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  • Cells, Cultured  (154)
  • American Association for the Advancement of Science (AAAS)  (154)
  • American Institute of Physics (AIP)
  • 1985-1989  (154)
Collection
Publisher
  • American Association for the Advancement of Science (AAAS)  (154)
  • American Institute of Physics (AIP)
Years
Year
  • 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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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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: 1989-12-22
    Description: Certain inflammatory stimuli render cultured human vascular endothelial cells hyperadhesive for neutrophils. This state is transient and reversible, in part because activated endothelial cells secrete a leukocyte adhesion inhibitor (LAI). LAI was identified as endothelial interleukin-8 (IL-8), the predominant species of which is an extended amino-terminal IL-8 variant. At nanomolar concentrations, purified endothelial IL-8 and recombinant human IL-8 inhibit neutrophil adhesion to cytokine-activated endothelial monolayers and protect these monolayers from neutrophil-mediated damage. These findings suggest that endothelial-derived IL-8 may function to attenuate inflammatory events at the interface between vessel wall and blood.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gimbrone, M A Jr -- Obin, M S -- Brock, A F -- Luis, E A -- Hass, P E -- Hebert, C A -- Yip, Y K -- Leung, D W -- Lowe, D G -- Kohr, W J -- P01-HL-36028/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1989 Dec 22;246(4937):1601-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2688092" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Biological Factors/pharmacology ; Cell Adhesion/drug effects ; Cells, Cultured ; Chemotactic Factors/*isolation & purification/pharmacology ; Culture Media/analysis ; Cytokines ; Endothelium, Vascular/cytology/drug effects/*physiology ; Humans ; Interleukin-1/*pharmacology ; Interleukin-8 ; Interleukins/*isolation & purification/pharmacology ; Molecular Sequence Data ; Neutrophils/cytology/drug effects/*physiology ; Recombinant Proteins/pharmacology
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  • 7
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-03-24
    Description: The N-methyl-D-aspartate (NMDA) class of excitatory amino acid receptors regulates the strength and stability of excitatory synapses and appears to play a major role in excitotoxic neuronal death associated with stroke and epilepsy. The conductance increase gated by NMDA is potentiated by the amino acid glycine, which acts at an allosteric site tightly coupled to the NMDA receptor. Indole-2-carboxylic acid (I2CA) specifically and competitively inhibits the potentiation by glycine of NMDA-gated current. In solutions containing low levels of glycine, I2CA completely blocks the response to NMDA, suggesting that NMDA alone is not sufficient for channel activation. I2CA will be useful for defining the interaction of glycine with NMDA receptors and for determining the in vivo role of glycine in excitotoxicity and synapse stabilization.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huettner, J E -- HL-35034/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1989 Mar 24;243(4898):1611-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Harvard Medical School, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2467381" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aspartic Acid/*analogs & derivatives/physiology ; Cells, Cultured ; Electric Conductivity ; Glycine/*antagonists & inhibitors ; In Vitro Techniques ; Indoles/*pharmacology ; Ion Channels/drug effects ; N-Methylaspartate ; Neural Inhibition ; Rats ; Receptors, N-Methyl-D-Aspartate ; Receptors, Neurotransmitter/*drug effects ; Structure-Activity Relationship
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  • 8
    Publication Date: 1989-12-22
    Description: The murine acquired immunodeficiency syndrome is induced by a defective retrovirus. To study the role of virus replication in this disease, helper-free stocks of defective Duplan virus were produced. These stocks were highly pathogenic in absence of detectable replicating murine leukemia viruses (MuLVs) other than xenotropic MuLV. They induced expansion of the infected cell population (over 1000-fold), and this cell expansion was oligoclonal in origin and, most likely, arose through cell division. These results suggest that this defective virus is oncogenic, inducing a primary neoplasia associated with an acquired immunodeficiency syndrome as a paraneoplastic syndrome. These data emphasize the need to determine whether virus replication is necessary for the progression of other immunodeficiency diseases, including acquired immunodeficiency syndrome, and whether these diseases also represent paraneoplastic syndromes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huang, M -- Simard, C -- Jolicoeur, P -- New York, N.Y. -- Science. 1989 Dec 22;246(4937):1614-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Biology, Clinical Research Institute of Montreal, Quebec, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2480643" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blotting, Southern ; Cells, Cultured ; DNA, Viral/isolation & purification ; Defective Viruses/isolation & purification/*pathogenicity ; Helper Viruses/isolation & purification ; Immunologic Deficiency Syndromes/*microbiology ; Leukemia Virus, Murine/pathogenicity ; Lymph Nodes/microbiology ; Lymphocytes/microbiology ; Mice ; Mice, Inbred C57BL ; RNA-Directed DNA Polymerase/analysis ; Retroviridae/isolation & purification/*pathogenicity ; Retroviridae Infections/*microbiology ; Spleen/microbiology
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  • 9
    Publication Date: 1989-06-09
    Description: Voltage-dependent Ca2+ channels (VDCCs) are modulators of synaptic plasticity, oscillatory behavior, and rhythmic firing in brain regions such as the hippocampus. The distribution and lateral mobility of VDCCs on CA1 hippocampal neurons have been determined with biologically active fluorescent and biotinylated derivatives of the selective probe omega-conotoxin in conjunction with circular dityndallism, digital fluorescence imaging, and photobleach recovery microscopy. On noninnervated cell bodies, VDCCs were found to be organized in multiple clusters, whereas after innervation the VDCCs were concentrated and immobilized at synaptic contact sites. On dendrites, VDCC distribution was punctate and was interrupted by extensive bare regions or abruptly terminated. More than 85% of the dendritic VDCCs were found to be immobile by fluorescence photobleach recovery. Thus, before synaptic contact, specific mechanisms target, segregate, and immobilize VDCCs to neuronal cell bodies and to specialized dendritic sites. Regulation of this distribution may be critical in determining the firing activity and integrative properties of hippocampal CA1 neurons.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jones, O T -- Kunze, D L -- Angelides, K J -- NS01218/NS/NINDS NIH HHS/ -- NS23575/NS/NINDS NIH HHS/ -- NS24606/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1989 Jun 9;244(4909):1189-93.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology and Molecular Biophysics, Baylor College of Medicine, Houston, TX 77030.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2543080" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium Channel Blockers/*pharmacology ; Calcium Channels/drug effects/*physiology ; Cells, Cultured ; Electric Conductivity ; Hippocampus/*physiology ; Membrane Potentials/drug effects ; Mollusk Venoms/*pharmacology ; Neurons/drug effects/*physiology ; Pyramidal Tracts/*physiology ; *omega-Conotoxins
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  • 10
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-01-20
    Description: DNA and nuclear proteins were transferred into cells simultaneously at more than 95% efficiency by means of vesicle complexes. The DNA was rapidly transported into the nuclei of cultured cells, and its expression reached a maximum within 6 to 8 hours after its introduction. Moreover, when the plasmid DNA and nuclear protein were cointroduced into nondividing cells in rat liver by injection into the portal veins of adult rats, the plasmid DNA was carried into liver cell nuclei efficiently by nuclear protein. The expression of the DNA in adult rat liver, on introduction of the DNA with nuclear protein, was more than five times as great as with nonnuclear protein.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaneda, Y -- Iwai, K -- Uchida, T -- New York, N.Y. -- Science. 1989 Jan 20;243(4889):375-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Molecular and Cellular Biology, Osaka University, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2911748" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blotting, Northern ; Cell Compartmentation ; Cell Nucleus/metabolism ; Cells, Cultured ; DNA/*metabolism/pharmacokinetics ; High Mobility Group Proteins/*metabolism ; Liver/*metabolism ; Mice ; Rats ; Transformation, Genetic
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  • 11
    Publication Date: 1989-02-17
    Description: Mouse 3T3 cell lines capable of constitutively synthesizing an RNA complementary to the messenger RNA encoding TIMP, tissue inhibitor of metalloproteinases, were constructed by transfection with appropriate plasmid constructs. Many of the lines were down-modulated for TIMP messenger RNA levels and secreted less TIMP into the culture medium. In comparison to noninvasive, nontumorigenic controls, these cells not only were invasive in a human amnion invasion assay, but also were tumorigenic and metastatic in athymic mice. These results indicate that TIMP suppresses oncogenicity, at least in immortal murine 3T3 cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Khokha, R -- Waterhouse, P -- Yagel, S -- Lala, P K -- Overall, C M -- Norton, G -- Denhardt, D T -- New York, N.Y. -- Science. 1989 Feb 17;243(4893):947-50.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, University of Western Ontario, London, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2465572" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; *Cell Transformation, Neoplastic ; Cells, Cultured ; Enzyme Inhibitors/*genetics/metabolism ; Female ; Metalloendopeptidases/antagonists & inhibitors ; Mice ; Mice, Nude ; Neoplasm Metastasis ; Pituitary Neoplasms/genetics/pathology ; RNA/*genetics ; RNA, Antisense ; RNA, Messenger/*antagonists & inhibitors/genetics ; Tissue Inhibitor of Metalloproteinases ; Transfection
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  • 12
    Publication Date: 1989-07-07
    Description: Basic fibroblast growth factor (bFGF) participates in many processes including early developmental events, angiogenesis, wound healing, and maintenance of neuronal cell viability. A 130-kilodalton protein was isolated on the basis of its ability to specifically bind to bFGF. A complementary DNA clone was isolated with an oligonucleotide probe corresponding to determined amino acid sequences of tryptic peptide fragments of the purified protein. The putative bFGF receptor encoded by this complementary DNA is a transmembrane protein that contains three extracellular immunoglobulin-like domains, an unusual acidic region, and an intracellular tyrosine kinase domain. These domains are arranged in a pattern that is different from that of any growth factor receptor described.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, P L -- Johnson, D E -- Cousens, L S -- Fried, V A -- Williams, L T -- CA 21765/CA/NCI NIH HHS/ -- R01 HL32898/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1989 Jul 7;245(4913):57-60.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Medicine, University of California, San Francisco 94143.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2544996" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cells, Cultured ; Chick Embryo ; *Cloning, Molecular ; DNA/*genetics ; Fibroblast Growth Factors/*genetics ; Kinetics ; Mice ; Molecular Sequence Data ; Peptide Fragments/analysis ; Receptors, Cell Surface/*genetics/metabolism ; Receptors, Fibroblast Growth Factor ; Recombinant Proteins/metabolism
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  • 13
    Publication Date: 1989-01-20
    Description: The patch-clamp technique was used to examine the effects of atrial natriuretic peptide (ANP) and its second messenger guanosine 3',5'-monophosphate (cGMP) on an amiloride-sensitive cation channel in the apical membrane of renal inner medullary collecting duct cells. Both ANP (10(-11) M) and dibutyryl guanosine 3',5'-monophosphate (10(-4) M) inhibited the channel in cell-attached patches, and cGMP (10(-5) M) inhibited the channel in inside-out patches. The inner medullary collecting duct is the first tissue in which ANP, via its second messenger cGMP, has been shown to regulate single ion channels. The results suggest that the natriuretic action of ANP is related in part to cGMP-mediated inhibition of electrogenic Na+ absorption by the inner medullary collecting duct.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Light, D B -- Schwiebert, E M -- Karlson, K H -- Stanton, B A -- DK-34533/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1989 Jan 20;243(4889):383-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, Dartmouth Medical School, Hanover, NH 03756.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2463673" target="_blank"〉PubMed〈/a〉
