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  • In Vitro Techniques  (61)
  • American Association for the Advancement of Science (AAAS)  (61)
  • American Chemical Society
  • Periodicals Archive Online (PAO)
  • 1985-1989  (61)
  • 1980-1984
  • 1965-1969
  • 1988  (39)
  • 1986  (22)
Collection
Keywords
Publisher
  • American Association for the Advancement of Science (AAAS)  (61)
  • American Chemical Society
  • Periodicals Archive Online (PAO)
Years
  • 1985-1989  (61)
  • 1980-1984
  • 1965-1969
Year
  • 1
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    Two forms of autosomal chronic granulomatous disease lack distinct neutrophil cytosol factors (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-12-02
    Description: Chronic granulomatous diseases of childhood (CGD) are a group of disorders of phagocytic cell superoxide (O2.-) production (respiratory burst). Anion exchange chromatography separated from normal neutrophil cytosol a 47-kilodalton neutrophil cytosol factor, NCF-1, that restored activity to defective neutrophil cytosol from most patients with autosomally inherited CGD in a cell-free O2.--generating system. A 65-kilodalton factor, NCF-2, restored activity to defective neutrophil cytosol from one patient with autosomal CGD. NCF-1, NCF-2, and a third cytosol fraction, NCF-3, were inactive alone or in pairs, but together replaced unfractionated cytosol in cell-free O2.- generation. Neutrophils deficient in NCF-1, but not NCF-2, did not phosphorylate the 47-kilodalton protein. It is proposed that NCF-1, NCF-2, and NCF-3 are essential for generation of O2.- by phagocytic cells and that genetic abnormalities of these cytosol components can result in the CGD phenotype.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nunoi, H -- Rotrosen, D -- Gallin, J I -- Malech, H L -- New York, N.Y. -- Science. 1988 Dec 2;242(4883):1298-301.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Bacterial Diseases Section, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2848319" target="_blank"〉PubMed〈/a〉
    Keywords: Blotting, Western ; Cell Membrane/metabolism ; Cytosol/metabolism ; Granulomatous Disease, Chronic/*metabolism ; Humans ; In Vitro Techniques ; Molecular Weight ; Neutrophils/*metabolism ; Phosphoproteins/metabolism ; Superoxides/*biosynthesis
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
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    Phosphatidylinositol-glycan anchors of membrane proteins: potential precursors of insulin mediators (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-04-22
    Description: BC3H1 myocytes release membrane-bound alkaline phosphatase to the incubation medium upon stimulation with insulin, following a time course that is consistent with the generation of dimyristoylglycerol and the appearance of a putative insulin mediator in the extracellular medium. The use of specific blocking agents shows, however, that alkaline phosphatase release and dimyristoylglycerol production are independent processes and that the blockade of either event inhibits the production of insulin mediator. These experiments suggest a new model of insulin action.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Romero, G -- Luttrell, L -- Rogol, A -- Zeller, K -- Hewlett, E -- Larner, J -- AI 18000/AI/NIAID NIH HHS/ -- AM 14334/AM/NIADDK NIH HHS/ -- AM 22125/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1988 Apr 22;240(4851):509-11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of Virginia School of Medicine, Charlottesville 22908.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3282305" target="_blank"〉PubMed〈/a〉
    Keywords: Alkaline Phosphatase/metabolism/secretion ; Animals ; Diglycerides/metabolism ; Enzyme Activation/drug effects ; Extracellular Space/enzymology ; Glycolipids/*physiology ; In Vitro Techniques ; Insulin/*pharmacology ; Kinetics ; Membrane Glycoproteins/*physiology ; Phosphatidylinositols/*physiology ; Pyruvate Dehydrogenase Complex/metabolism
    Print ISSN: 0036-8075
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  • 3
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    Antagonistic adrenergic-muscarinic regulation of M current in smooth muscle cells (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-01-08
    Description: The beta-adrenergic agonist isoproterenol and analogs of adenosine 3',5'-monophosphate (cAMP) induced a potassium current, M current, in freshly dissociated gastric smooth muscle cells. Muscarinic agonists suppress this current, apparently by acting at a locus downstream from regulation of cAMP levels by adenylate cyclase and phosphodiesterase. Thus, M current can be induced by an agent and regulated in antagonistic fashion by beta-adrenergic and muscarinic systems.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sims, S M -- Singer, J J -- Walsh, J V Jr -- DK 31620/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1988 Jan 8;239(4836):190-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, University of Massachusetts Medical School Worcester 01655.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2827305" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcholine/pharmacology ; Animals ; Bufo marinus ; Cyclic AMP/physiology ; Electric Conductivity ; In Vitro Techniques ; Isoproterenol/pharmacology ; Membrane Potentials/drug effects ; Muscarine/pharmacology ; Muscle, Smooth/*physiology ; Potassium/*physiology ; Receptors, Adrenergic, beta/*physiology ; Receptors, Muscarinic/*physiology ; Stomach/physiology
    Print ISSN: 0036-8075
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  • 4
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    A transcriptional enhancer 3' of C beta 2 in the T cell receptor beta locus (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-07-08
    Description: Run-on transcription experiments were used to demonstrate that transcription of T cell receptor beta chain V genes is activated by DNA rearrangement, in a manner similar to immunoglobulin genes. A transcriptional enhancer likely to be involved in this activation has been identified. A 25-kilobase region from J beta 1 to V beta 14 was tested for enhancer activity by transient transfections, and an enhancer was found 7.5 kilobases 3' of C beta 2. The beta enhancer has low activity relative to the simian virus 40 viral enhancer, does not display a preference for V beta promoters, has a T cell-specific activity, and binds two purified immunoglobulin heavy chain enhancer factors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McDougall, S -- Peterson, C L -- Calame, K -- GM29361/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1988 Jul 8;241(4862):205-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Chemistry, UCLA School of Medicine 90024.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2968651" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromosome Mapping ; *Enhancer Elements, Genetic ; Gene Expression Regulation ; Genes, Immunoglobulin ; Immunoglobulin Heavy Chains/genetics ; In Vitro Techniques ; Mice ; Nuclear Proteins/physiology ; Receptors, Antigen, T-Cell/*genetics ; Receptors, Antigen, T-Cell, alpha-beta ; *Regulatory Sequences, Nucleic Acid ; Transcription Factors/physiology ; Transcription, Genetic
    Print ISSN: 0036-8075
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  • 5
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    Identification of a putative regulator of early T cell activation genes (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-07-08
    Description: Molecules involved in the antigen receptor-dependent regulation of early T cell activation genes were investigated with the use of functional sequences of the T cell activation-specific enhancer of interleukin-2 (IL-2). One of these sequences forms a protein complex, NFAT-1, specifically with nuclear extracts of activated T cells. This complex appeared 10 to 25 minutes before the activation of the IL-2 gene. Studies with inhibitors of protein synthesis indicated that the time of synthesis of the activator of the IL-2 gene in Jurkat T cells corresponds to the time of appearance of NFAT-1. NFAT-1, or a very similar protein, bound functional sequences of the long terminal repeat (LTR) of the human immunodeficiency virus type 1; the LTR of this virus is known to be stimulated during early T cell activation. The binding site for this complex activated a linked promoter after transfection into antigen receptor-activated T cells but not other cell types. These characteristics suggest that NFAT-1 transmits signals initiated at the T cell antigen receptor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shaw, J P -- Utz, P J -- Durand, D B -- Toole, J J -- Emmel, E A -- Crabtree, G R -- CA 01048/CA/NCI NIH HHS/ -- CA 39612/CA/NCI NIH HHS/ -- HL 33942/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1988 Jul 8;241(4862):202-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Stanford University, CA 94305.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3260404" target="_blank"〉PubMed〈/a〉
    Keywords: Binding Sites ; DNA-Binding Proteins/*physiology ; *Enhancer Elements, Genetic ; HIV/genetics ; Humans ; In Vitro Techniques ; Interleukin-2/genetics ; *Lymphocyte Activation ; Nuclear Proteins/*physiology ; Receptors, Antigen, T-Cell/*physiology ; *Regulatory Sequences, Nucleic Acid ; T-Lymphocytes/*physiology ; Transcription Factors/*physiology
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  • 6
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    Newly identified brain potassium channels gated by the guanine nucleotide binding protein Go (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-12-09
    Description: Potassium channels in neurons are linked by guanine nucleotide binding (G) proteins to numerous neurotransmitter receptors. The ability of Go, the predominant G protein in the brain, to stimulate potassium channels was tested in cell-free membrane patches of hippocampal pyramidal neurons. Four distinct types of potassium channels, which were otherwise quiescent, were activated by both isolated brain G0 and recombinant Go alpha. Hence brain Go can couple diverse brain potassium channels to neurotransmitter receptors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉VanDongen, A M -- Codina, J -- Olate, J -- Mattera, R -- Joho, R -- Birnbaumer, L -- Brown, A M -- DK-19318/DK/NIDDK NIH HHS/ -- HL-31154/HL/NHLBI NIH HHS/ -- HL-37044/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1988 Dec 9;242(4884):1433-7.〈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/3144040" target="_blank"〉PubMed〈/a〉
    Keywords: Adenylyl Imidodiphosphate/pharmacology ; Animals ; Cattle ; Electric Conductivity ; GTP-Binding Proteins/*pharmacology ; Hippocampus/*physiology ; In Vitro Techniques ; Kinetics ; Macromolecular Substances ; Membrane Potentials/drug effects ; Potassium Channels/drug effects/*physiology ; Pyramidal Tracts/physiology ; Rats ; Recombinant Proteins/*pharmacology
    Print ISSN: 0036-8075
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  • 7
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    Identification of an intracellular peptide segment involved in sodium channel inactivation (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-09-23
    Description: Antibodies directed against a conserved intracellular segment of the sodium channel alpha subunit slow the inactivation of sodium channels in rat muscle cells. Of four site-directed antibodies tested, only antibodies against the short intracellular segment between homologous transmembrane domains III and IV slowed inactivation, and their effects were blocked by the corresponding peptide antigen. No effects on the voltage dependence of sodium channel activation or of steady-state inactivation were observed, but the rate of onset of the antibody effect and the extent of slowing of inactivation were voltage-dependent. Antibody binding was more rapid at negative potentials, at which sodium channels are not inactivated; antibody-induced slowing of inactivation was greater during depolarizations to more positive membrane potentials. The peptide segment recognized by this antibody appears to participate directly in rapid sodium channel inactivation during large depolarizations and to undergo a conformational change that reduces its accessibility to antibodies as the channel inactivates.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vassilev, P M -- Scheuer, T -- Catterall, W A -- NS 15751/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1988 Sep 23;241(4873):1658-61.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of Washington, School of Medicine, Seattle 98195.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2458625" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antibodies ; Cytoplasm/analysis ; In Vitro Techniques ; Ion Channels/*metabolism ; Membrane Potentials ; Molecular Sequence Data ; Peptides/*metabolism ; Rats ; Sodium/*metabolism
