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  • In Vitro Techniques  (13)
  • American Association for the Advancement of Science (AAAS)  (13)
  • American Geophysical Union
  • Blackwell Publishing Ltd
  • 2020-2023
  • 1985-1989  (13)
  • 1980-1984
  • 1970-1974
  • 1988  (13)
Collection
Keywords
Publisher
  • American Association for the Advancement of Science (AAAS)  (13)
  • American Geophysical Union
  • Blackwell Publishing Ltd
Years
  • 2020-2023
  • 1985-1989  (13)
  • 1980-1984
  • 1970-1974
Year
  • 1
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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
    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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    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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  • 3
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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
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    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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  • 5
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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
    Print ISSN: 0036-8075
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  • 6
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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
    Print ISSN: 0036-8075
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  • 7
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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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  • 8
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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)
    Details
    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
    Print ISSN: 0036-8075
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  • 9
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    Negative regulation by glucocorticoids through interference with a cAMP responsive enhancer (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    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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  • 10
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    Synaptic transmission between dissociated adult mammalian neurons and attached synaptic boutons (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    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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