    Keywords: Aminoquinolines/pharmacology ; Animals ; Atrial Natriuretic Factor/*pharmacology ; Cell Membrane/drug effects ; Cells, Cultured ; Cyclic GMP/pharmacology ; Ion Channels/*drug effects ; Kidney Medulla/drug effects ; Kidney Tubules/*drug effects ; Kidney Tubules, Collecting/*drug effects ; Natriuresis ; Rats ; Sodium/metabolism
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  • 14
    Publication Date: 1989-07-28
    Description: Astrocytes have many neuronal characteristics, such as neurotransmitter receptors, ion channels, and neurotransmitter uptake systems. Cultured astrocytes were shown to express certain neuropeptide genes, with specificity for both the gene expressed and the brain region from which the cells were prepared. Somatostatin messenger RNA and peptides were detected only in cerebellar astrocytes, whereas proenkephalin messenger RNA and enkephalin peptides were present in astrocytes of cortex, cerebellum, and striatum. Cholecystokinin was not expressed in any of the cells. These results support the hypothesis that peptides synthesized in astrocytes may play a role in the development of the central nervous system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shinoda, H -- Marini, A M -- Cosi, C -- Schwartz, J P -- New York, N.Y. -- Science. 1989 Jul 28;245(4916):415-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Clinical Neuroscience Branch, National Institute of Neurological Disorders and Stroke, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2569236" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Astrocytes/*metabolism ; Blotting, Northern ; Cells, Cultured ; Cerebellum/cytology/metabolism ; Cerebral Cortex/cytology/metabolism ; Corpus Striatum/cytology/metabolism ; Enkephalin, Methionine/biosynthesis/genetics ; Enkephalins/biosynthesis/genetics ; *Gene Expression Regulation ; Neuropeptides/biosynthesis/*genetics ; Protein Precursors/biosynthesis/genetics ; RNA, Messenger/analysis ; Radioimmunoassay ; Rats ; Somatostatin/biosynthesis/genetics
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  • 15
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-03-24
    Description: Clonal cultures and monoclonal antibodies against a lineage-specific epitope, stage-specific embryonic antigen-1 (SSEA-1) were used to analyze the commitment of quail neural crest cells to the sensory neuron pathway. There were two distinct populations of sensory cells at the time of gangliogenesis. Postmitotic neuroblasts that remained in close association with the neural tube coexisted with a large number of pluripotent cells that formed the leading edge of the emigrating cells and gave rise to sensory and autonomic neuroblasts and to melanocytes. The data suggest a dual origin of spinal sensory neuroblasts and a predominantly late divergence of the autonomic and sensory lineages.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sieber-Blum, M -- HD21423/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1989 Mar 24;243(4898):1608-11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy and Cellular Biology, Medical College of Wisconsin, Milwaukee 53226.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2564699" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/immunology ; Antigens, CD15 ; Cell Differentiation ; Cell Division ; Cells, Cultured ; Coturnix ; Glycolipids/*physiology ; Neural Crest/*cytology ; Neurons, Afferent/*embryology ; Pigmentation
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  • 16
    Publication Date: 1989-06-09
    Description: The neuron-specific protein GAP-43 is associated with the membrane of the nerve growth cone and thus may be important to the activity of this distinctive neuronal structure. Transient transfection of COS and NIH 3T3 cells with appropriate vectors resulted in expression of GAP-43 in these non-neuronal cells; as in neurons, transfected GAP-43 associated with the membrane. In addition, many long fine filopodial processes extended from the periphery of such transfected cells. Stable CHO cell lines expressing GAP-43 also exhibited processes that were more numerous, far longer, and more complex than those of CHO cell lines not transfected or transfected with control plasmids. Thus GAP-43 may directly contribute to growth cone activity by regulating cell membrane structure and enhancing extension of filopodial processes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zuber, M X -- Goodman, D W -- Karns, L R -- Fishman, M C -- New York, N.Y. -- Science. 1989 Jun 9;244(4909):1193-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Developmental Biology Laboratory, Massachusetts General Hospital Cancer Center, Boston.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2658062" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cell Membrane/*ultrastructure ; Cells, Cultured ; Fluorescent Antibody Technique ; GAP-43 Protein ; Growth Substances/*physiology ; Membrane Proteins/genetics/*physiology ; Mice ; Nerve Tissue Proteins/genetics/*physiology ; Recombinant Proteins/pharmacology ; Transfection
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  • 17
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-02-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J L -- New York, N.Y. -- Science. 1989 Feb 10;243(4892):737-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2783787" target="_blank"〉PubMed〈/a〉
    Keywords: Cells, Cultured ; Electrophoresis/methods ; Humans ; Hypoxanthine Phosphoribosyltransferase/genetics ; *Mutagenicity Tests ; T-Lymphocytes/drug effects
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  • 18
    Publication Date: 1989-04-28
    Description: The rapid transductional sequences initiated by interferon-gamma (IFN-gamma) on binding to its receptor regulate functional and genomic responses in many cells but are not well defined. Induction of macrophage activation is an example of such functional and genomic changes in response to IFN-gamma. Addition of IFN-gamma to murine macrophages, at activating concentrations, produced rapid (within 60 seconds) alkalinization of the cytosol and a concomitant, rapid influx of 22Na+. Amiloride inhibited the ion fluxes and the accumulation of specific messenger RNA for two genes induced by IFN-gamma (the early gene JE and the beta chain of the class II major histocompatibility complex gene I-A). The data indicate that IFN-gamma initiates rapid exchange of Na+ and H+ by means of the Na+/H+ antiporter and that these amiloride-sensitive ion fluxes are important to some of the genomic effects of IFN-gamma.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Prpic, V -- Yu, S F -- Figueiredo, F -- Hollenbach, P W -- Gawdi, G -- Herman, B -- Uhing, R J -- Adams, D O -- New York, N.Y. -- Science. 1989 Apr 28;244(4903):469-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Duke University Medical Center, Durham, NC 27710.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2541500" target="_blank"〉PubMed〈/a〉
    Keywords: Amiloride/pharmacology ; Animals ; Carrier Proteins/antagonists & inhibitors/metabolism ; Cells, Cultured ; Cytosol/metabolism ; *Gene Expression Regulation ; Histocompatibility Antigens Class II/*genetics ; Hydrogen-Ion Concentration ; Interferon-gamma/*physiology ; Kinetics ; Macrophage Activation ; Macrophages/drug effects/metabolism ; Mice ; *Protons ; RNA, Messenger/biosynthesis ; Sodium/*metabolism ; Sodium-Hydrogen Antiporter
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  • 19
    Publication Date: 1989-01-20
    Description: Both interleukin-1 (IL-1) and platelet-derived growth factor (PDGF) induce proliferation of cultured fibroblasts and smooth muscle cells. These polypeptide mediators are released by activated macrophages and other cell types in response to injury and are thought to have a role in tissue remodeling and a number of pathologic processes. Analysis of the kinetics of [3H]thymidine incorporation by cultured fibroblasts demonstrated that the response to IL-1 is delayed approximately 8 hours relative to their response to PDGF. IL-1 transiently stimulated expression of the PDGF A-chain gene, with maximum induction after approximately 2 hours. Subsequent synthesis and release of PDGF activity into the medium was detected as early as 4 hours after IL-1 stimulation, and downregulation of the binding site for the PDGF-AA isoform of PDGF followed PDGF-AA secretion. Antibodies to PDGF completely block the mitogenic response to IL-1. Therefore, the mitogenic activity of IL-1 for fibroblasts and smooth muscle cells appears to be indirect and mediated by induction of the PDGF A-chain gene.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Raines, E W -- Dower, S K -- Ross, R -- HL-18645/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1989 Jan 20;243(4889):393-6.〈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/2783498" target="_blank"〉PubMed〈/a〉
    Keywords: Cells, Cultured ; Fibroblasts/cytology/*drug effects ; Gene Expression Regulation/drug effects ; Humans ; Interleukin-1/*pharmacology ; Muscle, Smooth/cytology/*drug effects ; Platelet-Derived Growth Factor/*physiology ; RNA, Messenger/genetics ; Time Factors
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  • 20
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-03-17
    Description: A central challenge in developmental neurobiology is to understand how an apparently homogeneous population of neuroepithelial cells in the early mammalian embryo gives rise to the great diversity of nerve cells (neurons) and supporting cells (glial cells) in the mature central nervous system. Because the optic nerve is one of the several types of glial cells but no intrinsic neurons, it is an attractive place to investigate how neuroepithelial cells diversify. Studies of developing rat optic nerve cells in culture suggest that both cell-cell interactions and intrinsic cellular programs play important parts in glial cell diversification.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Raff, M C -- New York, N.Y. -- Science. 1989 Mar 17;243(4897):1450-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2648568" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Astrocytes/cytology ; Brain/cytology ; Cell Differentiation ; Cell Movement ; Cells, Cultured ; Epithelial Cells ; Morphogenesis ; Neuroglia/*cytology ; Oligodendroglia/cytology ; Optic Nerve/*cytology ; Rats
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  • 21
    Publication Date: 1989-10-27
    Description: Activation of protein kinase C is thought to require association of the kinase with the cell membrane. It has been assumed that cellular substrates for the kinase must likewise be associated with membranes, and previous studies with membrane-associated myristoylated proteins have supported this view. It is now shown that a mutation that prevents the normal amino-terminal myristoylation of a prominent cellular substrate of protein kinase C, and appears to prevent its membrane association, does not prevent the normal phosphorylation of this protein in intact cells in response to phorbol esters. Thus, membrane association may not be required in order for protein kinase C substrates to undergo phosphorylation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Graff, J M -- Gordon, J I -- Blackshear, P J -- 2T32-GM 07171/GM/NIGMS NIH HHS/ -- AI27179/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1989 Oct 27;246(4929):503-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute Laboratories, Durham, NC 27710.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2814478" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cells, Cultured ; Chickens ; Enzyme Activation ; *Intracellular Signaling Peptides and Proteins ; Membrane Proteins/metabolism ; Mutation ; Myristic Acid ; Myristic Acids ; Phosphorylation ; Protein Kinase C/*metabolism ; Proteins/*metabolism ; Substrate Specificity ; Transfection
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  • 22
    Publication Date: 1989-02-10
    Description: A genomic sequence and cloned complementary DNA has been identified for a novel receptor-like gene of the PDGF receptor/CSF1 receptor subfamily (platelet-derived growth factor receptor/colony-stimulating factor type 1 receptor). The gene recognized a 6.4-kilobase transcript that was coexpressed in normal human tissues with the 5.3-kilobase PDGF receptor messenger RNA. Introduction of complementary DNA of the novel gene into COS-1 cells led to expression of proteins that were specifically detected with antiserum directed against a predicted peptide. When the new gene was transfected into COS-1 cells, a characteristic pattern of binding of the PDGF isoforms was observed, which was different from the pattern observed with the known PDGF receptor. Tyrosine phosphorylation of the receptor in response to the PDGF isoforms was also different from the known receptor. The new PDGF receptor gene was localized to chromosome 4q11-4q12. The existence of genes encoding two PDGF receptors that interact in a distinct manner with three different PDGF isoforms likely confers considerable regulatory flexibility in the functional responses to PDGF.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Matsui, T -- Heidaran, M -- Miki, T -- Popescu, N -- La Rochelle, W -- Kraus, M -- Pierce, J -- Aaronson, S -- New York, N.Y. -- Science. 1989 Feb 10;243(4892):800-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Cellular and Molecular Biology, National Cancer Institute, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2536956" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Cells, Cultured ; *Chromosomes, Human, Pair 4 ; Cloning, Molecular ; DNA/genetics ; Gene Expression Regulation ; *Genes ; Humans ; Molecular Sequence Data ; Multigene Family ; Platelet-Derived Growth Factor/*physiology ; Protein-Tyrosine Kinases/genetics ; RNA, Messenger/genetics ; Receptors, Cell Surface/*genetics ; Receptors, Platelet-Derived Growth Factor ; Tissue Distribution