    Print ISSN: 0036-8075
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  • 8
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    Regulation of a heart potassium channel by protein kinase A and C (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-10-07
    Description: The enzymes adenosine 3',5'-monophosphate (cAMP)-dependent protein kinase (protein kinase A) and protein kinase C regulate the activity of a diverse group of cellular proteins including membrane ion channel proteins. When protein kinase A was stimulated in cardiac ventricular myocytes with the membrane-soluble cAMP analog 8-chlorphenylthio cAMP (8-CPT cAMP), the amplitude of the delayed-rectifier potassium current (IK) doubled when recorded at 32 degrees C but was not affected at 22 degrees C. In contrast, modulation of the calcium current (ICa) by 8-CPT cAMP was independent of temperature with similar increases in ICa occurring at both temperatures. Stimulation of protein kinase C by phorbol 12,13-dibutyrate also enhanced IK in a temperature-dependent manner but failed to increase ICa at either temperature. Thus, cardiac delayed-rectifier potassium but not calcium channels are regulated by two distinct protein kinases in a similar temperature-dependent fashion.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Walsh, K B -- Kass, R S -- New York, N.Y. -- Science. 1988 Oct 7;242(4875):67-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, University of Rochester, School of Medicine and Dentistry, NY 14642.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2845575" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cyclic AMP/*analogs & derivatives/pharmacology ; Guinea Pigs ; Heart/*physiology ; Homeostasis ; In Vitro Techniques ; Kinetics ; Membrane Potentials ; Potassium Channels/*physiology ; Protein Kinase C/*metabolism ; Protein Kinases/*metabolism ; Thermodynamics ; Thionucleotides/*pharmacology ; Ventricular Function
    Print ISSN: 0036-8075
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  • 9
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    Unbelievable results spark a controversy (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-07-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pool, R -- New York, N.Y. -- Science. 1988 Jul 22;241(4864):407.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3393908" target="_blank"〉PubMed〈/a〉
    Keywords: Basophils/*physiology ; Dose-Response Relationship, Immunologic ; *Homeopathy ; Humans ; In Vitro Techniques ; Publishing
    Print ISSN: 0036-8075
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  • 10
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    Muscarinic depression of long-term potentiation in CA3 hippocampal neurons (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-10-07
    Description: Behavioral studies have suggested that muscarinic cholinergic systems have an important role in learning and memory. A muscarinic cholinergic agonist is now shown to affect synaptic plasticity in the CA3 region of the hippocampal slice. Long-term potentiation (LTP) of the mossy fiber-CA3 synapse was blocked by muscarine. Low concentrations of muscarine (1 micromolar) had little effect on low-frequency (0.2 hertz) synaptic stimulation but did significantly reduce the magnitude and probability of induction of LTP. Experiments under voltage clamp showed that muscarine blocked the increase in excitatory synaptic conductance normally associated with LTP at this synapse. These results suggest a possible role for cholinergic systems in synaptic plasticity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Williams, S -- Johnston, D -- HL31164/HL/NHLBI NIH HHS/ -- NS11535/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1988 Oct 7;242(4875):84-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, Baylor College of Medicine, Houston, TX 77030.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2845578" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Electric Conductivity ; Electric Stimulation ; Evoked Potentials/drug effects ; Hippocampus/drug effects/*physiology ; In Vitro Techniques ; Muscarine/*pharmacology ; Neurons/drug effects/*physiology ; Pyramidal Tracts/drug effects/*physiology ; Rats ; Reference Values ; Synapses/physiology ; Synaptic Transmission/drug effects
    Print ISSN: 0036-8075
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  • 11
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    A monoclonal antibody to the alpha subunit of Gk blocks muscarinic activation of atrial K+ channels (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-08-12
    Description: The activated heterotrimeric guanine nucleotide binding (G) protein Gk, at subpicomolar concentrations, mimics muscarinic stimulation of a specific atrial potassium current. Reconstitution studies have implicated the alpha and beta gamma subunits as mediators, but subunit coupling by the endogenous G protein has not been analyzed. To study this process, a monoclonal antibody (4A) that binds to alpha k but not to beta gamma was applied to the solution bathing an inside-out patch of atrial membrane; the antibody blocked carbachol-activated currents irreversibly. The state of the endogenous Gk determined its susceptibility to block by the antibody. When agonist was absent or when activation by muscarinic stimulation was interrupted by withdrawal of guanosine triphosphate (GTP) in the presence or absence of guanosine diphosphate (GDP), the effects of the antibody did not persist. Thus, monoclonal antibody 4A blocked muscarinic activation of potassium channels by binding to the activated G protein in its holomeric form or by binding to the dissociated alpha subunit.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yatani, A -- Hamm, H -- Codina, J -- Mazzoni, M R -- Birnbaumer, L -- Brown, A M -- DK19318/DK/NIDDK NIH HHS/ -- HL36930/HL/NHLBI NIH HHS/ -- HL37044/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1988 Aug 12;241(4867):828-31.〈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/2457252" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcholine/*pharmacology ; Animals ; *Antibodies, Monoclonal ; Atrial Function ; Carbachol/*pharmacology ; GTP-Binding Proteins/immunology/*physiology ; Guanosine 5'-O-(3-Thiotriphosphate) ; Guanosine Diphosphate/pharmacology ; Guanosine Triphosphate/analogs & derivatives/pharmacology ; Guinea Pigs ; In Vitro Techniques ; Ion Channels/drug effects/*physiology ; Myocardium/*metabolism ; Potassium/*metabolism ; Receptors, Muscarinic/drug effects/*physiology ; Thionucleotides/pharmacology
    Print ISSN: 0036-8075
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  • 12
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    Stimulation of RNA and protein synthesis by intracellular insulin (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-04-22
    Description: Like insulin-sensitive somatic cells, stage IV oocytes from Xenopus laevis increase their synthesis of RNA, protein, and glycogen in response to extracellular insulin. Synthesis of RNA and protein are also increased when oocytes are maintained under paraffin oil and insulin is microinjected into the cytoplasm. The effects of external and intracellular insulin are additive, suggesting separate mechanisms of action. Experiments with nuclei isolated under oil show that RNA synthesis can be stimulated by applying insulin to the nucleus directly. Thus, the nucleus appears to be one intracellular site of hormone action.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miller, D S -- New York, N.Y. -- Science. 1988 Apr 22;240(4851):506-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Cellular and Molecular Pharmacology, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2451860" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Nucleus/metabolism ; Glycogen/biosynthesis ; In Vitro Techniques ; Insulin/*pharmacology ; Microinjections ; *Protein Biosynthesis ; RNA/*biosynthesis ; Xenopus laevis
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  • 13
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    Antibody-enhanced infection by HIV-1 via Fc receptor-mediated entry (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-10-28
    Description: Monocytes and macrophages, which may play a central role in the pathogenesis of infection with human immunodeficiency virus type 1 (HIV-1), express the CD4 molecule and Fc receptors (FcR) for immunoglobulin G (IgG). To explore the possibility that FcR mediate HIV-1 infection of monocytes, studies were conducted with the human monocytic cell line U937. These cells were exposed to HIV-1 complexed with various concentrations of serum from HIV-1 antibody-positive individuals and monitored for HIV-1 replication. Serum samples from antibody-negative normal individuals did not affect virus yields. High concentrations of antibody-positive sera showed virus-neutralizing activity; however, cells infected with HIV-1 in the presence of antibody-positive sera at subneutralizing concentrations significantly enhanced virus replication. This infection enhancement was blocked by heat-aggregated gamma-globulin. Moreover, the IgG fraction from an HIV-1 antibody-positive serum enhanced HIV-1 infection at the same serum dilution equivalents. In contrast, IgG-F(ab')2 did not enhance HIV-1 infection but showed neutralizing activity with HIV-1. These results are compatible with the concept of FcR-mediated infection enhancement and suggest that this immunological response to HIV-1, instead of protecting the host, potentially facilitates the infection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Takeda, A -- Tuazon, C U -- Ennis, F A -- R01-AI24750/AI/NIAID NIH HHS/ -- T32-AI07272/AI/NIAID NIH HHS/ -- U01-AI26458/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1988 Oct 28;242(4878):580-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of Massachusetts Medical School, Worcester 01655.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2972065" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/immunology/*microbiology ; Antigen-Antibody Complex ; Antigens, Differentiation/*physiology ; Cell Line ; HIV Antibodies/*immunology ; HIV-1/immunology/*pathogenicity ; Humans ; In Vitro Techniques ; Monocytes/*microbiology ; Receptors, Fc/*physiology ; Receptors, IgG
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  • 14
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    Spatially resolved calcium dynamics of mammalian Purkinje cells in cerebellar slice (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-11-04
    Description: Microfluorometric imaging was used to study the correlation of intracellular calcium concentration with voltage-dependent electrical activity in guinea pig cerebellar Purkinje cells. The spatiotemporal dynamics of intracellular calcium concentration are demonstrated during spontaneous and evoked activity. The results are in agreement with hypotheses of dendritic segregation of calcium conductances suggested by electrophysiological experiments. These in vitro slice fluorescence imaging methods are applicable to a wide range of problems in central nervous system biochemical and electrophysiological functions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tank, D W -- Sugimori, M -- Connor, J A -- Llinas, R R -- NS-13742/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1988 Nov 4;242(4879):773-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Biophysics Research Department, AT&T Bell Laboratories, Murray Hill, NJ 07974.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2847315" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Benzofurans ; Calcium/*physiology ; Calcium Channels/*physiology ; Dendrites/*physiology ; Fura-2 ; Guinea Pigs ; Image Processing, Computer-Assisted ; In Vitro Techniques ; Membrane Potentials ; Neurotoxins/pharmacology ; Periodicity ; Purkinje Cells/*physiology ; Spider Venoms/pharmacology
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  • 15
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    Yeast KEX2 endopeptidase correctly cleaves a neuroendocrine prohormone in mammalian cells (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-07-08
