetics/*metabolism/pharmacology ; Protein-Tyrosine Kinases/*metabolism ; Receptors, Cell Surface/genetics/*metabolism ; Receptors, Platelet-Derived Growth Factor ; Recombinant Proteins/pharmacology ; Transfection
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  • 48
    Publication Date: 1988-06-10
    Description: Previous studies involving platelet-derived growth factor (PDGF) have been based on the premise that a single cell-surface receptor binds all three isoforms of PDGF (AA, BB, and AB). It is now shown that two populations of PDGF receptor exist and can be distinguished by their ligand binding specificity. The B receptor binds only the BB dimer, whereas the A/B receptor binds AA, BB, and AB dimers. Human dermal fibroblasts appear to express seven times as much B receptor as A/B receptor. The B receptor is responsible for most PDGF receptor phosphorylation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hart, C E -- Forstrom, J W -- Kelly, J D -- Seifert, R A -- Smith, R A -- Ross, R -- Murray, M J -- Bowen-Pope, D F -- DE07063-11/DE/NIDCR NIH HHS/ -- GM35501/GM/NIGMS NIH HHS/ -- HL18645/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1988 Jun 10;240(4858):1529-31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, University of Washington, Seattle 98195.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2836952" target="_blank"〉PubMed〈/a〉
    Keywords: Binding, Competitive ; Cell Membrane/metabolism ; Cells, Cultured ; Fibroblasts/metabolism ; Humans ; Kinetics ; Platelet-Derived Growth Factor/*metabolism ; Receptors, Cell Surface/*metabolism ; Receptors, Platelet-Derived Growth Factor ; Skin/*metabolism ; Structure-Activity Relationship
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 49
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-03-25
    Description: The elastin receptor complex contains a component of 67 kilodaltons that binds to a glycoconjugate affinity column containing beta-galactoside residues and is eluted from this column with lactose. This protein component is also released from the surface of cultured chondroblasts by incubation with lactose, and its association with immobilized elastin is inhibited by lactose. Since lactose also blocks elastic fiber formation by cultured chondroblasts, the galactoside-binding property of the elastin receptor is implicated in this process.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hinek, A -- Wrenn, D S -- Mecham, R P -- Barondes, S H -- HL-26499/HL/NHLBI NIH HHS/ -- HL-29594/HL/NHLBI NIH HHS/ -- HL-38627/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1988 Mar 25;239(4847):1539-41.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology and Physiology, Jewish Hospital, Washington University Medical Center, St. Louis, MO 63110.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2832941" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cartilage/analysis ; Cattle ; Cells, Cultured ; Chromatography, Affinity ; Elastin/metabolism ; Extracellular Matrix/drug effects/metabolism ; Galactosides/*metabolism ; Glycoconjugates/metabolism ; Glycosides/*metabolism ; Immunoassay ; Immunohistochemistry ; Lactose/pharmacology ; Lung/*analysis ; Microscopy, Electron ; Receptors, Cell Surface/drug effects/isolation & purification/*metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 50
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1986-06-27
    Description: Electrical activity may regulate a number of neuronal functions in addition to its role in transmitting signals along nerve cells. The hypothesis that electrical activity affects neurite elongation in sprouting neurons was tested by stimulating individual snail neurons isolated in cell culture. The findings demonstrated that growth cone advance, and thus neurite elongation, is reversibly stopped during periods when action potentials are experimentally evoked. A decrease in filopodial number and growth cone area was also observed. Thus, action potentials can mediate the cessation of neurite outgrowth and thereby may influence structure and connectivity within the nervous system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohan, C S -- Kater, S B -- HD18577/HD/NICHD NIH HHS/ -- NS15350/NS/NINDS NIH HHS/ -- NS21217/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1986 Jun 27;232(4758):1638-40.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3715470" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Axons/*physiology ; Cells, Cultured ; Electrophysiology ; Neurons/physiology ; Snails ; Synapses/physiology
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  • 51
    Publication Date: 1986-07-11
    Description: Cells with properties characteristic of mononuclear phagocytes were evaluated for infectivity with five different isolates of the AIDS virus, HTLV-III/LAV. Mononuclear phagocytes cultured from brain and lung tissues of AIDS patients harbored the virus. In vitro-infected macrophages from the peripheral blood, bone marrow, or cord blood of healthy donors produced large quantities of virus. Virus production persisted for at least 40 days and was not dependent on host cell proliferation. Giant multinucleated cells were frequently observed in the macrophage cultures and numerous virus particles, often located within vacuole-like structures, were present in infected cells. The different virus isolates were compared for their ability to infect macrophages and T cells. Isolates from lung- and brain-derived macrophages had a significantly higher ability to infect macrophages than T cells. In contrast, the prototype HTLV-III beta showed a 10,000-fold lower ability to infect macrophages than T cells and virus production was one-tenth that in macrophage cultures infected with other isolates, indicating that a particular variant of HTLV-III/LAV may have a preferential tropism for macrophages or T cells. These results suggest that mononuclear phagocytes may serve as primary targets for infection and agents for virus dissemination and that these virus-infected cells may play a role in the pathogenesis of the disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gartner, S -- Markovits, P -- Markovitz, D M -- Kaplan, M H -- Gallo, R C -- Popovic, M -- New York, N.Y. -- Science. 1986 Jul 11;233(4760):215-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3014648" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/*immunology ; Brain/cytology ; Cells, Cultured ; Child ; DNA, Viral/genetics ; Deltaretrovirus/isolation & purification ; Humans ; Lung/cytology ; Macrophages/physiology ; Nucleic Acid Hybridization ; Phagocytes/*physiology