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  • 23
    Publication Date: 1989-05-12
    Description: Methotrexate coupled to maleylated bovine serum albumin was taken up efficiently through the "scavenger" receptors present on macrophages and led to selective killing of intracellular Leishmania mexicana amazonensis amastigotes in cultured hamster peritoneal macrophages. The drug conjugate was nearly 100 times as effective as free methotrexate in eliminating the intracellular parasites. Furthermore, in a model of experimental cutaneous leishmaniasis in hamsters, the drug conjugate brought about more than 90% reduction in the size of footpad lesions within 11 days. In contrast, the free drug at a similar concentration did not significantly affect lesion size. These studies demonstrate the potential of receptor-mediated drug delivery in the therapy of macrophage-associated diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mukhopadhyay, A -- Chaudhuri, G -- Arora, S K -- Sehgal, S -- Basu, S K -- New York, N.Y. -- Science. 1989 May 12;244(4905):705-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Microbial Technology, Chandigarh, India.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2717947" target="_blank"〉PubMed〈/a〉
    Keywords: Albumins/*administration & dosage/metabolism ; Animals ; Cells, Cultured ; Cricetinae ; Female ; Kinetics ; Leishmania mexicana/*drug effects ; Leishmaniasis/*drug therapy ; Macrophages/metabolism/*parasitology ; Male ; *Membrane Proteins ; Mesocricetus ; Methotrexate/*administration & dosage/pharmacology/therapeutic use ; *Receptors, Immunologic/metabolism ; *Receptors, Lipoprotein ; Receptors, Scavenger ; Scavenger Receptors, Class B ; Serum Albumin, Bovine
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  • 24
    Publication Date: 1989-12-22
    Description: T cell clones obtained from a human volunteer immunized with Plasmodium falciparum sporozoites specifically recognized the native circumsporozoite (CS) antigen expressed on P. falciparum sporozoites, as well as bacteria- and yeast-derived recombinant falciparum CS proteins. The response of these CD4+ CD8- cells was species-specific, since the clones did not proliferate or secrete gamma interferon when challenged with sporozoites or recombinant CS proteins of other human, simian, or rodent malarias. The epitope recognized by the sporozoite-specific human T cell clones mapped to the 5' repeat region of the CS protein and was contained in the NANPNVDPNANP sequence.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nardin, E H -- Herrington, D A -- Davis, J -- Levine, M -- Stuber, D -- Takacs, B -- Caspers, P -- Barr, P -- Altszuler, R -- Clavijo, P -- AI25085/AI/NIAID NIH HHS/ -- AI62533/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1989 Dec 22;246(4937):1603-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical and Molecular Parasitology, New York University, NY 10010.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2480642" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antigens, CD4/*immunology ; Antigens, Protozoan/*immunology ; Cells, Cultured ; Clone Cells ; Epitopes/*analysis ; Humans ; Interferon-gamma/biosynthesis ; Lymphocyte Activation ; Malaria/*immunology ; Molecular Sequence Data ; Plasmodium falciparum/*immunology ; *Protozoan Proteins ; Recombinant Proteins/immunology ; T-Lymphocytes/*immunology
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  • 25
    Publication Date: 1989-07-28
    Description: The activity of an oncoprotein and the secretion of a pheromone can be affected by an unusual protein modification. Specifically, posttranslational modification of yeast a-factor and Ras protein requires an intermediate of the cholesterol biosynthetic pathway. This modification is apparently essential for biological activity. Studies of yeast mutants blocked in sterol biosynthesis demonstrated that the membrane association and biological activation of the yeast Ras2 protein require mevalonate, a precursor of sterols and other isoprenes such as farnesyl pyrophosphate. Furthermore, drugs that inhibit mevalonate biosynthesis blocked the in vivo action of oncogenic derivatives of human Ras protein in the Xenopus oocyte assay. The same drugs and mutations also prevented the posttranslational processing and secretion of yeast a-factor, a peptide that is farnesylated. Thus, the mevalonate requirement for Ras activation may indicate that attachment of a mevalonate-derived (isoprenoid) moiety to Ras proteins is necessary for membrane association and biological function. These observations establish a connection between the cholesterol biosynthetic pathway and transformation by the ras oncogene and offer a novel pharmacological approach to investigating, and possibly controlling, ras-mediated malignant transformations.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schafer, W R -- Kim, R -- Sterne, R -- Thorner, J -- Kim, S H -- Rine, J -- CA-45593/CA/NCI NIH HHS/ -- GM21841/GM/NIGMS NIH HHS/ -- GM31105/GM/NIGMS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1989 Jul 28;245(4916):379-85.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, University of California, Berkeley 94720.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2569235" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cells, Cultured ; Drosophila ; Electrophoresis, Polyacrylamide Gel ; Fungal Proteins/genetics/*metabolism ; *Genes, ras ; Humans ; Hydroxymethylglutaryl CoA Reductases/genetics ; Hydroxymethylglutaryl-CoA Synthase/genetics ; Immunoblotting ; Mevalonic Acid/biosynthesis ; Molecular Sequence Data ; Peptides/genetics/metabolism ; Precipitin Tests ; Protein Processing, Post-Translational ; Proto-Oncogene Proteins/genetics/*metabolism ; Proto-Oncogene Proteins p21(ras) ; Saccharomyces cerevisiae/genetics/physiology ; *Saccharomyces cerevisiae Proteins ; *Suppression, Genetic ; Xenopus ; *ras Proteins
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  • 26
    Publication Date: 1989-12-22
    Description: The purified human immunodeficiency virus type-l (HIV-l) Tat protein inhibited lymphocyte proliferation induced by tetanus toxoid or Candida antigens by 66 to 97% at nanomolar concentrations of Tat. In contrast, Tat did not cause a significant reduction of lymphocyte proliferation in response to mitogens such as phytohemagglutinin or pokeweed mitogen. Inhibition was blocked by oxidation of the cysteine-rich region of Tat or by incubation with an antibody to Tat before the assay. A synthetic Tat peptide (residues 1 to 58) also inhibited antigen-stimulated proliferation. Experiments with H9 and U937 cell lines showed that Tat can easily enter both lymphocytes and monocytes. The specific inhibition of antigen-induced lymphocyte proliferation by Tat mimics the effect seen with lymphocytes from HIV-infected individuals and suggests that Tat might directly contribute to the immunosuppression associated with HIV infection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Viscidi, R P -- Mayur, K -- Lederman, H M -- Frankel, A D -- AI29135/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1989 Dec 22;246(4937):1606-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, MD 21205.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2556795" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/immunology ; Cells, Cultured ; Concanavalin A ; DNA Replication/drug effects ; Gene Products, tat/immunology/*pharmacology ; HIV-1/genetics/*immunology ; HeLa Cells/metabolism ; Humans ; Immunosuppression ; Lymphocyte Activation/*drug effects ; Lymphocytes/drug effects/immunology ; Pokeweed Mitogens ; Promoter Regions, Genetic ; Recombinant Proteins/immunology/pharmacology ; Staphylococcal Protein A ; Trans-Activators/*pharmacology ; Transcriptional Activation ; tat Gene Products, Human Immunodeficiency Virus
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  • 27
    Publication Date: 1989-03-03
    Description: Sindbis virus, an enveloped virus with a single-stranded RNA genome, was engineered to express a bacterial protein, chloramphenicol acetyltransferase (CAT), in cultured insect, avian, and mammalian cells. The vectors were self-replicating and gene expression was efficient and rapid; up to 10(8) CAT polypeptides were produced per infected cell in 16 to 20 hours. CAT expression could be made temperature-sensitive by means of a derivative that incorporated a temperature-sensitive mutation in viral RNA synthesis. Vector genomic RNAs were packaged into infectious particles when Sindbis helper virus was used to supply virion structural proteins. The vector RNAs were stable to at least seven cycles of infection. The expression of CAT increased about 10(3)-fold, despite a 10(15)-fold dilution during the passaging. Sindbis virus vectors should prove useful for expressing large quantities of gene products in a variety of animal cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Xiong, C -- Levis, R -- Shen, P -- Schlesinger, S -- Rice, C M -- Huang, H V -- AG05681/AG/NIA NIH HHS/ -- AI11377/AI/NIAID NIH HHS/ -- AI24134/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1989 Mar 3;243(4895):1188-91.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, Washington University School of Medicine, St. Louis, MO 63110.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2922607" target="_blank"〉PubMed〈/a〉
    Keywords: Aedes ; Animals ; Bacteria/enzymology ; Cells, Cultured ; Chick Embryo ; Chloramphenicol O-Acetyltransferase/*genetics ; Codon ; Cricetinae ; DNA/genetics ; Drosophila ; Gene Amplification ; Gene Expression Regulation ; *Genetic Engineering ; *Genetic Vectors ; Humans ; Quail ; RNA, Viral/*genetics ; Sindbis Virus/*genetics ; Transcription, Genetic ; Transfection
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  • 28
    Publication Date: 1989-12-15
    Description: A protein secreted by cultured rat heart cells can direct the choice of neurotransmitter phenotype made by cultured rat sympathetic neurons. Structural analysis and biological assays demonstrated that this protein is identical to a protein that regulates the growth and differentiation of embryonic stem cells and myeloid cells, and that stimulates bone remodeling and acute-phase protein synthesis in hepatocytes. This protein has been termed D factor, DIA, DIF, DRF, HSFIII, and LIF. Thus, this cytokine, like IL-6 and TGF beta, regulates growth and differentiation in the embryo and in the adult in many tissues, now including the nervous system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yamamori, T -- Fukada, K -- Aebersold, R -- Korsching, S -- Fann, M J -- Patterson, P H -- New York, N.Y. -- Science. 1989 Dec 15;246(4936):1412-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Biology Division, California Institute of Technology, Pasadena 91125.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2512641" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cell Differentiation ; Cells, Cultured ; Choline/*physiology ; Cloning, Molecular ; DNA/genetics ; *Growth Inhibitors/genetics/pharmacology/secretion ; Humans ; Immunosorbent Techniques ; *Interleukin-6 ; Leukemia Inhibitory Factor ; *Lymphokines ; Mice ; Molecular Sequence Data ; Myocardium/*metabolism ; Neurons/*cytology ; Rats ; Sequence Homology, Nucleic Acid
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  • 29
    Publication Date: 1989-07-21
    Description: To characterize cell surface molecules involved in control of growth of malignant lymphocytes, monoclonal antibodies were raised against the human B lymphoblast cell line SKW6.4. One monoclonal antibody, anti-APO-1, reacted with a 52-kilodalton antigen (APO-1) on a set of activated human lymphocytes, on malignant human lymphocyte lines, and on some patient-derived leukemic cells. Nanogram quantities of anti-APO-1 completely blocked proliferation of cells bearing APO-1 in vitro in a manner characteristic of a process called programmed cell death or apoptosis. Cell death was preceded by changes in cell morphology and fragmentation of DNA. This process was distinct from antibody- and complement-dependent cell lysis and was mediated by the antibody alone. A single intravenous injection of anti-APO-1 into nu/nu mice carrying a xenotransplant of a human B cell tumor induced regression of this tumor within a few days. Histological thin sections of the regressing tumor showed that anti-APO-1 was able to induce apoptosis in vivo. Thus, induction of apoptosis as a consequence of a signal mediated through cell surface molecules like APO-1 may be a useful therapeutic approach in treatment of malignancy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Trauth, B C -- Klas, C -- Peters, A M -- Matzku, S -- Moller, P -- Falk, W -- Debatin, K M -- Krammer, P H -- New York, N.Y. -- Science. 1989 Jul 21;245(4915):301-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Immunology and Genetics, German Cancer Research Center, Heidelberg.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2787530" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/*immunology/therapeutic use ; Antigens, Neoplasm/immunology ; Autoradiography ; B-Lymphocytes/immunology ; Burkitt Lymphoma/immunology/therapy ; Cell Survival ; Cells, Cultured ; Electrophoresis, Polyacrylamide Gel ; Humans ; Leukemia, B-Cell/*immunology/pathology/therapy ; Mice ; Mice, Nude ; Precipitin Tests ; Remission Induction ; T-Lymphocytes/immunology ; Tumor Cells, Cultured