    Description: Mammalian cell lines (BSC-40, NG108-15, and GH4C1) that cannot process the murine neuroendocrine peptide precursor prepro-opiomelanocortin (mPOMC) when its synthesis is directed by a vaccinia virus vector were coinfected with a second recombinant vaccinia virus carrying the yeast KEX2 gene, which encodes an endopeptidase that cleaves at pairs of basic amino acid residues. mPOMC was cleaved intracellularly to a set of product peptides normally found in vivo, including mature gamma-lipotropin and beta-endorphin1-31. In GH4C1 cells (a rat pituitary line), product peptides were incorporated into stored secretory granules. These results suggest that the inability of any particular cell line to process a prohormone precursor is due to the absence of a suitable endogenous processing enzyme.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thomas, G -- Thorne, B A -- Thomas, L -- Allen, R G -- Hruby, D E -- Fuller, R -- Thorner, J -- AI20563/AI/NIAID NIH HHS/ -- DK37274/DK/NIDDK NIH HHS/ -- HD18438/HD/NICHD NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1988 Jul 8;241(4862):226-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Vollum Institute for Advanced Biomedical Research, Oregon Health Sciences University, Portland 97201.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3291117" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Cloning, Molecular ; DNA, Recombinant ; Endopeptidases/*metabolism ; In Vitro Techniques ; Pro-Opiomelanocortin/*metabolism ; Protein Precursors/*metabolism ; Protein Processing, Post-Translational ; Saccharomyces cerevisiae/enzymology
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  • 16
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    Amiloride selectively blocks the low threshold (T) calcium channel (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-04-08
    Description: More than one type of voltage-gated calcium channel has been identified in muscle cells and neurons. Many specific organic and inorganic blockers of the conventional, slowly inactivating high threshold (L) calcium channel have been reported. No specific blockers of the low threshold (T) channel have been as yet identified. Amiloride, a potassium sparing diuretic, has now been shown to selectively block the low threshold calcium channel in mouse neuroblastoma and chick dorsal root ganglion neurons. The selective blockade of the T-type calcium channel will allow identification of this channel in different tissues and characterization of its specific physiological role.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tang, C M -- Presser, F -- Morad, M -- 1 K08 NS-01104/NS/NINDS NIH HHS/ -- R01 HL-16152/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1988 Apr 8;240(4849):213-5.〈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/2451291" target="_blank"〉PubMed〈/a〉
    Keywords: Amiloride/*pharmacology ; Animals ; Calcium/*physiology ; Chickens ; Dose-Response Relationship, Drug ; Electric Conductivity ; In Vitro Techniques ; Ion Channels/*drug effects ; Mice ; Neurons/*physiology ; Sodium/physiology ; Tumor Cells, Cultured
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  • 17
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    GABAA-receptor function in hippocampal cells is maintained by phosphorylation factors (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-07-15
    Description: Gamma aminobutyric acid (GABA) mediates fast synaptic inhibition in the central nervous system by activating the chloride-permeable GABAA channel. The GABAA conductance progressively diminishes with time when the intracellular contents of hippocampal neurons are perfused with a minimal intracellular medium. This "run down" of the GABA-activated conductance can be prevented by the inclusion of magnesium adenosine triphosphate and calcium buffer in the intracellular medium. The amount of chloride conductance that can be activated by GABA is determined by competition between a calcium-dependent process that reduces the conductance and a phosphorylation process that maintains the conductance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stelzer, A -- Kay, A R -- Wong, R K -- NS 24519/NS/NINDS NIH HHS/ -- NS 24682/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1988 Jul 15;241(4863):339-41.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, College of Physicians and Surgeons, Columbia University, New York, NY 10032.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2455347" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/pharmacology ; Animals ; Calcium/physiology ; Chlorides/physiology ; Egtazic Acid/pharmacology ; Electric Conductivity ; Guinea Pigs ; Hippocampus/*physiology ; In Vitro Techniques ; Ion Channels/physiology ; Magnesium/pharmacology ; *Neural Inhibition ; Phosphorylation ; Receptors, GABA-A/*physiology ; gamma-Aminobutyric Acid/*physiology
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  • 18
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    Effects of intracellular free magnesium on calcium current in isolated cardiac myocytes (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-02-12
    Description: Magnesium ions play a fundamental role in cellular function, but the effects of changes in the concentration of intracellular ionized magnesium ([Mg2+]i) on cell physiology have only recently received experimental attention. Increasing [Mg2+]i from 0.3 to 3.0 mM in cardiac cells by internal perfusion has only small effects on the basal voltage-gated calcium current (ICa) or on ICa elevated by dihydropyridine calcium channel agonists. In contrast, ICa elevated by cyclic adenosine monophosphate (cAMP)-dependent phosphorylation decreases by more than 50 percent. The effect of [Mg2+]i is not due to changes in the concentration of cAMP or in the velocity of phosphorylation but rather appears to be a direct effect on the phosphorylated channel or on channel dephosphorylation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉White, R E -- Hartzell, H C -- HL21195/HL/NHLBI NIH HHS/ -- HL27385/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1988 Feb 12;239(4841 Pt 1):778-80.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy and Cell Biology, Emory University School of Medicine, Atlanta, GA 30322.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2448878" target="_blank"〉PubMed〈/a〉
    Keywords: 8-Bromo Cyclic Adenosine Monophosphate/pharmacology ; Animals ; Calcium/*metabolism/pharmacology ; Cyclic AMP/physiology ; Heart/drug effects/*physiology ; In Vitro Techniques ; Ion Channels/drug effects/*physiology ; Isoproterenol/pharmacology ; Magnesium/pharmacology/*physiology ; Membrane Potentials ; Phosphorylation ; Ranidae ; Ventricular Function
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  • 19
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    An origin unwinding activity regulates initiation of DNA replication during mammalian cell cycle (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-09-16
    Description: An in vitro assay was developed to study the positive factors that regulate the onset of DNA replication during the mammalian cell cycle. Extracts prepared from cells at defined positions in the cell cycle were used to examine the replication of SV40 DNA in a cell free system. Extracts prepared from S phase cells were ten times more efficient at initiating replication at the SV40 origin than were extracts from G1 cells, whereas elongation rates were similar in G1 and S reactions. At a discrete point in the cell cycle, just before the cell's entry into S, an activity appeared that was required, in conjunction with SV40 T antigen, for site specific initiation at the SV40 origin. This factor had a role in unwinding DNA at the replication origin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roberts, J M -- D'Urso, G -- AG0005/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 1988 Sep 16;241(4872):1486-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Fred Hutchinson Cancer Research Center, Seattle, WA 98104.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2843984" target="_blank"〉PubMed〈/a〉
    Keywords: Antigens, Polyomavirus Transforming/physiology ; *Cell Cycle ; Cell Line ; Cell-Free System ; *DNA Replication ; Humans ; In Vitro Techniques ; Interphase ; Simian virus 40/genetics ; Virus Replication
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  • 20
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    Activation of muscarinic potassium currents by ATP gamma S in atrial cells (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-10-21
    Description: Intracellular perfusion of atrial myocytes with adenosine 5'-(gamma-thio) triphosphate (ATP gamma S), an ATP analog, elicits a progressive increase of the muscarinic potassium channel current, IK(M), in the absence of agonists. In this respect, ATP gamma S mimics the actions of guanosine triphosphate (GTP) analogs, which produce direct, persistent activation of the guanyl nucleotide-binding (G) protein controlling the K+(M) channel. The effect of ATP gamma S on IK(M), however, differs from that produced by GTP analogs in two aspects: it requires relatively large ATP gamma S concentrations, and it appears after a considerable delay, suggesting a rate-limiting step not present in similar experiments performed with guanosine 5'-(gamma-thio) triphosphate (GTP gamma S). Incubation of atrial homogenates with [35S]ATP gamma S leads to formation of significant amounts of [35S]GTP gamma S, suggesting that activation of IK(M) by ATP gamma S arises indirectly through its conversion into GTP gamma S by cellular enzymes. ATP gamma S is often used to demonstrate the involvement of protein phosphorylation in the control of various cellular processes. The finding that cytosolic application of ATP gamma S can also lead to G-protein activation implies that experiments with ATP gamma S must be interpreted with caution.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Otero, A S -- Breitwieser, G E -- Szabo, G -- HL07458/HL/NHLBI NIH HHS/ -- HL37127/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1988 Oct 21;242(4877):443-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology and Biophysics, University of Texas Medical Branch, Galveston 77550.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3051383" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/*analogs & derivatives/metabolism/pharmacology ; Adenylyl Imidodiphosphate/pharmacology ; Animals ; Atrial Function ; Guanosine 5'-O-(3-Thiotriphosphate) ; Guanosine Triphosphate/analogs & derivatives/metabolism/pharmacology ; Heart/*physiology ; Heart Atria/drug effects ; In Vitro Techniques ; Membrane Potentials/drug effects ; Potassium Channels/drug effects/*physiology ; Rana catesbeiana ; Receptors, Muscarinic/drug effects/*physiology ; Thionucleotides/metabolism/pharmacology
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  • 21
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    Associative induction of posttetanic and long-term potentiation in CA1 neurons of rat hippocampus (1986)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1986-05-23
    Description: Electrical stimulation of fibers in the stratum radiatum causes an excitatory postsynaptic potential in CA1 neurons of the hippocampus. Other excitatory inputs to or direct depolarization of these CA1 neurons during stimulation of the stratum radiatum caused a subsequent increase in the excitatory postsynaptic potential. This enhancement was characterized as a brief potentiation (2 to 3 minutes, similar to posttetanic potentiation) and a long-term potentiation (presumed to be involved in learning and memory). These potentiations are probably induced by an interaction of the postsynaptic cell or other presynaptic terminals with the test presynaptic terminals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sastry, B R -- Goh, J W -- Auyeung, A -- New York, N.Y. -- Science. 1986 May 23;232(4753):988-90.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3010459" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Brain Mapping ; Calcium/physiology ; Conditioning (Psychology)/physiology ; Electric Stimulation ; Hippocampus/*physiology ; In Vitro Techniques ; Learning/physiology ; Membrane Potentials ; Rats ; Synapses/physiology ; Synaptic Transmission
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  • 22
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    Guanosine triphosphatase activating protein (GAP) interacts with the p21 ras effector binding domain (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-04-22