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  • 52
    Publication Date: 1986-10-31
    Description: Neuroleukin is a lymphokine product of lectin-stimulated T cells that induces immunoglobulin secretion by cultured human peripheral blood mononuclear cells. Neuroleukin acts early in the in vitro response that leads to formation of antibody-secreting cells, but continued production of immunoglobulin by differentiated antibody-secreting cells is neuroleukin-independent. Although the factor is not directly mitogenic, cellular proliferation is a late component of the response to neuroleukin. Neuroleukin does not have B-cell growth factor (BCGF) or B-cell differentiation factor (BCDF) activity in defined assays. Neuroleukin-evoked induction of immunoglobulin secretion is both monocyte- and T-cell-dependent.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gurney, M E -- Apatoff, B R -- Spear, G T -- Baumel, M J -- Antel, J P -- Bania, M B -- Reder, A T -- 5PO1 NS24412/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1986 Oct 31;234(4776):574-81.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3020690" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/drug effects/physiology ; Bone Marrow/metabolism ; Cell Line ; Cells, Cultured ; Deltaretrovirus/genetics ; Glucose-6-Phosphate Isomerase ; Growth Substances/genetics/pharmacology/*physiology ; Humans ; Immunity, Cellular/drug effects ; Immunoglobulins/biosynthesis ; Lectins/pharmacology ; Leukemia/metabolism ; Lymphokines/genetics/pharmacology/*physiology ; Lymphoma/metabolism ; Mice ; Pokeweed Mitogens/pharmacology ; Sequence Homology, Nucleic Acid ; T-Lymphocytes/drug effects/*physiology
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  • 53
    Publication Date: 1986-03-07
    Description: The mechanism by which the estrogen receptor and other steroid hormone receptors regulate gene expression in eukaryotic cells is not well understood. In this study, a complementary DNA clone containing the entire translated portion of the messenger RNA for the estrogen receptor from MCF-7 human breast cancer cells was sequenced and then expressed in Chinese hamster ovary (CHO-K1) cells to give a functional protein. An open reading frame of 1785 nucleotides in the complementary DNA corresponded to a polypeptide of 595 amino acids and a molecular weight of 66,200, which is in good agreement with published molecular weight values of 65,000 to 70,000 for the estrogen receptor. Homogenates of transformed Chinese hamster ovary cells containing a protein that bound [3H]estradiol and sedimented as a 4S complex in salt-containing sucrose gradients and as an 8 to 9S complex in the absence of salt. Interaction of this receptor-[3H]estradiol complex with a monoclonal antibody that is specific for primate ER confirms the identity of the expressed complementary DNA as human estrogen receptor. Amino acid sequence comparisons revealed significant regional homology among the human estrogen receptor, the human glucocorticoid receptor, and the putative v-erbA oncogene product. This suggests that steroid receptor genes and the avian erythroblastosis viral oncogene are derived from a common primordial gene. The homologous region, which is rich in cysteine, lysine, and arginine, may represent the DNA-binding domain of these proteins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Greene, G L -- Gilna, P -- Waterfield, M -- Baker, A -- Hort, Y -- Shine, J -- CA-02897/CA/NCI NIH HHS/ -- HD17103/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1986 Mar 7;231(4742):1150-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3753802" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Amino Acids/analysis ; Antibodies, Monoclonal ; Base Sequence ; Cells, Cultured ; Cloning, Molecular ; DNA/*metabolism ; Female ; Humans ; Molecular Weight ; Receptors, Estrogen/*genetics ; Transformation, Genetic
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  • 54
    Publication Date: 1986-10-31
    Description: A novel 56,000-dalton growth factor found in mouse salivary gland was purified, molecularly cloned, and expressed in monkey COS cells. The protein is a neurotrophic factor and also, surprisingly, a lymphokine product of lectin-stimulated T cells. The factor was therefore named neuroleukin. Neuroleukin promotes the survival in culture of a subpopulation of embryonic spinal neurons that probably includes skeletal motor neurons. Neuroleukin also supports the survival of cultured sensory neurons that are insensitive to nerve growth factor, but has no effect on sympathetic or parasympathetic neurons. The amino acid sequence of neuroleukin is partly homologous to a highly conserved region of the external envelope protein of HTLV-III/LAV, the retrovirus that causes acquired immune deficiency syndrome.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gurney, M E -- Heinrich, S P -- Lee, M R -- Yin, H S -- 5PO1 NS-21442/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1986 Oct 31;234(4776):566-74.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3764429" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cells, Cultured ; Chick Embryo ; Cloning, Molecular ; DNA/genetics ; Glucose-6-Phosphate Isomerase ; Growth Substances/genetics/*physiology ; Lymphokines/genetics/*physiology ; Male ; Mice ; Mice, Inbred BALB C ; Motor Neurons/drug effects ; Muscles/innervation ; Nerve Growth Factors/genetics/isolation & purification/*physiology ; Neurons/drug effects ; Neurons, Afferent/drug effects ; Salivary Glands/metabolism ; Spinal Cord/cytology
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  • 55
    facet.materialart.