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  • 30
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-03-17
    Description: The beta-amyloid protein is progressively deposited in Alzheimer's disease as vascular amyloid and as the amyloid cores of neuritic plaques. Contrary to its metabolically inert appearance, this peptide may have biological activity. To evaluate this possibility, a peptide ligand homologous to the first 28 residues of the beta-amyloid protein (beta 1-28) was tested in cultures of hippocampal pyramidal neurons for neurotrophic or neurotoxic effects. The beta 1-28 appeared to have neurotrophic activity because it enhanced neuronal survival under the culture conditions examined. This finding may help elucidate the sequence of events leading to plaque formation and neuronal damage in Alzheimer's disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Whitson, J S -- Selkoe, D J -- Cotman, C W -- AG00538/AG/NIA NIH HHS/ -- AG07918/AG/NIA NIH HHS/ -- MH19691/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1989 Mar 17;243(4897):1488-90.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychobiology, University of California, Irvine 92717.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2928783" target="_blank"〉PubMed〈/a〉
    Keywords: Amyloid/*pharmacology ; *Amyloid beta-Peptides ; *Amyloid beta-Protein Precursor ; Animals ; Cell Adhesion/drug effects ; Cell Survival ; Cells, Cultured ; Hippocampus/*cytology/embryology ; Neurons/cytology ; Peptide Fragments/*pharmacology ; Rats ; Structure-Activity Relationship
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  • 31
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-07-07
    Description: beta-Adrenergic agonists activate the G protein, Gs, which stimulates cardiac calcium currents by both cytoplasmic, indirect and membrane-delimited, direct pathways. To test whether beta-adrenergic agonists might use both pathways in the heart, isoproterenol was rapidly applied to cardiac myocytes, resulting in a biphasic increase in cardiac calcium channel currents that had time constants of 150 milliseconds and 36 seconds. beta-Adrenergic antagonists of a G protein inhibitor blocked both the fast and slow responses, whereas the adenylyl cyclase activator forskolin produced only the slow response. The presence of a fast pathway in the heart can explain what the slow pathway cannot account for: the ability of cardiac sympathetic nerves to change heart rate within a single beat.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yatani, A -- Brown, A M -- HL36930/HL/NHLBI NIH HHS/ -- HL37044/HL/NHLBI NIH HHS/ -- NS23877/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1989 Jul 7;245(4913):71-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Physiology and Biophysics, Baylor College of Medicine, Houston, TX 77030.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2544999" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Atrial Function ; Calcium Channels/drug effects/*physiology ; Carbachol/pharmacology ; Cells, Cultured ; Colforsin/pharmacology ; GTP-Binding Proteins/*physiology ; Guinea Pigs ; Heart/*physiology ; Isoproterenol/*pharmacology ; Kinetics ; Membrane Potentials/drug effects ; *Signal Transduction
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  • 32
    Publication Date: 1989-06-16
    Description: The possibility of using the vascular endothelial cell as a target for gene replacement therapy was explored. Recombinant retroviruses were used to transduce the lacZ gene into endothelial cells harvested from mongrel dogs. Prosthetic vascular grafts seeded with the genetically modified cells were implanted as carotid interposition grafts into the dogs from which the original cells were harvested. Analysis of the graft 5 weeks after implantation revealed genetically modified endothelial cells lining the luminal surface of the graft. This technology could be used in the treatment of atherosclerosis disease and the design of new drug delivery systems.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wilson, J M -- Birinyi, L K -- Salomon, R N -- Libby, P -- Callow, A D -- Mulligan, R C -- New York, N.Y. -- Science. 1989 Jun 16;244(4910):1344-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute, Cambridge, MA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2734614" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Blood Vessel Prosthesis ; Carotid Arteries/surgery ; Cells, Cultured ; Dogs ; Endothelium, Vascular/*cytology/physiology/transplantation ; Genetic Vectors ; Retroviridae/genetics ; *Transfection
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  • 33
    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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  • 34
    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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  • 35
    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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  • 36
    Publication Date: 1989-03-17
    Description: Wall shear stress generated by blood flow may regulate the expression of fibrinolytic proteins by endothelial cells. Tissue plasminogen activator (tPA) and plasminogen activator inhibitor, type 1 (PAI-1) secretion by cultured human endothelial cells were not affected by exposure to venous shear stress (4 dynes/cm2). However, at arterial shear stresses of 15 and 25 dynes/cm2, the tPA secretion rate was 2.1 and 3.0 times greater, respectively, than the basal tPA secretion rate. PAI-1 secretion was unaffected by shear stress over the entire physiological range.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Diamond, S L -- Eskin, S G -- McIntire, L V -- HL 18672/HL/NHLBI NIH HHS/ -- HL 23016/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1989 Mar 17;243(4897):1483-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Rice University, Biomedical Engineering Laboratory, Houston, TX 77251.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2467379" target="_blank"〉PubMed〈/a〉
    Keywords: 1-Methyl-3-isobutylxanthine/pharmacology ; Cells, Cultured ; Endothelium, Vascular/*secretion ; Epoprostenol/pharmacology ; Glycoproteins/secretion ; Humans ; Iloprost ; In Vitro Techniques ; Indomethacin/pharmacology ; Plasminogen Inactivators ; Rheology ; Secretory Rate/drug effects ; Stress, Mechanical ; Time Factors ; Tissue Plasminogen Activator/*secretion
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  • 37
    Publication Date: 1989-02-03
    Description: Two autocrine proteins of 14 and 12 kilodaltons that induce the synthesis of rabbit fibroblast collagenase were identified. The proteins were purified from serum-free culture medium taken from rabbit synovial fibroblasts stimulated with phorbol myristate acetate. The amino-terminal sequences of the 14- and 12-kilodalton species were approximately 60 to 80 percent homologous with serum amyloid A and beta 2 microglobulin, respectively. The polyacrylamide gel-eluted proteins retained the ability to induce collagenase synthesis in rabbit and human fibroblasts. These autocrine proteins may provide a means to modulate collagenase synthesis in normal remodeling as well as in inflammation and disease states.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brinckerhoff, C E -- Mitchell, T I -- Karmilowicz, M J -- Kluve-Beckerman, B -- Benson, M D -- AM-20582/AM/NIADDK NIH HHS/ -- AM-7448/AM/NIADDK NIH HHS/ -- RR-00750/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1989 Feb 3;243(4891):655-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Dartmouth Medical School, Hanover, NH 03756.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2536953" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cells, Cultured ; Chromatography, High Pressure Liquid ; DNA Probes ; Enzyme Induction/drug effects ; Fibroblasts/enzymology ; Humans ; Immunosorbent Techniques ; Isoelectric Focusing ; Microbial Collagenase/*biosynthesis ; Molecular Sequence Data ; Nucleic Acid Hybridization ; RNA, Messenger ; Rabbits ; Serum Amyloid A Protein/genetics/isolation & purification/*pharmacology ; Synovial Membrane/*enzymology ; Tetradecanoylphorbol Acetate/pharmacology ; beta 2-Microglobulin/genetics/isolation & purification/*pharmacology
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  • 38
    Publication Date: 1989-01-13
    Description: A cellular sheath, the perineurium, forms a protective barrier around fascicles of nerve fibers throughout the peripheral nervous system. In a study to determine the cellular origin of perineurium, a culture system was used in which perineurium forms after purified populations of sensory neurons, Schwann cells, and fibroblasts are recombined. Before recombination, the Schwann cells or the fibroblasts were labeled by infection with a defective recombinant retrovirus whose gene product, beta-galactosidase, is histochemically detectable in the progeny of infected cells. Perineurial cells were labeled when fibroblasts had been infected but not when Schwann cells had been infected. Thus, perineurium arises from fibroblasts in vitro and, by implication, in vivo as well.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bunge, M B -- Wood, P M -- Tynan, L B -- Bates, M L -- Sanes, J R -- NS09923/NS/NINDS NIH HHS/ -- NS22828/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1989 Jan 13;243(4888):229-31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy and Neurobiology, Washington University School of Medicine, St. Louis, MO 63110.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2492115" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/ultrastructure ; Cell Transformation, Viral ; Cells, Cultured ; *Connective Tissue Cells ; Fetus ; Fibroblasts/*cytology ; Ganglia, Spinal/*cytology ; Genes ; Neurons/*cytology ; Rats ; Retroviridae/enzymology/*genetics ; Schwann Cells/cytology ; beta-Galactosidase/analysis/genetics
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  • 39
    Publication Date: 1989-10-20
    Description: A 73-kilodalton (kD) intracellular protein was found to bind to peptide regions that target intracellular proteins for lysosomal degradation in response to serum withdrawal. This protein cross-reacted with a monoclonal antibody raised to a member of the 70-kD heat shock protein (hsp70) family, and sequences of two internal peptides of the 73-kD protein confirm that it is a member of this family. In response to serum withdrawal, the intracellular concentration of the 73-kD protein increased severalfold. In the presence of adenosine 5'-triphosphate (ATP) and MgCl2, the 73-kD protein enhanced protein degradation in two different cell-free assays for lysosomal proteolysis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chiang, H L -- Terlecky, S R -- Plant, C P -- Dice, J F -- AG06116/AG/NIA NIH HHS/ -- DK07542/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1989 Oct 20;246(4928):382-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, Tufts University School of Medicine, Boston, MA 02111.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2799391" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cells, Cultured ; Heat-Shock Proteins/genetics/*physiology ; Immunoblotting ; Lysosomes/*metabolism ; Molecular Sequence Data ; Rats ; Ribonuclease, Pancreatic/genetics/*metabolism ; Sequence Homology, Nucleic Acid
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  • 40
    Publication Date: 1989-09-29
    Description: Autocrine growth due to dysregulated growth factor production may have a role in the development of neoplasia. Whether autocrine growth is stimulated by growth factor secretion in an autocrine loop or by intracellular binding of the growth factor to a receptor has been unclear. The carboxyl-terminus coding sequence for murine interleukin-3 (IL-3) was extended with an oligonucleotide encoding a four-amino acid endoplasmic reticulum retention signal. IL-3-dependent hematopoietic cells became growth factor-independent when the modified IL-3 gene was introduced by retroviral gene transfer, despite lack of secretion of the modified IL-3. Hence autocrine growth can occur as a result of the intracellular action of a growth factor and this mechanism may be important in neoplastic and normal cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dunbar, C E -- Browder, T M -- Abrams, J S -- Nienhuis, A W -- New York, N.Y. -- Science. 1989 Sep 29;245(4925):1493-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Clinical Hematology Branch, National Heart, Lung, and Blood Institute, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2789432" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Division/drug effects ; Cell Transformation, Neoplastic ; Cells, Cultured ; Clone Cells ; Interleukin-3/genetics/metabolism/*physiology ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Recombinant Fusion Proteins/pharmacology
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  • 41
    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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  • 42
    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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  • 43
    facet.materialart.