    Description: A cytoplasmic protein that greatly enhances the guanosine triphosphatase (GTPase) activity of N-ras protein but does not affect the activity of oncogenic ras mutants has been recently described. This protein (GAP) is shown here to be ubiquitous in higher eukaryotes and to interact with H-ras as well as with N-ras proteins. To identify the region of ras p21 with which GAP interacts, 21 H-ras mutant proteins were purified and tested for their ability to undergo stimulation of GTPase activity by GAP. Mutations in nonessential regions of H-ras p21 as well as mutations in its carboxyl-terminal domain (residues 165-185) and purine binding region (residues 117 and 119) did not decrease the ability of the protein to respond to GAP. In addition, an antibody against the carboxyl-terminal domain did not block GAP activity, supporting the conclusion that GAP does not interact with this region. Transforming mutations at positions 12, 59, and 61 (the phosphoryl binding region) abolished GTPase stimulation by GAP. Point mutations in the putative effector region of ras p21 (amino acids 35, 36, and 38) were also insensitive to GAP. However, a point mutation at position 39, shown previously not to impair effector function, did not alter GAP-p21 interaction. These results indicate that GAP interaction may be essential for ras p21 biological activity and that it may be a ras effector protein.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Adari, H -- Lowy, D R -- Willumsen, B M -- Der, C J -- McCormick, F -- New York, N.Y. -- Science. 1988 Apr 22;240(4851):518-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Cetus Corporation, Emeryville, CA 94608.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2833817" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antibodies, Monoclonal/immunology ; DNA Mutational Analysis ; Enzyme Activation ; GTP Phosphohydrolases/*metabolism ; GTP-Binding Proteins/*metabolism ; GTPase-Activating Proteins ; *Genes, ras ; Immunologic Techniques ; In Vitro Techniques ; Phosphoric Monoester Hydrolases/*metabolism ; Proteins/*metabolism ; Proto-Oncogene Proteins/*metabolism ; Structure-Activity Relationship ; ras GTPase-Activating Proteins
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  • 23
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    Negative regulation by glucocorticoids through interference with a cAMP responsive enhancer (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-07-15
    Description: Although steroid hormone receptors are known to activate gene expression by binding to specific hormone-dependent enhancers, the mechanisms by which steroids inhibit the transcription of specific genes are unknown. It is shown here by gene transfer studies that the same glucocorticoid receptor that activates gene expression can negatively regulate expression of the human glycoprotein hormone alpha-subunit gene. Glucocorticoid inhibition was conferred by a 52-nucleotide region that also contains elements crucial both for adenosine 3',5'-monophosphate (cAMP) responsiveness and for placental-specific expression of this gene and was observed only under conditions in which these elements were functioning as enhancers. Purified glucocorticoid receptor was found to bind to DNA that overlap the cAMP responsive elements sites in this region. It is hypothesized that steroid receptors negatively regulate gene expression by interfering with the activity or binding of other important transcription factors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Akerblom, I E -- Slater, E P -- Beato, M -- Baxter, J D -- Mellon, P L -- R01 HD020377/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1988 Jul 15;241(4863):350-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Regulatory Biology Laboratory, Salk Institute for Biological Studies, La Jolla, CA 92037.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2838908" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Chorionic Gonadotropin/*genetics ; Cyclic AMP/*physiology ; DNA-Binding Proteins/physiology ; Dexamethasone/*pharmacology ; *Enhancer Elements, Genetic ; *Gene Expression Regulation ; Humans ; In Vitro Techniques ; Receptors, Steroid/*physiology ; *Regulatory Sequences, Nucleic Acid ; Transcription Factors/physiology
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  • 24
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    Long-term synaptic potentiation (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-11-04
    Description: Long-term synaptic potentiation (LTP) is a leading candidate for a synaptic mechanism of rapid learning in mammals. LTP is a persistent increase in synaptic efficacy that can be quickly induced. The biophysical process that controls one type of LTP is formally similar to a synaptic memory mechanism postulated decades ago by the psychologist Donald Hebb. A key aspect of the modification process involves the N-methyl-D-aspartate (NMDA) receptor-ionophore complex. This ionophore allows calcium influx only if the endogenous ligand glutamate binds to the NMDA receptor and if the voltage across the associated channel is also sufficiently depolarized to relieve a magnesium block. According to one popular hypothesis, the resulting increase in the intracellular calcium concentration activates protein kinases that enhance the postsynaptic conductance. Further biophysical and molecular understanding of the modification process should facilitate detailed explorations of the mnemonic functions of LTP.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brown, T H -- Chapman, P F -- Kairiss, E W -- Keenan, C L -- New York, N.Y. -- Science. 1988 Nov 4;242(4879):724-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychology, Yale University, New Haven, CT 06520.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2903551" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; In Vitro Techniques ; Learning/*physiology ; Neuronal Plasticity ; Neurotransmitter Agents/physiology ; Receptors, Neurotransmitter/physiology ; Synapses/*physiology
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  • 25
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    The alpha subunit of the GTP binding protein activates muscarinic potassium channels of the atrium (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-06-24
    Description: It has been debated whether the potassium channel of the atrium is activated by the alpha subunit or by the beta gamma subunits of guanine nucleotide binding (G) proteins, which dissociate on activation with guanosine triphosphate (GTP). Therefore, the channel-activating effectiveness of these subunits on isolated guinea pig atrial cells was tested. The activated alpha K subunit from human erythrocytes activated the channel in subpicomolar concentrations. The beta gamma dimer from bovine brain activated the channel in nanomolar concentrations. These results support the view that, physiologically, the alpha subunit activates the channel.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cerbai, E -- Klockner, U -- Isenberg, G -- New York, N.Y. -- Science. 1988 Jun 24;240(4860):1782-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Applied Physiology, University of Cologne, Koln, FRG.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2454511" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Atrial Function ; Electric Conductivity ; GTP-Binding Proteins/*metabolism ; Guinea Pigs ; Humans ; In Vitro Techniques ; Ion Channels/*physiology ; Macromolecular Substances ; Potassium/*physiology ; Receptors, Muscarinic/*physiology
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  • 26
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    Synaptic transmission between dissociated adult mammalian neurons and attached synaptic boutons (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-09-30
    Description: In most studies of synaptic currents in mammalian central neurons, preparations have been used in which synaptic currents are recorded at some distance from the synapse itself. This procedure introduces problems in interpretation of the kinetics and voltage-dependent properties of the synaptic current. These problems have now been overcome by the development of a preparation in which presynaptic vesicle-containing boutons have been coisolated with the soma of individual neurons, thus providing the opportunity to study synaptic currents under conditions of both adequate voltage control and internal ionic perfusion. Spontaneous synaptic currents mediated by gamma-aminobutyric acid and excitatory amino acids were recorded from neurons isolated from a mammalian medial solitary tract nucleus. Calcium- and depolarization-dependent spontaneous currents of several to hundreds of picoamperes occurred with rapid rise times of 0.8 to 3 milliseconds and decays at least ten times as long.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Drewe, J A -- Childs, G V -- Kunze, D L -- HL36840/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1988 Sep 30;241(4874):1810-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology and Biophysics, University of Texas Medical Branch, Galveston 77550.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2459774" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/physiology ; Glutamates/physiology ; Guinea Pigs ; In Vitro Techniques ; Ion Channels/physiology ; Membrane Potentials ; Neurons/*physiology ; Potassium/physiology ; Synapses/*physiology ; *Synaptic Transmission ; gamma-Aminobutyric Acid/physiology
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  • 27
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    Chemotransduction in the carotid body: K+ current modulated by PO2 in type I chemoreceptor cells (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Selective activation of transcription by a novel CCAAT binding factor (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-07-29
    Description: A novel CCAAT binding factor (CBF) composed of two different subunits has been extensively purified from rat liver. Both subunits are needed for specific binding to DNA. Addition of this purified protein to nuclear extracts of NIH 3T3 fibroblasts stimulates transcription from several promoters including the alpha 2(I) collagen, the alpha 1(I) collagen, the Rous sarcoma virus long terminal repeat (RSV-LTR), and the adenovirus major late promoter. Point mutations in the CCAAT motif that show either no binding or a decreased binding of CBF likewise abolish or reduce activation of transcription by CBF. Activation of transcription requires, therefore, the specific binding of CBF to its recognition sites.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Maity, S N -- Golumbek, P T -- Karsenty, G -- de Crombrugghe, B -- New York, N.Y. -- Science. 1988 Jul 29;241(4865):582-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics, Univesity of Texas, M.D. Anderson Cancer Center, Houston 77030.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3399893" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Nucleus/physiology ; Collagen/genetics ; DNA-Binding Proteins/*physiology ; In Vitro Techniques ; Macromolecular Substances ; Mice ; Nuclear Proteins/physiology ; *Promoter Regions, Genetic ; Rats ; *Regulatory Sequences, Nucleic Acid ; Transcription Factors/*physiology ; *Transcription, Genetic
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  • 29
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    Postsynaptic calcium is sufficient for potentiation of hippocampal synaptic transmission (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-10-07
    Description: Brief repetitive activation of excitatory synapses in the hippocampus leads to an increase in synaptic strength that lasts for many hours. This long-term potentiation (LTP) of synaptic transmission is the most compelling cellular model in the vertebrate brain for learning and memory. The critical role of postsynaptic calcium in triggering LTP has been directly examined using three types of experiment. First, nitr-5, a photolabile nitrobenzhydrol tetracarboxylate calcium chelator, which releases calcium in response to ultraviolet light, was used. Photolysis of nitr-5 injected into hippocampal CA1 pyramidal cells resulted in a large enhancement of synaptic transmission. Second, in agreement with previous results, buffering intracellular calcium at low concentrations blocked LTP. Third, depolarization of the postsynaptic membrane so that calcium entry is suppressed prevented LTP. Taken together, these results demonstrate that an increase in postsynaptic calcium is necessary to induce LTP and sufficient to potentiate synaptic transmission.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Malenka, R C -- Kauer, J A -- Zucker, R S -- Nicoll, R A -- MH00437/MH/NIMH NIH HHS/ -- MH38256/MH/NIMH NIH HHS/ -- NS24205/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1988 Oct 7;242(4875):81-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, School 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/2845577" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/*physiology ; Chelating Agents/pharmacology ; Egtazic Acid/analogs & derivatives/pharmacology ; Evoked Potentials/drug effects ; Hippocampus/*physiology ; In Vitro Techniques ; Kinetics ; Photolysis ; Pyramidal Tracts/physiology ; Rats ; Synapses/*physiology ; *Synaptic Transmission
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    Three-dimensional structure of an antigen-antibody complex at 2.8 A resolution (1986)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1986-08-15