    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1986-03-28
    Description: The peripheral nervous system of vertebrates arises from the neural crest and the ectodermal placodes. Construction of quail-chick chimaeras has provided significant information on the migration and fate of the neural crest and placodal cells. Transplantation of neural crest tissue to various sites in these chimaeras has demonstrated that the differentiation of neural crest cells is controlled by environmental influences during their migration and, particularly, during gangliogenesis. Experiments with in vitro and monoclonal antibody techniques have shown that these environmental cues act on a heterogeneous population of neural crest cells whose developmental potencies are partly restricted to definite differentiation pathways.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Le Douarin, N M -- New York, N.Y. -- Science. 1986 Mar 28;231(4745):1515-22.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3952494" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal ; Cell Differentiation ; Cells, Cultured ; Chick Embryo ; Chimera ; Coturnix/embryology ; Ganglia/cytology/*embryology/growth & development ; Neural Crest/cytology/immunology/*physiology/transplantation ; Neuronal Plasticity ; Peripheral Nerves/*embryology
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  • 56
    Publication Date: 1986-05-23
    Description: The virulence loci of Agrobacterium tumefaciens are a set of linked transcriptional units that play an essential role in the early stages of plant tumorigenesis. These loci are induced upon cocultivation of the bacteria with plant cells. Seven phenolic compounds that are widely distributed among the angiosperm plants--catechol, gallic acid, pyrogallic acid, p-hydroxybenzoic acid, protocatechuic acid, beta-resorcylic acid, and vanillin--are able to induce the expression of the virulence loci. These phenolics in combination induce each transcriptional locus of the vir loci. Furthermore, this induction displays similar kinetics and genetic control to that observed during cocultivation of the bacteria with plant cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bolton, G W -- Nester, E W -- Gordon, M P -- R01 GM32618/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1986 May 23;232(4753):983-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3085219" target="_blank"〉PubMed〈/a〉
    Keywords: Cells, Cultured ; Culture Media ; Dose-Response Relationship, Drug ; Gene Expression Regulation/drug effects ; Genetic Engineering ; Phenols/*pharmacology ; Rhizobium/*genetics/pathogenicity ; beta-Galactosidase/genetics
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  • 57
    Publication Date: 1986-05-23
    Description: Cachectin (tumor necrosis factor) is a macrophage hormone strongly implicated in the pathogenesis of endotoxin-induced shock. The availability of a DNA probe complementary to the cachectin messenger RNA (mRNA), as well as a specific antibody capable of recognizing the cachectin gene product, has made it possible to analyze the regulation of cachectin gene expression under a variety of conditions. Thioglycollate-elicited peritoneal macrophages obtained from mice contain a pool of cachectin mRNA that is not expressed as protein. When the cells are stimulated with endotoxin, large quantity of additional cachectin mRNA is produced, and immunoreactive cachectin is secreted. Macrophages from mice of the C3H/HeJ strain do not produce cachectin in response to endotoxin. A dual defect appears to prevent cachectin expression. First, a diminished quantity of cachectin mRNA is expressed in response to low concentrations of endotoxin. Second, a post-transcriptional defect prevents the production of cachectin protein. Macrophages from endotoxin-sensitive mice do not produce cachectin if they are first treated with dexamethasone, apparently for similar reasons. These findings give new insight into the nature of the C3H/HeJ mutation and suggest an important mechanism by which glucocorticoids may act to suppress inflammation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Beutler, B -- Krochin, N -- Milsark, I W -- Luedke, C -- Cerami, A -- AI21359/AI/NIAID NIH HHS/ -- AM01314/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1986 May 23;232(4753):977-80.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3754653" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Dexamethasone/pharmacology ; Drug Resistance ; Endotoxins/*pharmacology ; Gene Expression Regulation/drug effects ; In Vitro Techniques ; Macrophages/drug effects/*metabolism ; Mice ; Mice, Inbred C3H/physiology ; *Protein Biosynthesis ; Proteins/genetics ; RNA, Messenger/metabolism ; Transcription, Genetic/drug effects ; Tumor Necrosis Factor-alpha
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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