    Unknown
    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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  • 44
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1989-01-20
    Description: The relation between terminal mitosis and the events that determine the developmental fate of embryonic precursor cells is not well understood. This relation has now been investigated with [3H]thymidine autoradiography to determine the time of cell birth and with a culture system that allows the testing of the developmental potential of cells isolated from the chick embryo retina. Contrary to the situation in vivo, where neuronal differentiation always precedes photoreceptor differentiation, photoreceptor differentiation occurs prematurely and precedes neuronal differentiation when precursor cells are isolated from the retina at early embryonic stages. Thus, cells born by embryonic day 5 (ED-5) give rise predominantly to photoreceptors when isolated for culture on ED-6 but develop mainly as neurons when isolated on ED-8. This suggests that retinal precursor cells retain after terminal mitosis the capacity to develop either as neurons or as photoreceptors. Moreover, photoreceptor differentiation appears to represent a constitutive or "default" pathway that precursor cells follow in the absence of neuron-inducing signals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Adler, R -- Hatlee, M -- NEI 04859/PHS HHS/ -- New York, N.Y. -- Science. 1989 Jan 20;243(4889):391-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wilmer Eye Institute, School of Medicine, Johns Hopkins University, Baltimore, MD 21205.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2911751" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Differentiation ; Cells, Cultured ; Chick Embryo ; Mitosis ; *Neuronal Plasticity ; Retina/cytology/*embryology
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  • 45
    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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  • 46
    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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  • 47
    facet.materialart.
    Unknown
    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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  • 48
    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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  • 49
    Publication Date: 1987-10-23
    Description: Exposure to bacterial endotoxins has long been known to stimulate the release of anterior pituitary hormones; administration of endotoxin was at one time a common clinical test of anterior pituitary function. Endotoxin is a potent stimulus for production of the endogenous pyrogenic protein, interleukin-1 (IL-1), by macrophages and monocytes. The possibility that IL-1 has a direct effect on the secretion of hormones by rat pituitary cells in a monolayer culture was investigated. Recombinant human IL-1 beta stimulated the secretion of adrenocorticotropic hormone, luteinizing hormone, growth hormone, and thyroid-stimulating hormone. Increased hormone secretion into culture supernatants was found with IL-1 concentrations ranging from 10(-9) M to 10(-12) M. Prolactin secretion by the monolayers was inhibited by similar doses. These concentrations of IL-1 are within the range reported for IL-1 in serum, suggesting that IL-1 generated peripherally by mononuclear immune cells may act directly on anterior pituitary cells to modulate hormone secretion in vivo. Incubation of IL-1 solutions with antibody to IL-1 neutralized these actions. These pituitary effects of IL-1 suggest that this monokine may be an important regulator of the metabolic adaptations to infectious stressors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bernton, E W -- Beach, J E -- Holaday, J W -- Smallridge, R C -- Fein, H G -- New York, N.Y. -- Science. 1987 Oct 23;238(4826):519-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Neuropsychiatry, Walter Reed Army Institute of Research, Washington, D.C. 20307-5100.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2821620" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenocorticotropic Hormone/secretion ; Animals ; Cells, Cultured ; Dinoprostone ; Female ; Growth Hormone/secretion ; Humans ; Infection/physiopathology ; Inflammation/physiopathology ; Interleukin-1/*physiology ; Luteinizing Hormone/secretion ; Pituitary Gland, Anterior/*secretion ; Pituitary Hormones, Anterior/*secretion ; Prolactin/secretion ; Prostaglandins E/secretion ; Rats ; Rats, Inbred Strains ; Recombinant Proteins/pharmacology ; Thyrotropin/secretion
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  • 50
    Publication Date: 1987-08-28
    Description: Li-Fraumeni syndrome is manifested in a variety of neoplasms that are transmitted in a dominantly inherited pattern. The noncancerous skin fibroblasts of family members exhibit a unique characteristic of being resistant to the killing effect of ionizing radiation. A three- to eightfold elevation in expression of c-myc and an apparent activation of c-raf-1 gene have been observed in these noncancerous skin fibroblasts. These results may provide insight into the heritable defect underlying the familial predisposition to a variety of cancers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chang, E H -- Pirollo, K F -- Zou, Z Q -- Cheung, H Y -- Lawler, E L -- Garner, R -- White, E -- Bernstein, W B -- Fraumeni, J W Jr -- Blattner, W A -- CA45158/CA/NCI NIH HHS/ -- CO7488/CO/NCI NIH HHS/ -- New York, N.Y. -- Science. 1987 Aug 28;237(4818):1036-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3616624" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Transformation, Neoplastic/radiation effects ; Cells, Cultured ; Fibroblasts/*radiation effects ; Humans ; Mice ; Mice, Nude ; Neoplastic Syndromes, Hereditary/*genetics ; Oncogenes/*radiation effects ; Pedigree ; *Radiation Tolerance ; Skin/cytology/*radiation effects ; Syndrome
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  • 51
    Publication Date: 1987-10-09
    Description: Oncogenes encoding serine/threonine or tyrosine kinases were introduced into the established rodent fibroblast cell line NIH 3T3 and tested for tumorigenic and metastatic behavior in T cell-deficient nude mice. Transforming oncogenes of the ras family were capable of converting fibroblast cell lines to fully metastatic tumors. Cell lines transformed by the kinase oncogenes mos, raf, src, fes, and fms formed experimental metastases and (in some cases) these genes were more efficient at metastatic conversion than a mutant ras gene. In contrast, cells transformed by either of two nuclear oncogenes, myc or p53, were tumorigenic when injected subcutaneously but were virtually nonmetastatic after intravenous injection. These data demonstrate that, in addition to ras, a structurally divergent group of kinase oncogenes can induce the metastatic phenotype.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Egan, S E -- Wright, J A -- Jarolim, L -- Yanagihara, K -- Bassin, R H -- Greenberg, A H -- New York, N.Y. -- Science. 1987 Oct 9;238(4824):202-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Manitoba Institute of Cell Biology, University of Manitoba, Winnipeg, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3659911" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Transformation, Neoplastic ; Cells, Cultured ; *Genes ; Mice ; *Neoplasm Metastasis ; *Oncogenes ; Phenotype ; Protein Kinases/*genetics
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  • 52
    Publication Date: 1987-08-21
    Description: The molecular basis for the marked difference between primate and rodent cells in sensitivity to the cardiac glycoside ouabain has been established by genetic techniques. A complementary DNA encoding the entire alpha 1 subunit of the mouse Na+- and K+-dependent adenosine triphosphatase (ATPase) was inserted into the expression vector pSV2. This engineered DNA molecule confers resistance against 10(-4) M ouabain to monkey CV-1 cells. Deletion of sequences encoding the carboxyl terminus of the alpha 1 subunit abolish the activity of the complementary DNA. The ability to assay the biological activity of this ATPase in a transfection protocol permits the application of molecular genetic techniques to the analysis of structure-function relationships for the enzyme that establishes the internal Na+/K+ environment of most animal cells. The full-length alpha 1 subunit complementary DNA will also be useful as a dominant selectable marker for somatic cell genetic studies utilizing ouabain-sensitive cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kent, R B -- Emanuel, J R -- Ben Neriah, Y -- Levenson, R -- Housman, D E -- CA-07919/CA/NCI NIH HHS/ -- CA-26712/CA/NCI NIH HHS/ -- CA-38992/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1987 Aug 21;237(4817):901-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3039660" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Cercopithecus aethiops ; DNA/genetics ; Drug Resistance ; Gene Expression Regulation ; Macromolecular Substances ; Mice ; Ouabain/*pharmacology ; Sodium-Potassium-Exchanging ATPase/antagonists & inhibitors/*genetics ; Species Specificity ; Structure-Activity Relationship ; Transfection
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  • 53
    facet.materialart.
    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1987-05-15
    Description: Neoplasms produce substances that induce blood vessel formation (angiogenesis). Fractions from ethanol extracts of the Walker 256 carcinoma were isolated by silica column chromatography and C18 reversed-phase high-performance liquid chromatography. Two of the isolated fractions induced neovascularization when tested in the rabbit corneal micropocket assay. One of the fractions was identified as nicotinamide by desorption-electron impact mass spectrometry, nuclear magnetic resonance spectroscopy, and gas chromatography-mass spectrometry. The second active fraction contained nicotinamide as part of a more complex, as yet unidentified, molecular arrangement. Microgram quantities of commercial nicotinamide induced neovascularization in the corneal micropocket assay and in the chick chorioallantoic membrane assay.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kull, F C Jr -- Brent, D A -- Parikh, I -- Cuatrecasas, P -- New York, N.Y. -- Science. 1987 May 15;236(4803):843-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2437656" target="_blank"〉PubMed〈/a〉
    Keywords: Angiogenesis Inducing Agents/*isolation & purification/pharmacology ; Animals ; Carcinoma 256, Walker/*physiopathology ; Cells, Cultured ; Chick Embryo ; Cornea/blood supply ; Endothelium/cytology/drug effects ; Gas Chromatography-Mass Spectrometry ; Growth Substances/*isolation & purification ; Magnetic Resonance Spectroscopy ; Mass Spectrometry ; Mice ; Neovascularization, Pathologic ; Niacinamide/isolation & purification/pharmacology
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  • 54
    Publication Date: 1987-10-02
    Description: Epidermal growth factor (EGF) is a potent polypeptide mitogen originally isolated from the adult male mouse submaxillary gland. It also acts as a gastrointestinal hormone. EGF-immunoreactive material has recently been identified within neuronal fibers and terminals in rodent brain. In the present study, EGF was found to enhance survival and process outgrowth of primary cultures of subneocortical telencephalic neurons of neonatal rat brain in a dose-dependent manner. This effect was observed with EGF concentrations as low as 100 picograms per milliliter (0.016 nanomolar) and was dependent on the continuous presence of EGF in the medium. Similar effects were observed with basic fibroblast growth factor, but several other growth-promoting substances, including other mitogens for glial elements, were without effect. Thus EGF, in addition to its mitogenic and hormonal activities, may act as a neurite elongation and maintenance factor for select neurons of the rodent central nervous system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Morrison, R S -- Kornblum, H I -- Leslie, F M -- Bradshaw, R A -- NS19319/NS/NINDS NIH HHS/ -- NS19964/NS/NINDS NIH HHS/ -- T32-CA0905A/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1987 Oct 2;238(4823):72-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Chemistry, College of Medicine, University of California, Irvine 92717.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3498986" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Brain/*cytology ; Cell Survival/drug effects ; Cells, Cultured ; Epidermal Growth Factor/*physiology ; Growth Substances/pharmacology ; Rats
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  • 55
    Publication Date: 1987-07-10
    Description: Inhibin is a gonadal glycoprotein hormone that regulates the production of follicle-stimulating hormone (FSH) by the anterior pituitary gland and exhibits intragonadal actions as well. The present study shows that inhibin-like immunoreactivity (inhibin-LI) is present in cells of the cytotrophoblast layer of human placenta at term and in primary cultures of human trophoblasts. Human chorionic gonadotropin (hCG) stimulated secretion of inhibin-LI from these cultured placental cells. This effect was mimicked by 8-bromo-cyclic adenosine monophosphate (8-bromo-cAMP), forskolin, and cholera toxin, suggesting that the mechanism of hCG induction of placental inhibin-LI secretion is cAMP-dependent. Incubation with an antiserum that binds the alpha-subunit of human inhibin increased the secretion of hCG and gonadotropin-releasing hormone-like immunoreactivity (GnRH-LI) from trophoblast cells in culture, suggesting a local tonic inhibitory action of endogenous inhibin on hCG and GnRH-LI release. The action of inhibin on hCG secretion may partially require the presence of placental GnRH, as suggested by evidence that a synthetic GnRH antagonist partially reverses the hCG increase induced by inhibin immunoneutralization. Results suggest paracrine roles for both inhibin and GnRH in the regulation of placental hCG production.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Petraglia, F -- Sawchenko, P -- Lim, A T -- Rivier, J -- Vale, W -- AM26741/AM/NIADDK NIH HHS/ -- HD13527/HD/NICHD NIH HHS/ -- NS21182/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1987 Jul 10;237(4811):187-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3299703" target="_blank"〉PubMed〈/a〉