    Description: The 2.8 A resolution three-dimensional structure of a complex between an antigen (lysozyme) and the Fab fragment from a monoclonal antibody against lysozyme has been determined and refined by x-ray crystallographic techniques. No conformational changes can be observed in the tertiary structure of lysozyme compared with that determined in native crystalline forms. The quaternary structure of Fab is that of an extended conformation. The antibody combining site is a rather flat surface with protuberances and depressions formed by its amino acid side chains. The antigen-antibody interface is tightly packed, with 16 lysozyme and 17 antibody residues making close contacts. The antigen contacting residues belong to two stretches of the lysozyme polypeptide chain: residues 18 to 27 and 116 to 129. All the complementarity-determining regions and two residues outside hypervariable positions of the antibody make contact with the antigen. Most of these contacts (10 residues out of 17) are made by the heavy chain, and in particular by its third complementarity-determining region. Antigen variability and antibody specificity and affinity are discussed on the basis of the determined structure.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Amit, A G -- Mariuzza, R A -- Phillips, S E -- Poljak, R J -- New York, N.Y. -- Science. 1986 Aug 15;233(4765):747-53.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2426778" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antibodies, Monoclonal ; *Antigen-Antibody Complex ; Chickens ; Egg White ; Epitopes ; *Immunoglobulin Fab Fragments ; Immunoglobulin Heavy Chains ; Immunoglobulin Light Chains ; In Vitro Techniques ; Kinetics ; Models, Molecular ; Muramidase/*immunology ; Protein Conformation ; X-Ray Diffraction
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    Dynamics of lymphocyte-endothelial interactions in vivo (1986)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1986-01-24
    Description: The dynamics of the attachment of lymphocytes to the endothelium of high endothelial venules in murine Peyer's patches were studied in vivo. Lymphocytes adhered readily to the endothelium lining these vessels, but most of the adhering cells detached within a few seconds. Many lymphocytes, however, experienced multiple collisions with the high endothelial venules, and this substantially increased the efficiency of lymphocyte collection by these vessels.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bjerknes, M -- Cheng, H -- Ottaway, C A -- New York, N.Y. -- Science. 1986 Jan 24;231(4736):402-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3941903" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Endothelium/physiology ; Female ; In Vitro Techniques ; Lymphocytes/*physiology ; Mice ; Mice, Inbred BALB C ; Microscopy, Fluorescence ; Peyer's Patches/*physiology
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    Human beta-adrenoceptors: relation of myocardial and lymphocyte beta-adrenoceptor density (1986)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1986-03-28
    Description: In human right atria obtained from 21 patients during open-heart surgery, beta-adrenoceptor density [assessed by iodine-125-labeled (-)-cyanopindolol binding] and responsiveness (positive inotropic responses to isoprenaline) were linearly related to the beta-adrenoceptor density in the corresponding circulating lymphocytes. This direct relation of human myocardial and lymphocyte beta-adrenoceptor alterations, therefore, makes it possible to monitor drug- or disease-induced beta-adrenoceptor changes in tissues not easily accessible in humans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brodde, O E -- Kretsch, R -- Ikezono, K -- Zerkowski, H R -- Reidemeister, J C -- New York, N.Y. -- Science. 1986 Mar 28;231(4745):1584-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3006250" target="_blank"〉PubMed〈/a〉
    Keywords: Female ; Heart Atria ; Humans ; In Vitro Techniques ; Isoproterenol/pharmacology ; Lymphocytes/*metabolism ; Male ; Middle Aged ; Myocardial Contraction/drug effects ; Myocardium/*metabolism ; Receptors, Adrenergic, beta/*metabolism
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    A low threshold calcium spike mediates firing pattern alterations in pontine reticular neurons (1986)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1986-11-07
    Description: Intracellular electrical recordings in an in vitro slice preparation of the brainstem medial pontine reticular formation, a region thought to be important in mediation of desynchronized sleep phenomena, demonstrate a population of neurons that have a calcium-dependent, low threshold spike. This low threshold spike was inactivated at relatively depolarized membrane potential levels and, when this spike was deinactivated, it induced a burst of action potentials. The membrane potential dependence of the spike may underlie changes in action potential firing patterns associated with behavioral state change because the baseline membrane potential in neurons of the medial pontine reticular population depolarizes during passage from waking and slow wave sleep to desynchronized sleep, which is characterized by the absence of burst firing.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Greene, R W -- Haas, H L -- McCarley, R W -- MH 39,683/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1986 Nov 7;234(4777):738-40.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3775364" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Calcium/physiology ; Electric Stimulation ; In Vitro Techniques ; Membrane Potentials ; Pons/cytology/*physiology ; Rats
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    Inhibition of endothelial regeneration by type-beta transforming growth factor from platelets (1986)
    American Association for the Advancement of Science (AAAS)
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    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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    The role of chloride transport in postsynaptic inhibition of hippocampal neurons (1986)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1986-06-13
    Description: Hippocampal inhibitory postsynaptic potentials are depolarizing in granule cells but hyperpolarizing in CA3 neurons because the reversal potentials and membrane potentials of these cells differ. Here the hippocampal slice preparation was used to investigate the role of chloride transport in these inhibitory responses. In both cell types, increasing the intracellular chloride concentration by injection shifted the reversal potential of these responses in a positive direction, and blocking the outward transport of chloride with furosemide slowed their recovery from the injection. In addition, hyperpolarizing and depolarizing inhibitory responses and the hyperpolarizing and depolarizing responses to the inhibitory neurotransmitter gamma-aminobutyric acid decreased in the presence of furosemide. These effects of furosemide suggest that the internal chloride activity of an individual hippocampal neuron is regulated by two transport processes, one that accumulates chloride and one that extrudes chloride.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Misgeld, U -- Deisz, R A -- Dodt, H U -- Lux, H D -- New York, N.Y. -- Science. 1986 Jun 13;232(4756):1413-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2424084" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Transport/drug effects ; Cell Membrane Permeability/drug effects ; Chlorides/*physiology ; Furosemide/pharmacology ; Guinea Pigs ; Hippocampus/*physiology ; In Vitro Techniques ; Ion Channels/drug effects ; Membrane Potentials/drug effects ; *Neural Inhibition ; gamma-Aminobutyric Acid/*physiology
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    A macrophage-derived factor required by plasmacytomas for survival and proliferation in vitro (1986)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1986-08-01
    Description: Plasmacytoma (PCT) cell lines dependent for proliferation and survival on a factor elaborated by the murine macrophage cell line, P388D1, were established in vitro. Adherent peritoneal cells induced by pristane produced 50-fold greater amounts of this activity in vitro than did resident cells. The molecules responsible for plasmacytoma growth were distinct from a number of characterized factors including interleukin-1, -2, and -3, macrophage colony-stimulating factor, B-cell stimulatory factor-1, B-cell growth factor II, epidermal growth factor, transforming growth factor-beta, and gamma- and beta-interferon, none of which were able to support the growth of the factor-dependent PCT cell lines. These results suggest that PCT growth factor may be a novel factor that has not been previously characterized and, further, that its production is associated with the pristane-induced, chronic peritoneal inflammatory response that precedes plasmacytoma formation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nordan, R P -- Potter, M -- New York, N.Y. -- Science. 1986 Aug 1;233(4763):566-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3726549" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Division/drug effects ; Cell Line ; *Cell Survival/drug effects ; Growth Substances/*isolation & purification/pharmacology/physiology ; Humans ; In Vitro Techniques ; Macrophages/*physiology ; Mice ; Plasmacytoma/*physiopathology
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    Effect of antibodies to recombinant and synthetic peptides on P. falciparum sporozoites in vitro (1986)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1986-01-10
    Description: Antibodies were raised in mice immunized with several recombinant and synthetic peptides of the circumsporozoite protein of Plasmodium falciparum. The antibodies were evaluated for protective activity in a human hepatocyte culture system. They exerted their protective effect against the parasite at three points: sporozoite attachment to the hepatocyte surface, entry, and subsequent intracellular development. Inhibition of attachment and entry were found to be related to the antibody titer against the authentic circumsporozoite protein on the sporozoite surface, especially when peptides were administered with alum or complete Freund's adjuvant. Even when invasion was not totally inhibited, the presence of abnormal trophozoites and a frequent inhibition of schizont development in long-term cultures suggested continued activity of antibodies at the intracellular level after sporozoite penetration had been completed.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mazier, D -- Mellouk, S -- Beaudoin, R L -- Texier, B -- Druilhe, P -- Hockmeyer, W -- Trosper, J -- Paul, C -- Charoenvit, Y -- Young, J -- New York, N.Y. -- Science. 1986 Jan 10;231(4734):156-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3510455" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies/*immunology ; Antigens, Protozoan/*immunology ; Fluorescent Antibody Technique ; Humans ; In Vitro Techniques ; Liver/cytology/parasitology ; Mice ; Peptides/immunology ; Plasmodium falciparum/*immunology ; Recombinant Proteins/immunology
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    Calcium channels in planar lipid bilayers: insights into mechanisms of ion permeation and gating (1986)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1986-03-28
    Description: Electrophysiological recordings were used to analyze single calcium channels in planar lipid bilayers after membranes from bovine cardiac sarcolemmal vesicles had been incorporated into the bilayer. In these cell-free conditions, channels in the bilayer showed unitary barium or calcium conductances, gating kinetics, and pharmacological responses that were similar to dihydropyridine-sensitive calcium channels in intact cells. The open channel current varied in a nonlinear manner with voltage under asymmetric (that is, physiological) ionic conditions. However, with identical solutions on both sides of the bilayer, the current-voltage relation was linear. In matched experiments, calcium channels from skeletal muscle T-tubules differed significantly from cardiac calcium channels in their conductance properties and gating kinetics.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rosenberg, R L -- Hess, P -- Reeves, J P -- Smilowitz, H -- Tsien, R W -- New York, N.Y. -- Science. 1986 Mar 28;231(4745):1564-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2420007" target="_blank"〉PubMed〈/a〉
    Keywords: 3-Pyridinecarboxylic acid, ; 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester ; Animals ; Calcium/*physiology ; Cattle ; Electric Conductivity ; Heart/physiology ; In Vitro Techniques ; Ion Channels/*physiology ; Lipid Bilayers ; Nicotinic Acids/pharmacology ; Nifedipine/analogs & derivatives/pharmacology ; Nimodipine ; Potassium/physiology ; Sarcolemma ; Sodium/physiology