    Keywords: 8-Bromo Cyclic Adenosine Monophosphate/pharmacology ; Cells, Cultured ; Cholera Toxin/pharmacology ; Chorionic Gonadotropin/pharmacology/*secretion ; Chorionic Villi/analysis ; Colforsin/pharmacology ; Feedback ; Female ; Gonadotropin-Releasing Hormone/antagonists & inhibitors/pharmacology/secretion ; Humans ; Infant, Newborn ; Inhibins/analysis/*physiology ; Male ; Pregnancy ; Secretory Rate/drug effects ; Trophoblasts/analysis/drug effects/*secretion
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  • 56
    Publication Date: 1987-09-11
    Description: The validity of mouse liver tumor end points in assessing the potential hazards of chemical exposure to humans is a controversial but important issue, since liver neoplasia in mice is the most frequent tumor target tissue end point in 2-year carcinogenicity studies. The ability to distinguish between promotion of background tumors versus a genotoxic mechanism of tumor initiation by chemical treatment would aid in the interpretation of rodent carcinogenesis data. Activated oncogenes in chemically induced and spontaneously occurring mouse liver tumors were examined and compared as one approach to determine the mechanism by which chemical treatment caused an increased incidence of mouse liver tumors. Data suggest that furan and furfural caused an increased incidence in mouse liver tumors at least in part by induction of novel weakly activating point mutations in ras genes even though both chemicals did not induce mutations in Salmonella assays. In addition to ras oncogenes, two activated raf genes and four non-ras transforming genes were detected. The B6C3F1 mouse liver may thus provide a sensitive assay system to detect various classes of proto-oncogenes that are susceptible to activation by carcinogenic insult. As illustrated with mouse liver tumors, analysis of activated oncogenes in spontaneously occurring and chemically induced rodent tumors will provide information at a molecular level to aid in the use of rodent carcinogenesis data for risk assessment.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Reynolds, S H -- Stowers, S J -- Patterson, R M -- Maronpot, R R -- Aaronson, S A -- Anderson, M W -- New York, N.Y. -- Science. 1987 Sep 11;237(4820):1309-16.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3629242" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; *Cell Transformation, Neoplastic ; Cells, Cultured ; Liver Neoplasms/*genetics ; Mice ; Mutation ; Nucleic Acid Hybridization ; *Oncogenes ; *Proto-Oncogenes ; Risk
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  • 57
    Publication Date: 1987-11-27
    Description: In density-arrested monolayer cultures of Balb/c 3T3 cells, platelet-derived growth factor (PDGF) stimulates expression of the c-myc and c-fos proto-oncogenes, as well as the functionally uncharacterized genes, JE, KC, and JB. These genes are not coordinately regulated. Under ordinary conditions, c-fos, JE, KC, and JB respond to PDGF only when the cells are in a state of G0 growth arrest at the time of PDGF addition. The c-myc gene is regulated in opposition to the other genes, responding best to PDGF in cycling cultures.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rollins, B J -- Morrison, E D -- Stiles, C D -- CA 20042-09/CA/NCI NIH HHS/ -- GM 31489-04/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1987 Nov 27;238(4831):1269-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Medicine, Dana-Farber Cancer Institute, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3685976" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Cycle/drug effects ; Cell Division/drug effects ; Cells, Cultured ; Gene Expression Regulation/*drug effects ; Interphase ; Mice ; Mice, Inbred BALB C ; Platelet-Derived Growth Factor/*pharmacology ; Proto-Oncogenes/*drug effects ; Transcription, Genetic/*drug effects
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  • 58
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1987-12-18
    Description: The traditional view that quantal release of neurotransmitter results from the fusion of transmitter-containing vesicles with the neuronal membrane has been recently challenged. Although various alternative mechanisms have been proposed, a common element among them is the release of cytoplasmic transmitter, which, in one view, could occur through large conductance channels on the presynaptic membrane. Six nerve-muscle cell pairs were examined with a whole-cell patch clamp for the presence of such channels that are associated with the production of miniature end-plate potentials. Examination of the neuronal membrane current during the occurrence of 822 miniature end-plate potentials produced no evidence of large channels. Thus it is unlikely that quantal release is mediated by such channels in the neuromuscular junction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Young, S H -- Chow, I -- New York, N.Y. -- Science. 1987 Dec 18;238(4834):1712-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, UCLA School of Medicine 90024.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2891190" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Membrane/*physiology ; Cells, Cultured ; Membrane Potentials ; Motor Endplate/cytology/*physiology ; Neuromuscular Junction/*physiology ; Neurons/cytology/*physiology ; Neurotransmitter Agents/*secretion ; Xenopus
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  • 59
    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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  • 60
    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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  • 61
    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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  • 62
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    Unknown
    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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  • 63
    Publication Date: 1985-10-18
    Description: Developments in microscope, sensor, and image-processing technologies have led to integrated systems for the quantification of low-light-level emission signals from biological samples. Specificity is provided in the form of monoclonal antibodies and other ligands or enzyme substrates conjugated with efficient fluorophores. Fluorescent probes are also available for cellular macromolecular constituents and for free ions of biological interest such as H+ and Ca2+. The entire spectrum of photophysical phenomena can be exploited. Representative data are presented from studies of DNA conformation and architecture in polytene chromosomes and from studies of receptor-mediated endocytosis, calcium distribution, and the organization of the contractile apparatus in muscle cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Arndt-Jovin, D J -- Robert-Nicoud, M -- Kaufman, S J -- Jovin, T M -- FO6 TWOO960/TW/FIC NIH HHS/ -- New York, N.Y. -- Science. 1985 Oct 18;230(4723):247-56.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/4048934" target="_blank"〉PubMed〈/a〉
    Keywords: Analog-Digital Conversion ; Animals ; Cell Cycle ; Cells/*cytology ; Cells, Cultured ; Chromosomes/ultrastructure ; Drosophila ; Fluorescent Dyes ; Kinetics ; Microscopy, Fluorescence/instrumentation/*methods ; Salivary Glands/cytology
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  • 64
    Publication Date: 1985-05-31
    Description: The carcinogenic process is extremely complex and is affected by diverse environmental and host factors. The mechanism for the gradual development of the transformed phenotype (a process termed "progression") was studied in type 5 adenovirus (Ad5)-transformed rat embryo cells. Progression was not correlated with major changes in the pattern of integration of viral DNA sequences. Instead, it was associated with an increased methylation of integrated viral sequences other than those corresponding to the E1 transforming genes of Ad5. A single exposure of progressed cells to the demethylating agent 5-azacytidine (Aza) resulted in a stable reversion to the unprogressed state of the original parental clone. A further selection of cells after growth in agar allowed the isolation of Aza-treated clones that had regained the progressed phenotype. These observations indicate that progression is a reversible process and suggest that progression may be associated with changes in the state of methylation of one or more specific genes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Babiss, L E -- Zimmer, S G -- Fisher, P B -- CA-33434/CA/NCI NIH HHS/ -- CA-35675/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1985 May 31;228(4703):1099-101.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2581317" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoviruses, Human/*genetics ; Animals ; Azacitidine/*pharmacology ; Cell Division ; Cell Transformation, Viral/*drug effects ; Cells, Cultured ; DNA, Neoplasm/genetics ; DNA, Viral/genetics ; Gene Expression Regulation ; Genes, Viral ; *Methylation ; Mice ; Neoplasms, Experimental/*pathology ; Rats ; Rats, Inbred Strains/embryology ; Transcription, Genetic
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  • 65
    Publication Date: 1985-06-07
    Description: Many higher plants produce economically important organic compounds such as oils, resins, tannins, natural rubber, gums, waxes, dyes, flavors and fragrances, pharmaceuticals, and pesticides. However, most species of higher plants have never been described, much less surveyed for chemical or biologically active constituents, and new sources of commercially valuable materials remain to be discovered. Advances in biotechnology, particularly methods for culturing plant cells and tissues, should provide new means for the commercial processing of even rare plants and the chemicals they produce. These new technologies will extend and enhance the usefulness of plants as renewable resources of valuable chemicals. In the future, biologically active plant-derived chemicals can be expected to play an increasingly significant role in the commercial development of new products for regulating plant growth and for insect and weed control.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Balandrin, M F -- Klocke, J A -- Wurtele, E S -- Bollinger, W H -- New York, N.Y. -- Science. 1985 Jun 7;228(4704):1154-60.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3890182" target="_blank"〉PubMed〈/a〉
    Keywords: Antineoplastic Agents, Phytogenic/isolation & purification ; Cells, Cultured ; Insecticides/isolation & purification ; Plant Extracts/analysis ; Plant Growth Regulators/isolation & purification ; *Plants/analysis ; *Plants, Medicinal
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  • 66
    Publication Date: 1985-12-06
    Description: Rat atrial natriuretic factor (ANF) is translated as a 152-amino acid precursor preproANF. PreproANF is converted to the 126-amino acid proANF, the storage form of ANF in the atria. ANF isolated from the blood is approximately 25 amino acids long. It is demonstrated here that rat cardiocytes in culture store and secrete proANF. Incubation of proANF with serum produced a smaller ANF peptide. PreproANF seems to be processed to proANF in the atria, and proANF appears to be released into the blood, where it is converted by a protease to a smaller peptide.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bloch, K D -- Scott, J A -- Zisfein, J B -- Fallon, J T -- Margolies, M N -- Seidman, C E -- Matsueda, G R -- Homcy, C J -- Graham, R M -- Seidman, J G -- 1R23CA33570/CA/NCI NIH HHS/ -- HL07208/HL/NHLBI NIH HHS/ -- HL26215/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1985 Dec 6;230(4730):1168-71.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2933808" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Atrial Natriuretic Factor/*biosynthesis/genetics/secretion ; Autoradiography ; Cells, Cultured ; Electrophoresis, Polyacrylamide Gel ; Heart/physiology ; Immune Sera/immunology ; Myocardium/*cytology/metabolism ; Protein Precursors/*biosynthesis/genetics/secretion ; RNA, Messenger/genetics ; Rabbits/immunology ; Rats
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  • 67
    Publication Date: 1985-06-21
    Description: Fibroblasts possess several distinct mechanisms that control cellular adhesion to extracellular matrix macromolecules. Monoclonal antibodies to a 140-kilodalton (kD) cell surface glycoprotein inhibited the adhesion of fibroblastic Chinese hamster ovary cells to fibronectin-coated substrata but did not inhibit adhesion to substrata coated with vitronectin, laminin, serum, or other adhesive macromolecules. Thus the 140-kD glycoprotein appears to be involved in the fibronectin-mediated adhesion mechanism but not in other adhesion processes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brown, P J -- Juliano, R L -- GM26165/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1985 Jun 21;228(4706):1448-51.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/4012302" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal ; *Cell Adhesion ; Cell Membrane/immunology/*metabolism ; Cells, Cultured ; Cricetinae ; Cricetulus ; Fibroblasts/metabolism ; Fibronectins/*metabolism ; Glycoproteins/immunology/*metabolism ; Molecular Weight
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  • 68
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1985-06-28
    Description: Both elemental distribution and ion transport in cultured cells have been imaged by ion microscopy. Morphological and chemical information was obtained with a spatial resolution of approximately 0.5 micron for sodium, potassium, calcium, and magnesium in freeze-fixed, cryofractured, and freeze-dried normal rat kidney cells and Chinese hamster ovary cells. Ion transport was successfully demonstrated by imaging Na+-K+ fluxes after the inhibition of Na+- and K+ -dependent adenosine triphosphatase with ouabain. This method allows measurements of elemental (isotopic) distribution to be related to cell morphology, thereby providing the means for studying ion distribution and ion transport under different physiological, pathological, and toxicological conditions in cell culture systems.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chandra, S -- Morrison, G H -- R01GM24314/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1985 Jun 28;228(4707):1543-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2990033" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/analysis ; Cell Line ; Cells, Cultured ; Cricetinae ; Elements/*analysis ; Female ; Freeze Fracturing ; Kidney/*ultrastructure ; Magnesium/analysis ; Microscopy/methods ; Ouabain/pharmacology ; Ovary/*ultrastructure ; Potassium/analysis ; Rats ; Sodium/analysis ; Sodium-Potassium-Exchanging ATPase/antagonists & inhibitors ; Tissue Distribution
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  • 69
    Publication Date: 1985-03-22
    Description: Fibrinogen fragment D, which is heterogeneous, has several important biological functions. Human fibrinogen fragments D94 (molecular weight, 94,000), D78 (78,000), and E (52,000) were purified. Fragments D78 and D94 but not purified fibrinogen or fragment E specifically caused disorganization of bovine aortic endothelial cells cultured as monolayers. Within 2 hours of exposure to pathophysiological concentrations of fragment D, the confluent endothelial cells retracted from each other and projected pseudopodia. These disturbed cells subsequently became rounded and detached from the substrate. The actin present in stress fibers in stationary monolayer cells was diffusely redistributed in cells with fragment D-induced alterations in morphology. This effect was not observed in monolayers of kidney epithelial cells. The results demonstrate a specific effect of fibrinogen fragment D on the disorganization of cultured vascular endothelial cell monolayers and suggest that fragment D plays a role in the pathogenesis of syndromes with vascular endothelial damage.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dang, C V -- Bell, W R -- Kaiser, D -- Wong, A -- New York, N.Y. -- Science. 1985 Mar 22;227(4693):1487-90.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/4038818" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/analysis ; Animals ; Aorta ; Cattle ; Cell Adhesion/drug effects ; Cell Line ; Cells, Cultured ; Cytoskeleton/drug effects ; Endothelium/analysis/*cytology/drug effects/ultrastructure ; Epithelial Cells ; Fibrin Fibrinogen Degradation Products/*pharmacology ; Humans ; Kidney ; Pseudopodia/drug effects
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  • 70
    Publication Date: 1985-03-15
    Description: Human lymphocytes were exposed in vitro to ultrasound from two clinical devices, one of which was previously reported to have increased the frequency of sister chromatid exchanges. The ultrasonic exposures had no significant effect on the frequency of sister chromatid exchanges from three blood donors. Exposure to ultrasound also had no effect on cell cycle progression. A concomitant positive control (mitomycin C) resulted in a significant increase in sister chromatid exchanges.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ciaravino, V -- Brulfert, A -- Miller, M W -- Jacobson-Kram, D -- Morgan, W F -- ES03000/ES/NIEHS NIH HHS/ -- ES03238/ES/NIEHS NIH HHS/ -- GM22680/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1985 Mar 15;227(4692):1349-51.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3883487" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Cycle ; Cells, Cultured ; Humans ; Lymphocytes ; *Sister Chromatid Exchange ; Ultrasonography/*adverse effects
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  • 71
    Publication Date: 1985-12-20
    Description: A retroviral expression vector (N2) containing the selectable gene, neoR, has been used to determine the optimal conditions for infecting murine hematopoietic progenitor cells at high efficiency. After infected bone marrow cells were introduced into lethally irradiated mice, the presence, stability, and expression of the vector DNA sequences were analyzed either in individual spleen foci 10 days later or in the blood, bone marrow, and spleens of mice 4 months later. When bone marrow cells were cultured in medium containing virus with titers of more than 10(6) colony-forming units per milliliter in the presence of purified murine interleukin-3, more than 85 percent of the resulting foci contained vector DNA. This proviral vector DNA was intact. Efficient expression of the neoR gene was demonstrated in most of the DNA-positive foci examined. The spleens of reconstituted animals (over a long term) contained intact "vector DNA" and the blood and bone marrow expressed the neoR gene in some animals. Thus, a retroviral vector can be used to introduce intact exogenous DNA sequences into hematopoietic stem cells with high efficiency and with substantial expression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Eglitis, M A -- Kantoff, P -- Gilboa, E -- Anderson, W F -- New York, N.Y. -- Science. 1985 Dec 20;230(4732):1395-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2999985" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Bone Marrow/microbiology ; Cells, Cultured ; DNA Transposable Elements ; DNA, Viral/genetics ; *Genes, Viral ; *Genetic Vectors ; Mice ; Moloney murine leukemia virus/*genetics ; Spleen/microbiology ; *Transcription, Genetic
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  • 72
    Publication Date: 1985-02-15
    Description: Isolated rat hepatocytes were incubated in the presence or absence of extracellular calcium and alpha-tocopherol succinate with three different toxic chemicals; namely, adriamycin in combination with 1,3-bis(2-chloroethyl)-1-nitrosourea, ethyl methanesulfonate, and the calcium ionophore A23187. In the absence of extracellular calcium these three compounds were far more toxic to the cells than in its presence. The addition of vitamin E to calcium-free medium, however, protected hepatocytes against toxic injury, whereas cells incubated in medium containing calcium were not protected. Hepatocyte viability during each toxic insult correlated well with the cellular alpha-tocopherol content but not with the presence or absence of extracellular calcium. These results suggest that cellular alpha-tocopherol maintains the viability of the cell during a toxic insult and that the presence or absence of vitamin E in the incubation medium probably explains the conflicting reports on the role of extracellular calcium in toxic cell death.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fariss, M W -- Pascoe, G A -- Reed, D J -- ES01978/ES/NIEHS NIH HHS/ -- ES07060/ES/NIEHS NIH HHS/ -- New York, N.Y. -- Science. 1985 Feb 15;227(4688):751-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3918345" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcimycin/toxicity ; Calcium/*physiology ; Carmustine/toxicity ; Cell Survival/*drug effects ; Cells, Cultured ; Doxorubicin/toxicity ; Ethyl Methanesulfonate/toxicity ; Liver/cytology/*drug effects ; Male ; Rats ; Rats, Inbred Strains ; Vitamin E/*physiology
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  • 73
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1985-04-26
    Description: The interleukins, which have a regulatory role in immune function, may also mediate inflammation associated with injury to the brain. In experiments to determine the effect of these peptide hormones on glial cell proliferation in culture, interleukin-1 was a potent mitogen for astroglia but had no effect on oligodendroglia. Interleukin-2 did not alter the growth of either type of glial cell. Activity similar to that of interleukin-1 was detected in brains of adult rats 10 days after the brains had been injured. These findings suggest that interleukin-1, released by inflammatory cells, may promote the formation of scars by astroglia in the damaged mammalian brain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Giulian, D -- Lachman, L B -- EY04915/EY/NEI NIH HHS/ -- R01CA38043/CA/NCI NIH HHS/ -- RR5511/RR/NCRR NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1985 Apr 26;228(4698):497-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3872478" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Astrocytes/*pathology ; Brain Injuries/*pathology ; Cells, Cultured ; Chromatography, High Pressure Liquid/methods ; Chromatography, Ion Exchange/methods ; Interleukin-1/isolation & purification/*physiology ; Interleukin-2/physiology ; Isoelectric Focusing ; *Mitogens ; Oligodendroglia/pathology ; Rats
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  • 74
    Publication Date: 1985-11-29
    Description: The transfer of the human gene for hypoxanthine phosphoribosyltransferase (HPRT) into human bone marrow cells was accomplished by use of a retroviral vector. The cells were infected in vitro with a replication-incompetent murine retroviral vector that carried and expressed a mutant HPRT complementary DNA. The infected cells were superinfected with a helper virus and maintained in long-term culture. The production of progeny HPRT virus by the bone marrow cells was demonstrated with a colony formation assay on cultured HPRT-deficient, ouabain-resistant murine fibroblasts. Hematopoietic progenitor cells able to form colonies of granulocytes or macrophages (or both) in semisolid medium in the presence of colony stimulating factor were present in the nonadherent cell population. Colony forming units cloned in agar and subsequently cultured in liquid medium produced progeny HPRT virus, indicating infection of this class of hematopoietic progenitor cell.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gruber, H E -- Finley, K D -- Hershberg, R M -- Katzman, S S -- Laikind, P K -- Seegmiller, J E -- Friedmann, T -- Yee, J K -- Jolly, D J -- AM 13622/AM/NIADDK NIH HHS/ -- GM 28223/GM/NIGMS NIH HHS/ -- HD20034/HD/NICHD NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1985 Nov 29;230(4729):1057-61.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3864246" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Gene Expression Regulation ; *Genetic Engineering ; Genetic Vectors ; Hematopoietic Stem Cells/*physiology ; Humans ; Hypoxanthine Phosphoribosyltransferase/*genetics ; Mice ; Retroviridae/*genetics ; Transfection
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  • 75
    Publication Date: 1985-04-05
    Description: Formaldehyde, a common environmental pollutant, inhibits repair of O6-methylguanine and potentiates the mutagenicity of an alkylating agent, N-methyl-N-nitrosourea, in normal human fibroblasts. Because formaldehyde alone also causes mutations in human cells, the compound may cause genotoxicity by a dual mechanism of directly damaging DNA and inhibiting repair of mutagenic and carcinogenic DNA lesions caused by other chemical and physical carcinogens.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grafstrom, R C -- Curren, R D -- Yang, L L -- Harris, C C -- New York, N.Y. -- Science. 1985 Apr 5;228(4695):89-91.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3975633" target="_blank"〉PubMed〈/a〉
    Keywords: Bronchi/cytology ; Cells, Cultured ; DNA Repair/*drug effects ; Drug Synergism ; Fibroblasts/drug effects ; Formaldehyde/*adverse effects/pharmacology ; Guanine/analogs & derivatives/metabolism ; Humans ; Methylnitrosourea/pharmacology ; Mutagens/*pharmacology
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  • 76
    Publication Date: 1985-01-25
    Description: An in vitro model was developed to study the hepatic phase of Plasmodium falciparum, the only malaria parasite lethal to man. Primary cultures of human hepatocytes were inoculated with sporozoites of Brazilian and African strains of P. falciparum. On days 1 through 7 after inoculation examination of fluorescence-labeled and Giemsa-stained preparations demonstrated the presence of many intracellular parasites. In three separate sets of experiments all cultures were found to be infected with as many as 650 liver schizonts measuring up to 40 micrometers. After the addition of red blood cells, intraerythrocytic forms of P. falciparum were detected on days 12 and 13 by an immunofluorescence assay, indicating that the hepatic cycle had been completed in vitro.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mazier, D -- Beaudoin, R L -- Mellouk, S -- Druilhe, P -- Texier, B -- Trosper, J -- Miltgen, F -- Landau, I -- Paul, C -- Brandicourt, O -- New York, N.Y. -- Science. 1985 Jan 25;227(4685):440-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3880923" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Azure Stains ; Cells, Cultured ; Culture Media ; Erythrocytes/parasitology ; Fluorescent Antibody Technique ; Liver/*parasitology ; Plasmodium falciparum/cytology/*growth & development ; Time Factors
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  • 77
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1985-07-19
    Description: In addition to nerve growth factor (NGF), many proteins present in soluble tissue extracts and in the extracellular matrix influence the survival and development of cultured neurons. The structure, synthesis, and mechanism of action of NGF as a neurotrophic factor are considered along with the experiments on the new putative trophic molecules.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thoenen, H -- Edgar, D -- New York, N.Y. -- Science. 1985 Jul 19;229(4710):238-42.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2409599" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cattle ; Cell Survival ; Cells, Cultured ; Chick Embryo ; Chickens ; Cyclic AMP/physiology ; DNA/genetics ; Extracellular Matrix/physiology ; Humans ; Ion Channels/physiology ; Male ; Mice ; Molecular Weight ; Myocardium/cytology ; Nerve Growth Factors/genetics/isolation & purification/*physiology ; Neurons/physiology ; Protein Precursors/genetics ; RNA, Messenger/metabolism ; Rats ; Receptors, Cell Surface/physiology ; Receptors, Nerve Growth Factor ; Sympathetic Nervous System/cytology
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  • 78
    Publication Date: 1985-03-22