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  • 39
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    Direct polyclonal activation of human B lymphocytes by the acquired immune deficiency syndrome virus (1986)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1986-09-05
    Description: When B lymphocytes from normal human peripheral blood were incubated for 1 hour with the retrovirus that causes the acquired immune deficiency syndrome (AIDS), the B cells showed marked proliferation and differentiation. Proliferative responses to the virus peaked on day 4 and appeared to be independent of accessory cells. This finding was repeated with three separate viral isolates, one of which was from a patient from Zaire. The magnitude of the observed responses was comparable to that seen with standard polyclonal B-cell activators. This phenomenon may be at least partially responsible for the polyclonal B-cell activation seen in patients with AIDS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schnittman, S M -- Lane, H C -- Higgins, S E -- Folks, T -- Fauci, A S -- New York, N.Y. -- Science. 1986 Sep 5;233(4768):1084-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3016902" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/*immunology ; B-Lymphocytes/*immunology ; Cell Differentiation ; Deltaretrovirus/*immunology ; Humans ; Immunoglobulins/metabolism ; In Vitro Techniques ; Lymphocyte Activation ; Receptors, Virus/physiology
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    Direct cloning and sequence analysis of enzymatically amplified genomic sequences (1986)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1986-09-05
    Description: A method is described for directly cloning enzymatically amplified segments of genomic DNA into an M13 vector for sequence analysis. A 110-base pair fragment of the human beta-globin gene and a 242-base pair fragment of the human leukocyte antigen DQ alpha locus were amplified by the polymerase chain reaction method, a procedure based on repeated cycles of denaturation, primer annealing, and extension by DNA polymerase I. Oligonucleotide primers with restriction endonuclease sites added to their 5' ends were used to facilitate the cloning of the amplified DNA. The analysis of cloned products allowed the quantitative evaluation of the amplification method's specificity and fidelity. Given the low frequency of sequence errors observed, this approach promises to be a rapid method for obtaining reliable genomic sequences from nanogram amounts of DNA.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Scharf, S J -- Horn, G T -- Erlich, H A -- New York, N.Y. -- Science. 1986 Sep 5;233(4768):1076-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3461561" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Cloning, Molecular/*methods ; Coliphages/*genetics ; DNA Polymerase I/metabolism ; Gene Amplification ; *Genetic Vectors ; Globins/*genetics ; HLA-DQ Antigens ; Histocompatibility Antigens Class II/*genetics ; Humans ; In Vitro Techniques ; Polymorphism, Genetic
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    Induction of kappa transcription by interferon-gamma without activation of NF-kappa B (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-11-18
    Description: The induction of immunoglobulin kappa light chain expression in 70Z/3 pre-B cells treated with bacterial lipopolysaccharide (LPS) requires the activation of the B cell-specific factor NF-kappa B, which binds to the kappa enhancer motif, GGGACTTTCC. This sequence alone can function as a tissue-specific enhancer for LPS-induced gene expression. A potent inhibitor of B lymphopoiesis [transforming growth factor-beta (TGF-beta)] was used to explore the mechanisms in the activation of kappa transcription by LPS and by interferon-gamma (IFN-gamma). TGF-beta inhibited LPS-induced kappa transcription but not the activation and in vitro binding of NF-kappa B. This indicates that NF-kappa B activation, while necessary, is not sufficient for LPS-induced kappa transcription. TGF-beta had no effect on IFN-gamma-induced kappa transcription, and NF-kappa B was not activated by IFN-gamma. These results reveal that LPS and IFN-gamma activate transcription through different mechanisms.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Briskin, M -- Kuwabara, M D -- Sigman, D S -- Wall, R -- CA 12800/CA/NCI NIH HHS/ -- GM 21199/GM/NIGMS NIH HHS/ -- GM 40185/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1988 Nov 18;242(4881):1036-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Biology Institute, UCLA School of Medicine, University of California 90024.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3143155" target="_blank"〉PubMed〈/a〉
    Keywords: B-Lymphocytes/*physiology ; Cell Line ; Enhancer Elements, Genetic ; Gene Expression Regulation/drug effects ; *Genes, Immunoglobulin ; Immunoglobulin kappa-Chains/*genetics ; Immunoglobulin mu-Chains/genetics ; In Vitro Techniques ; Interferon-gamma/*pharmacology ; Lipopolysaccharides/pharmacology ; Transcription Factors/*physiology ; Transcription, Genetic/*drug effects ; Transforming Growth Factors/pharmacology
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    RNA processing generates the mature 3' end of yeast CYC1 messenger RNA in vitro (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-12-02
    Description: In whole cell extracts of Saccharomyces cerevisiae, incubation of precursor mRNA transcripts encoding the sequences essential in vivo for forming the 3' end of the iso-1-cytochrome c mRNA (CYC1) revealed an endonuclease activity with the characteristics required for producing the mature mRNA 3' end. The observed cleavage in vitro is (i) accurate, occurring at or near the polyadenylation site of CYC1 RNA, (ii) 30 to 50 percent efficient, (iii) adenosine triphosphate dependent, (iv) specific for the 3' ends of at least two yeast pre-mRNA's, and (v) absent with related pre-mRNA's carrying mutations that abolish correct 3' end formation in vivo. In addition, a second activity in the extract polyadenylates the product under appropriate conditions. Thus, the mature 3' ends of yeast mRNA's may be generated by endonucleolytic cleavage and polyadenylation rather than by transcription termination.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Butler, J S -- Platt, T -- 5-RO1-GM35658/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1988 Dec 2;242(4883):1270-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, University of Rochester Medical Center, NY 14642.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2848317" target="_blank"〉PubMed〈/a〉
    Keywords: Cytochrome c Group/*genetics ; *Cytochromes c ; Endoribonucleases/metabolism ; In Vitro Techniques ; Nucleotides/metabolism ; Poly A/*genetics ; *RNA Processing, Post-Transcriptional ; RNA, Messenger/*genetics ; Saccharomyces cerevisiae/*genetics ; *Saccharomyces cerevisiae Proteins ; Transcription, Genetic
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    Fish oils inhibit endothelial cell production of platelet-derived growth factor-like protein (1988)
    American Association for the Advancement of Science (AAAS)
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    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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    Solid phase synthesis (1986)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1986-04-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Merrifield, B -- New York, N.Y. -- Science. 1986 Apr 18;232(4748):341-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3961484" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Chemical Phenomena ; Chemistry ; In Vitro Techniques ; Methods ; Nucleotides/*chemical synthesis ; Peptide Fragments/metabolism ; Peptides/*chemical synthesis ; Ribonuclease, Pancreatic/chemical synthesis/metabolism ; Structure-Activity Relationship
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  • 45
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    Hyperthermia protects against light damage in the rat retina (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-09-30
    Description: An increase in the synthesis of heat shock proteins that is induced in cells in vitro by hyperthermia or other types of metabolic stress correlates with enhanced cell survival upon further stress. To determine if a similar increase in stress tolerance could be elicited in vivo, rats were made hyperthermic, and then their retinas were tested for sensitivity to light damage. This treatment resulted in a marked decrease in photoreceptor degeneration after exposure to bright light as compared to normothermic animals. Concomitant with such protection was an increase in retinal synthesis of three heat shock proteins. Thus, a physiological rise in body temperature enhances the stress tolerance of nerve tissue, perhaps by increasing heat shock protein production.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barbe, M F -- Tytell, M -- Gower, D J -- Welch, W J -- 1 R01 EY07616/EY/NEI NIH HHS/ -- GM 33551-06/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1988 Sep 30;241(4874):1817-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy, Medical College of Pennsylvania, Philadelphia 19144.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3175623" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blotting, Western ; Heat-Shock Proteins/*physiology ; *Hot Temperature ; In Vitro Techniques ; Rats ; Retina/pathology/physiology/*radiation effects ; Time Factors
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    Growth and transparency in the lens, an epithelial tissue, stimulated by pulses of PDGF (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-11-04
    Description: The rat lens undergoes dramatic growth during early postnatal development. Lens weight increased by a factor of 23 in 26 days. Growth rate per day oscillated between 0 and 87 percent. A new culture system was designed to study the oscillations in growth during development. Lens growth and transparency in vitro required pulsatile delivery of platelet-derived growth factor (PDGF) in HL-1 serum-free medium. Continuous delivery of HL-1 medium with PDGF or pulsatile delivery of HL-1 medium without PDGF resulted in lens opacity and no growth. These results provide direct evidence that PDGF stimulates an epithelial tissue and that oscillations in growth occur during normal development of the rat lens.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brewitt, B -- Clark, J I -- EY-04542/EY/NEI NIH HHS/ -- EY-07031/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 1988 Nov 4;242(4879):777-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Structure, University of Washington, School of Medicine, Seattle 98195.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3187521" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Drug Administration Schedule ; Epithelium/physiology ; In Vitro Techniques ; Lens, Crystalline/anatomy & histology/*growth & development ; Organ Size ; Periodicity ; Platelet-Derived Growth Factor/administration & dosage/*pharmacology ; Rats ; Time Factors
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  • 47
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    Relaxation of isolated ventricular cardiomyocytes by a voltage-dependent process (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-08-12
    Description: Cell contraction and relaxation were measured in single voltage-clamped guinea pig cardiomyocytes to investigate the contribution of sarcolemmal Na+-Ca2+ exchange to mechanical relaxation. Cells clamped from -80 to 0 millivolts displayed initial phasic and subsequent tonic contractions; caffeine reduced or abolished the phasic and enlarged the tonic contraction. The rate of relaxation from tonic contractions was steeply voltage-dependent and was significantly slowed in the absence of a sarcolemmal Na+ gradient. Tonic contractions elicited in the absence of a Na+ gradient promptly relaxed when external Na+ was applied, reflecting activation of Na+-Ca2+ exchange. It appears that a voltage-dependent Na+-Ca2+ exchange can rapidly mechanically relax mammalian heart muscle.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bridge, J H -- Spitzer, K W -- Ershler, P R -- HL31140/HL/NHLBI NIH HHS/ -- HL34288/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1988 Aug 12;241(4867):823-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Nora Eccles Harrison Cardiovascular Research and Training Institute, Salt Lake City, UT.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3406740" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caffeine/pharmacology ; Electric Stimulation ; Guinea Pigs ; Heart/*physiology ; In Vitro Techniques ; Membrane Potentials/drug effects ; *Myocardial Contraction/drug effects ; Perfusion ; Sarcolemma/drug effects/physiology