    Description: An earlier finding that lymphocytes from African patients with the acquired immune deficiency syndrome (AIDS) react with rabbit antiserum to purified antigens of bovine leukemia virus (BLV) prompted a study of the possible cross-reactions between a BLV-infected ovine cell line and human lymphocytes inoculated with a strain of lymphadenopathy syndrome-associated virus (LAV). A solid-phase radioimmunoassay was used to detect antigenic markers of the retroviruses. Crude extracts from short-term cultures of lymphocytes infected with LAV bound rabbit antisera to the LAV glycoprotein gp13 (molecular weight 13,000) and the BLV proteins p24 and gp51, but did not bind antibodies to the p24 of human T-cell leukemia virus type I (HTLV-I). Antiserum to LAV gp13 reacted with an ovine cell line producing BLV but also weakly with virus-free ovine cells. Lymphocyte cultures from four African patients with AIDS expressed BLV-related antigens within 6 to 10 days of culture, at the moment when particle-bound reverse transcriptase was produced. BLV-related antigens were induced in lymphocyte cultures from healthy individuals by addition of filtered supernatant or irradiated cells of the original culture. The antisera to BLV used in this study may prove useful for the detection of AIDS-associated viruses in short-term cultures of lymphocytes from AIDS patients or their contacts.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thiry, L -- Sprecher-Goldberger, S -- Jacquemin, P -- Cogniaux, J -- Burny, A -- Bruck, C -- Portetelle, D -- Cran, S -- Clumeck, N -- New York, N.Y. -- Science. 1985 Mar 22;227(4693):1482-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2579433" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/*microbiology ; Animals ; Antigens, Viral/analysis/*immunology ; Cell Line ; Cells, Cultured ; Cross Reactions ; Deltaretrovirus/*immunology ; Epitopes/immunology ; Humans ; Leukemia Virus, Bovine/*immunology ; Lymph Nodes/microbiology ; Lymphocytes/immunology/*microbiology ; Radioimmunoassay ; Retroviridae/*immunology ; Sheep ; Viral Proteins/immunology
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  • 79
    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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  • 80
    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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  • 81
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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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  • 82
    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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  • 83
    Publication Date: 1985-08-23
    Description: The DNA genomes of human T-lymphotropic virus type III (HTLV-III) isolated from 18 individuals with AIDS or who were at risk for AIDS were evaluated for evidence of variation. Although all of the 18 viral DNA's hybridized throughout their entire genomes to a full-length cloned probe of the original HTLV-III isolate, each of the 18 isolates showed a different restriction enzyme pattern. The number of restriction site differences between isolates ranged from only 1 site in 23 to at least 16 sites in 31. No particular viral genotype was associated with a particular disease state and 2 of the 18 patients had evidence of concurrent infection by more than one viral genotype. Propagation of three different viral isolates in vitro for up to 9 months did not lead to detectable changes in their restriction patterns. These findings indicate that different isolates of HTLV-III comprise a spectrum of highly related but distinguishable viruses and have important implications regarding the pathogenicity of HTLV-III and attempts to develop effective diagnostic, therapeutic, and preventive measures for this virus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wong-Staal, F -- Shaw, G M -- Hahn, B H -- Salahuddin, S Z -- Popovic, M -- Markham, P -- Redfield, R -- Gallo, R C -- New York, N.Y. -- Science. 1985 Aug 23;229(4715):759-62.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2992084" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/*microbiology ; Carrier State ; Cells, Cultured ; DNA Restriction Enzymes ; Deltaretrovirus/*genetics ; Humans ; Polymorphism, Genetic
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  • 84
    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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  • 85
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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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  • 86
    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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  • 87
    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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  • 88
    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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  • 89
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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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  • 90
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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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  • 91
    Publication Date: 1987-08-21
    Description: The genome of the human immunodeficiency virus HIV-1 contains at least eight genes, of which three (sor, R, and 3' orf) have no known function. In this study, the role of the sor gene was examined by constructing a series of proviral genomes of HIV-1 that either lacked the coding sequences for sor or contained point mutations in sor. Analysis of four such mutants revealed that although each clone could generate morphologically normal virus particles upon transfection, the mutant viruses were limited in their capacity to establish stable infection. Virus derived from transfection of Cos-1 cells (OKT4-) with sor mutant proviral DNA's was resistant to transmission to OKT4+ "susceptible" cells under cell-free conditions, and was transmitted poorly by coculture. In contrast, virus derived from clones with an intact sor frame was readily propagated by either approach. Normal amounts of gag-, env-, and pol-derived proteins were produced by all four mutants and assays in both lymphoid and nonlymphoid cells indicated that their trans-activating capacity was intact and comparable with wild type. Thus the sor gene, although not absolutely required in HIV virion formation, influences virus transmission in vitro and is crucial in the efficient generation of infectious virus. The data also suggest that sor influences virus replication at a novel, post-translational stage and that its action is independent of the regulatory genes tat and trs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fisher, A G -- Ensoli, B -- Ivanoff, L -- Chamberlain, M -- Petteway, S -- Ratner, L -- Gallo, R C -- Wong-Staal, F -- New York, N.Y. -- Science. 1987 Aug 21;237(4817):888-93.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3497453" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Communication ; Cells, Cultured ; Cercopithecus aethiops ; Cytopathogenic Effect, Viral ; Genes, Viral ; HIV/*genetics ; T-Lymphocytes/microbiology ; Viral Proteins/*physiology ; *Virus Replication
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 92
    Publication Date: 1987-01-16
    Description: Second messenger systems may modulate neuronal activity through protein phosphorylation. However, interactions between two major second messenger pathways, the cyclic AMP and phosphatidylinositol systems, are not well understood. The effects of activators of cyclic AMP-dependent protein kinase and protein kinase C on resting membrane properties, action potentials, and currents recorded from mouse dorsal root ganglion neurons and cerebral hemisphere neurons grown in primary dissociated cell culture were investigated. Neither forskolin (FOR) nor phorbol 12,13-dibutyrate (PDBu) altered resting membrane properties but both increased the duration of calcium-dependent action potentials in both central and peripheral neurons. By means of the single-electrode voltage clamp technique, FOR and PDBu were shown to decrease the same voltage-dependent potassium conductance. This suggests that two independent second messenger systems may affect the same potassium conductance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grega, D S -- Werz, M A -- Macdonald, R L -- NS 07231/NS/NINDS NIH HHS/ -- NS 19613/NS/NINDS NIH HHS/ -- NS 19692/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1987 Jan 16;235(4786):345-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2432663" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials/*drug effects ; Animals ; Brain/cytology ; Calcium/physiology ; Cells, Cultured ; Colforsin/*pharmacology ; Electric Conductivity ; Ganglia, Spinal/cytology ; Ion Channels/physiology ; Membrane Potentials ; Mice ; Neurons/drug effects/*physiology ; Phorbol Esters/*pharmacology ; Potassium/*physiology
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  • 93
    Publication Date: 1987-08-07
    Description: Human peripheral blood eosinophils, cells often associated with allergic and parasitic diseases, were maintained in vitro for at least 14 days when they were cocultured with bovine endothelial cells and for at least 7 days when cultured with either bovine or human endothelial cell-derived conditioned medium. The cocultured eosinophils became hypodense and generated about three times as much leukotriene C4 upon activation with calcium ionophore and killed about three times as many antibody-coated larvae of Schistosoma mansoni as freshly isolated normodense eosinophils. That these cells can be maintained in vitro by coculture with endothelial cells, and the surprising finding that the cocultured eosinophils have biochemical, cytotoxic, and density properties similar to those of eosinophils in patients with allergic and other disorders, will facilitate investigation of the regulation and role of these cells in health and disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rothenberg, M E -- Owen, W F Jr -- Silberstein, D S -- Soberman, R J -- Austen, K F -- Stevens, R L -- AI-22531/AI/NIAID NIH HHS/ -- AI-23483/AI/NIAID NIH HHS/ -- AM-01401/AM/NIADDK NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1987 Aug 7;237(4815):645-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3110954" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibody-Dependent Cell Cytotoxicity ; Calcimycin/pharmacology ; Cattle ; *Cell Communication ; Cell Survival ; Cells, Cultured ; Endothelium/*cytology ; Eosinophils/*cytology ; Humans ; SRS-A/biosynthesis ; Schistosoma mansoni/immunology ; Time Factors
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 94
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1987-12-04
    Description: The establishment of a cell culture system for the clonal development of blood cells has made it possible to identify the proteins that regulate the growth and differentiation of different blood cell lineages and to discover the molecular basis of normal and abnormal cell development in blood forming tissues. A model system with myeloid blood cells has shown that (i) normal blood cells require different proteins to induce cell multiplication (growth inducers) and cell differentiation (differentiation inducers), (ii) there is a hierarchy of growth inducers as cells become more restricted in their developmental program, and (iii) a cascade of interactions between proteins determines the correct balance between immature and mature cells in normal blood cell development. Gene cloning has shown that there is a family of different genes for these proteins. Normal protein regulators of blood cell development can control the abnormal growth of certain types of leukemic cells and suppress malignancy by inducing differentiation to mature nondividing cells. Chromosome abnormalities that give rise to malignancy in these leukemic cells can be bypassed and their effects nullified by inducing differentiation, which stops cells from multiplying. These blood cell regulatory proteins are active in culture and in the body, and they can be used clinically to correct defects in blood cell development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sachs, L -- New York, N.Y. -- Science. 1987 Dec 4;238(4832):1374-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Weizmann Institute of Science, Rehovot, Israel.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3317831" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bone Marrow Cells ; Cell Differentiation/drug effects ; Cells, Cultured ; Clone Cells/cytology ; Colony-Stimulating Factors/physiology/therapeutic use ; *Hematopoiesis/drug effects ; Hematopoietic Stem Cells/cytology ; Humans ; Interleukin-3/physiology/therapeutic use ; Leukemia, Myeloid/drug therapy/physiopathology ; Mice ; Neoplastic Stem Cells/drug effects/pathology
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  • 95
    Publication Date: 1987-05-08
    Description: In a variety of human genetic diseases, replacement of the absent or defective protein provides significant therapeutic benefits. As a model for a somatic cell gene therapy system, cultured murine fibroblasts were transfected with a human growth hormone (hGH) fusion gene and cells from one of the resulting clonal lines were subsequently implanted into various locations in mice. Such implants synthesized and secreted hGH, which was detectable in the serum. The function of the implants depended on their location and size, and on the histocompatibility of the donor cells with their recipients. The expression of hGH could be modified by addition of regulatory effectors, and, with appropriate immunosuppression, the implants survived for more than 3 months. This approach to gene therapy, here termed "transkaryotic implantation," is potentially applicable to many genetic diseases in that the transfected cell line can be extensively characterized prior to implantation, several anatomical sites are suitable for implantation, and regulated expression of the gene of therapeutic interest can be obtained.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Selden, R F -- Skoskiewicz, M J -- Howie, K B -- Russell, P S -- Goodman, H M -- AM-07055/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1987 May 8;236(4802):714-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3472348" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; DNA, Recombinant ; Fibroblasts/immunology/*transplantation ; *Genetic Engineering ; Graft Survival ; Growth Hormone/biosynthesis/*genetics ; Humans ; Immunosuppression ; Kidney ; Kinetics ; Mice ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Plasmids ; Therapeutics ; Transfection
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  • 96
    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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  • 97
    facet.materialart.
    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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  • 98
    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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  • 99
    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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  • 100
    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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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