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    A c-myb antisense oligodeoxynucleotide inhibits normal human hematopoiesis in vitro (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-12-02
    Description: The nuclear protein encoded by the proto-oncogene c-myb has been hypothesized to play an important role in the process of hematopoiesis, but direct proof of this function has been lacking. To address this issue, normal human bone marrow mononuclear cells were exposed to c-myb sense and antisense synthetic oligodeoxynucleotides, and the effects on hematopoietic colony formation and maturation were examined. Exposure of these cells to c-myb antisense, oligodeoxynucleotides resulted in a decrease in both colony size and number, without apparent effect on the maturation of residual colony cells. Exposure to c-myb sense, or irrelevant antisense, oligonucleotides had no such effect. These results show that (i) c-myb plays a critical role in regulating normal human hematopoiesis and (ii) the combined use of antisense oligodeoxynucleotides and hematopoietic cell culture techniques will provide a powerful tool for studying the role of proteins encoded by proto-oncogenes, or other specific genes, in normal human hematopoiesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gewirtz, A M -- Calabretta, B -- CA 01324/CA/NCI NIH HHS/ -- CA 36896/CA/NCI NIH HHS/ -- CA 46782/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1988 Dec 2;242(4883):1303-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University School of Medicine, Philadelphia, PA 19140.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2461588" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Differentiation ; Cell Division ; Clone Cells ; *Hematopoiesis ; Humans ; In Vitro Techniques ; Nuclear Proteins/*physiology ; Oligodeoxyribonucleotides/chemical synthesis ; Peroxidase/genetics ; Proto-Oncogene Proteins/*physiology ; Proto-Oncogene Proteins c-myb ; Rna ; RNA, Antisense
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    Site-specific oligonucleotide binding represses transcription of the human c-myc gene in vitro (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-07-22
    Description: A 27-base-long DNA oligonucleotide was designed that binds to duplex DNA at a single site within the 5' end of the human c-myc gene, 115 base pairs upstream from the transcription origin P1. On the basis of the physical properties of its bound complex, it was concluded that the oligonucleotide forms a colinear triplex with the duplex binding site. By means of an in vitro assay system, it was possible to show a correlation between triplex formation at -115 base pairs and repression of c-myc transcription. The possibility is discussed that triplex formation (site-specific RNA binding to a DNA duplex) could serve as the basis for an alternative program of gene control in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cooney, M -- Czernuszewicz, G -- Postel, E H -- Flint, S J -- Hogan, M E -- New York, N.Y. -- Science. 1988 Jul 22;241(4864):456-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Princeton University, NJ 08544.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3293213" target="_blank"〉PubMed〈/a〉
    Keywords: Electrophoresis ; Gene Expression Regulation ; Humans ; In Vitro Techniques ; Nucleic Acid Hybridization ; Oligodeoxyribonucleotides/*pharmacology ; Proto-Oncogene Proteins/*genetics ; *Proto-Oncogenes ; *Transcription, Genetic/drug effects
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    Dominant role of N-type Ca2+ channels in evoked release of norepinephrine from sympathetic neurons (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-01-01
    Description: Multiple types of calcium channels have been found in neurons, but uncertainty remains about which ones are involved in stimulus-secretion coupling. Two types of calcium channels in rat sympathetic neurons were described, and their relative importance in controlling norepinephrine release was analyzed. N-type and L-type calcium channels differed in voltage dependence, unitary barium conductance, and pharmacology. Nitrendipine inhibited activity of L-type channels but not N-type channels. Potassium-evoked norepinephrine release was markedly reduced by cadmium and the conesnail peptide toxin omega-Conus geographus toxin VIA, agents that block both N- and L-type channels, but was little affected by nitrendipine at concentrations that strongly reduce calcium influx, as measured by fura-2. Thus N-type calcium channels play a dominant role in the depolarization-evoked release of norepinephrine.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hirning, L D -- Fox, A P -- McCleskey, E W -- Olivera, B M -- Thayer, S A -- Miller, R J -- Tsien, R W -- DA02121/DA/NIDA NIH HHS/ -- HL13306/HL/NHLBI NIH HHS/ -- NS24067/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1988 Jan 1;239(4835):57-61.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacological and Physiological Sciences, University of Chicago, IL 60637.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2447647" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/*physiology ; Calcium Channel Blockers/pharmacology ; Electric Conductivity ; Ganglia, Sympathetic/*physiology ; In Vitro Techniques ; Ion Channels/*physiology ; Membrane Potentials ; Norepinephrine/*secretion ; Rats ; Secretory Rate/drug effects
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    Overexpression of metallothionein confers resistance to anticancer drugs (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-09-30
    Description: Resistance to antineoplastic agents is the major obstacle to curative therapy of cancer. Tumor cell lines with acquired resistance to the antineoplastic agent cis-diamminedichloroplatinum(II) overexpressed metallothionein and demonstrated cross-resistance to alkylating agents such as chlorambucil and melphalan. Human carcinoma cells that maintained high levels of metallothionein because of chronic exposure to heavy metals were resistant to cis-diamminedichloroplatinum(II), melphalan, and chlorambucil. Furthermore, cells transfected with bovine papilloma virus expression vectors containing DNA encoding human metallothionein-IIA were resistant to cis-diamminedichloroplatinum(II), melphalan, and chlorambucil but not to 5-fluorouracil or vincristine. Thus, overexpression of metallothionein represents one mechanism of resistance to a subset of clinically important anticancer drugs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kelley, S L -- Basu, A -- Teicher, B A -- Hacker, M P -- Hamer, D H -- Lazo, J S -- CA-01012/CA/NCI NIH HHS/ -- CA-38497/CA/NCI NIH HHS/ -- CA-43917/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1988 Sep 30;241(4874):1813-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Pharmaceutical Research and Development Division, Bristol Myers Co., Wallingford, CT 06492.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3175622" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antineoplastic Agents ; Blotting, Northern ; Cells, Cultured ; *Drug Resistance ; In Vitro Techniques ; Metallothionein/*physiology ; Mice
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    Steroid hormone metabolites are barbiturate-like modulators of the GABA receptor (1986)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1986-05-23
    Description: Two metabolites of the steroid hormones progesterone and deoxycorticosterone, 3 alpha-hydroxy-5 alpha-dihydroprogesterone and 3 alpha, 5 alpha-tetrahydrodeoxycorticosterone, are potent barbiturate-like ligands of the gamma-aminobutyric acid (GABA) receptor-chloride ion channel complex. At concentrations between 10(-7) and 10(-5)M both steroids inhibited binding of the convulsant t-butylbicyclophosphorothionate to the GABA-receptor complex and increased the binding of the benzodiazepine flunitrazepam; they also stimulated chloride uptake (as measured by uptake of 36Cl-) into isolated brain vesicles, and potentiated the inhibitory actions of GABA in cultured rat hippocampal and spinal cord neurons. These data may explain the ability of certain steroid hormones to rapidly alter neuronal excitability and may provide a mechanism for the anesthetic and hypnotic actions of naturally occurring and synthetic anesthetic steroids.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Majewska, M D -- Harrison, N L -- Schwartz, R D -- Barker, J L -- Paul, S M -- New York, N.Y. -- Science. 1986 May 23;232(4753):1004-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2422758" target="_blank"〉PubMed〈/a〉
    Keywords: 20-alpha-Dihydroprogesterone/*analogs & derivatives/metabolism/pharmacology ; Animals ; Bicyclo Compounds/metabolism ; *Bicyclo Compounds, Heterocyclic ; Binding, Competitive ; Brain/metabolism ; Cells, Cultured ; Chlorides/metabolism ; Desoxycorticosterone/*analogs & derivatives/metabolism/pharmacology ; Drug Synergism ; Flunitrazepam/metabolism ; Hippocampus/metabolism ; In Vitro Techniques ; Ion Channels/metabolism ; Progesterone/*analogs & derivatives/metabolism/pharmacology ; Rats ; Receptors, GABA-A/*drug effects/metabolism ; Spinal Cord/metabolism
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    Dynamic instability of sheared microtubules observed by quasi-elastic light scattering (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-09-23
    Description: The kinetics of microtubule reassembly was studied in vitro by quasi-elastic light scattering (QELS). When microtubules assembled in the absence of microtubule-associated proteins (MAPs) were sheared, they rapidly depolymerized, recovered, and reassembled. The mean length of the recovered microtubules was the same as that observed just before shearing, implying that on average one fragment per original microtubule survived the fragmentation and recovery. When microtubules that contained 25 percent brain MAP were sheared, the fragments did not depolymerize extensively and the average length of the fragments decreased by a factor of 3 relative to the unsheared sample. The results support the dynamic instability model, which predicts that cellular microtubules are latently unstable structures protected on their ends by stabilizing caps.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Keates, R A -- Hallett, F R -- New York, N.Y. -- Science. 1988 Sep 23;241(4873):1642-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry and Biochemistry, University of Guelph, Ontario, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3420415" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Guanosine Diphosphate/physiology ; Guanosine Triphosphate/physiology ; In Vitro Techniques ; Kinetics ; Light ; Microtubule-Associated Proteins/metabolism ; Microtubules/*metabolism ; Scattering, Radiation ; Tubulin/metabolism
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    Heterogeneous nuclear ribonucleoproteins: role in RNA splicing (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-03-28
    Description: Splicing in vitro of a messenger RNA (mRNA) precursor (pre-mRNA) is inhibited by a monoclonal antibody to the C proteins (anti-C) of the heterogeneous nuclear RNA (hnRNA)-ribonucleoprotein (hnRNP) particles. This antibody, 4F4, inhibits an early step of the reaction: cleavage at the 3' end of the upstream exon and the formation of the intron lariat. In contrast, boiled 4F4, or a different monoclonal antibody (designated 2B12) to the C proteins, or antibodies to other hnRNP proteins (120 and 68 kilodaltons) and nonimmune mouse antibodies have no inhibitory effect. The 4F4 antibody does not prevent the adenosine triphosphate-dependent formation of a 60S splicing complex (spliceosome). Furthermore, the 60S splicing complex contains C proteins, and it can be immunoprecipitated with 4F4. Depletion of C proteins from the splicing extract by immunoadsorption with either of the two monoclonal antibodies to the C proteins (4F4 or 2B12) results in the loss of splicing activity, whereas mock-depletion with nonimmune mouse antibodies bodies has no effect. A 60S splicing complex does not form in a C protein-depleted nuclear extract. These results indicate an essential role for proteins of the hnRNP complex in the splicing of mRNA precursors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Choi, Y D -- Grabowski, P J -- Sharp, P A -- Dreyfuss, G -- New York, N.Y. -- Science. 1986 Mar 28;231(4745):1534-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3952495" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Antibodies, Monoclonal/*immunology ; HeLa Cells ; Heterogeneous-Nuclear Ribonucleoproteins ; Humans ; In Vitro Techniques ; Macromolecular Substances ; *RNA Splicing ; RNA, Heterogeneous Nuclear/metabolism ; Ribonucleoproteins/immunology/*physiology
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  • 55
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    Role of platelet-activating factor-acether in mediating guinea pig anaphylaxis (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-04-04
    Description: The pathophysiology of anaphylaxis is very complex, and the sequelae of events are not fully explained in terms of the effects of histamine and peptide leukotrienes alone. Platelet-activating factor (1-O-alkyl-2-acetyl-sn-glyceryl-3-phosphorylcholine, PAF-acether) has been detected in animals undergoing anaphylaxis. Injection of synthetic PAF-acether induces similar effects, including bronchoconstriction, respiratory arrest, systemic hypotension, neutropenia, and thrombocytopenia. The results reported here demonstrate that the histamine- and leukotriene-independent component of guinea pig anaphylaxis in vivo and in isolated lung parenchymal strips in vitro is mediated by PAF-acether. However, PAF-acether is not responsible for the anaphylaxis-induced thrombocytopenia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Darius, H -- Lefer, D J -- Smith, J B -- Lefer, A M -- HL-25575/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1986 Apr 4;232(4746):58-60.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3082008" target="_blank"〉PubMed〈/a〉
    Keywords: 4,5-Dihydro-1-(3-(trifluoromethyl)phenyl)-1H-pyrazol-3-amine ; Alprazolam ; *Anaphylaxis ; Animals ; Anti-Inflammatory Agents/pharmacology ; Benzodiazepines/pharmacology ; Blood Pressure ; Diphenhydramine/pharmacology ; Guinea Pigs ; In Vitro Techniques ; Kinetics ; Lung/drug effects/*immunology ; Male ; Ovalbumin ; Platelet Activating Factor/*immunology ; Platelet Count/drug effects ; Pyrazoles/pharmacology
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  • 56
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    Vasoconstriction: a new activity for platelet-derived growth factor (1986)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1986-04-04
    Description: Platelet-derived growth factor (PDGF) is a potent mitogen for vascular smooth muscle cells that has been implicated in the pathogenesis of atherosclerosis. The potential role of PDGF in the altered vasoreactivity of atherosclerotic vessels has been studied through an examination of its effects on contractility in the rat aorta. PDGF caused a concentration-dependent contraction of aortic strips and was significantly more potent on a molar basis than the classic vasoconstrictor peptide angiotensin II. Furthermore, PDGF increased the cytosolic free calcium concentration in cultured rat aortic smooth muscle cells. These observations suggest a new biological activity for PDGF that may contribute to the enhanced vasoreactivity of certain atherosclerotic vessels.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Berk, B C -- Alexander, R W -- Brock, T A -- Gimbrone, M A Jr -- Webb, R C -- HL20054/HL/NHLBI NIH HHS/ -- HL22602/HL/NHLBI NIH HHS/ -- HL35013/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1986 Apr 4;232(4746):87-90.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3485309" target="_blank"〉PubMed〈/a〉
    Keywords: Aminoquinolines ; Angiotensin II/pharmacology ; Animals ; Aorta/*drug effects/metabolism/physiology ; Calcium/metabolism ; Cytosol/metabolism ; Dose-Response Relationship, Drug ; Epidermal Growth Factor/pharmacology ; Fluorescent Dyes ; Homeostasis/drug effects ; Humans ; In Vitro Techniques ; Kinetics ; Platelet-Derived Growth Factor/*pharmacology ; Rats ; Vasoconstriction/*drug effects
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  • 57
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    Inhibition of vasopressin action by atrial natriuretic factor (1986)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1986-03-28
    Description: Atrial natriuretic factor results in diuresis in animals and humans, perhaps because atrial natriuretic factor increases renal blood flow. The possibility that this diuresis is due to direct inhibition of renal tubular epithelial water transport was examined in rabbit collecting tubules perfused in vitro. Atriopeptin III inhibition of the hydraulic conductivity response to the hormone arginine vasopressin but not to either 3'5'-cyclic adenosine monophosphate or forskolin was found. These results suggest that atriopeptin III acts proximal to cyclic adenosine monophosphate formation to directly affect vasopressin-stimulated water transport in the mammalian nephron. They also suggest a potential role for inhibition by atrial natriuretic factor of the renal response to arginine vasopressin as a contributor to a diuretic state.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dillingham, M A -- Anderson, R J -- 1K08 AM-01245/AM/NIADDK NIH HHS/ -- AM-26111/AM/NIADDK NIH HHS/ -- AM-30448/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1986 Mar 28;231(4745):1572-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3006248" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arginine Vasopressin/*antagonists & inhibitors ; Atrial Natriuretic Factor/*pharmacology ; Colforsin/pharmacology ; Cyclic AMP/physiology ; Cyclic GMP/physiology ; Diuresis/drug effects ; In Vitro Techniques ; Kidney Tubules/*drug effects ; Kidney Tubules, Collecting/*drug effects/physiology ; Rabbits
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  • 58
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    Activation of smooth muscle contraction: relation between myosin phosphorylation and stiffness (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-04-04
    Description: Contraction and myosin light-chain phosphorylation were measured in electrically stimulated tracheal smooth muscle. Latencies for the onset of force, stiffness, and light-chain phosphorylation were 500 milliseconds. Myosin light chain was phosphorylated from 0.04 to 0.80 mole of phosphate per mole of light chain with a pseudo-first-order rate of 1.1 per second with no evidence of an ordered or negatively cooperative process. Following the period of latency, stiffness increased with phosphorylation and both increased more rapidly than isometric force. The linear relation between stiffness and phosphorylation during activation suggests independent attachment of each myosin head upon phosphorylation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kamm, K E -- Stull, J T -- HL 26043/HL/NHLBI NIH HHS/ -- HL 32607/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1986 Apr 4;232(4746):80-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3754063" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carbachol/pharmacology ; Electric Stimulation ; In Vitro Techniques ; Kinetics ; *Muscle Contraction/drug effects ; Muscle, Smooth/*physiology ; Myosin-Light-Chain Kinase ; Myosins/*metabolism ; Phosphorylation ; Protein Kinases/metabolism ; Trachea/physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 59
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    Differential conditioning of associative synaptic enhancement in hippocampal brain slices (1986)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1986-04-04
    Description: An electrophysiological stimulation paradigm similar to one that produces Pavlovian conditioning was applied to synaptic inputs to pyramidal neurons of hippocampal brain slices. Persistent synaptic enhancement was induced in one of two weak synaptic inputs by pairing high-frequency electrical stimulation of the weak input with stimulation of a third, stronger input to the same region. Forward (temporally overlapping) but not backward (temporally separate) pairings caused this enhancement. Thus hippocampal synapses in vitro can undergo the conditional and selective type of associative modification that could provide the substrate for some of the mnemonic functions in which the hippocampus is thought to participate.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kelso, S R -- Brown, T H -- NS07408/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1986 Apr 4;232(4746):85-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3952501" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Conditioning, Classical ; Electric Stimulation ; Hippocampus/*physiology ; In Vitro Techniques ; Models, Neurological ; Models, Psychological ; Neurons/physiology ; Pyramidal Tracts/physiology ; Rats ; Synapses/*physiology ; Time Factors
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  • 60
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    Induction of synaptic potentiation in hippocampus by patterned stimulation involves two events (1986)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1986-05-23
    Description: Electrical stimulation of axons in the hippocampus with short high-frequency bursts that resemble in vivo activity patterns produces stable potentiation of postsynaptic responses when the bursts occur at intervals of 200 milliseconds but not 2 seconds. When a burst was applied to one input and a second burst applied to a different input to the same target neuron 200 milliseconds later, only the synapses activated by the second burst showed stable potentiation. This effect was observed even when the two inputs innervated completely different regions of the postsynaptic cells; but did not occur when the inputs were stimulated simultaneously or when the second burst was delayed by 2 seconds. Intracellular recordings indicated that the first burst extended the decay phase of excitatory postsynaptic potentials evoked 200 milliseconds later. These results suggest that a single burst of axonal stimulation produces a transient, spatially diffuse "priming" effect that prolongs responses to subsequent bursts, and that these altered responses trigger spatially restricted synaptic modifications. The similarity of the temporal parameters of the priming effect and the theta rhythm that dominates the hippocampal electroencephalogram (EEG) during learning episodes suggests that this priming may be involved in behaviorally induced synaptic plasticity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Larson, J -- Lynch, G -- New York, N.Y. -- Science. 1986 May 23;232(4753):985-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3704635" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Electric Stimulation ; Hippocampus/*physiology ; In Vitro Techniques ; Learning/physiology ; Membrane Potentials ; Neuronal Plasticity ; Periodicity ; Rats ; Synapses/physiology
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  • 61
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    Control of cachectin (tumor necrosis factor) synthesis: mechanisms of endotoxin resistance (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-05-23
    Description: Cachectin (tumor necrosis factor) is a macrophage hormone strongly implicated in the pathogenesis of endotoxin-induced shock. The availability of a DNA probe complementary to the cachectin messenger RNA (mRNA), as well as a specific antibody capable of recognizing the cachectin gene product, has made it possible to analyze the regulation of cachectin gene expression under a variety of conditions. Thioglycollate-elicited peritoneal macrophages obtained from mice contain a pool of cachectin mRNA that is not expressed as protein. When the cells are stimulated with endotoxin, large quantity of additional cachectin mRNA is produced, and immunoreactive cachectin is secreted. Macrophages from mice of the C3H/HeJ strain do not produce cachectin in response to endotoxin. A dual defect appears to prevent cachectin expression. First, a diminished quantity of cachectin mRNA is expressed in response to low concentrations of endotoxin. Second, a post-transcriptional defect prevents the production of cachectin protein. Macrophages from endotoxin-sensitive mice do not produce cachectin if they are first treated with dexamethasone, apparently for similar reasons. These findings give new insight into the nature of the C3H/HeJ mutation and suggest an important mechanism by which glucocorticoids may act to suppress inflammation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Beutler, B -- Krochin, N -- Milsark, I W -- Luedke, C -- Cerami, A -- AI21359/AI/NIAID NIH HHS/ -- AM01314/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1986 May 23;232(4753):977-80.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3754653" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Dexamethasone/pharmacology ; Drug Resistance ; Endotoxins/*pharmacology ; Gene Expression Regulation/drug effects ; In Vitro Techniques ; Macrophages/drug effects/*metabolism ; Mice ; Mice, Inbred C3H/physiology ; *Protein Biosynthesis ; Proteins/genetics ; RNA, Messenger/metabolism ; Transcription, Genetic/drug effects ; Tumor Necrosis Factor-alpha
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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