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  • 1
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    Primary structure of the beta subunit of the DHP-sensitive calcium channel from skeletal muscle (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-09-08
    Description: Complementary DNAs for the beta subunit of the dihydropyridine-sensitive calcium channel of rabbit skeletal muscle were isolated on the basis of peptide sequences derived from the purified protein. The deduced primary structure is without homology to other known protein sequences and is consistent with the beta subunit being a peripheral membrane protein associated with the cytoplasmic aspect of the sarcolemma. The protein contains sites that might be expected to be preferentially phosphorylated by protein kinase C and guanosine 3',5'-monophosphate-dependent protein kinase. A messenger RNA for this protein appears to be expressed in brain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ruth, P -- Rohrkasten, A -- Biel, M -- Bosse, E -- Regulla, S -- Meyer, H E -- Flockerzi, V -- Hofmann, F -- New York, N.Y. -- Science. 1989 Sep 8;245(4922):1115-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut fur Physiologische Chemie, Medizinische Fakultat, Homburg/Saar, Federal Republic of Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2549640" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Calcium Channel Blockers/*metabolism/pharmacology ; Calcium Channels/drug effects/*metabolism ; Dihydropyridines/*metabolism/pharmacology ; Molecular Sequence Data ; Muscles/*analysis ; Phosphorylation ; Protein Conformation ; RNA, Messenger/isolation & purification ; Rabbits ; Receptors, Nicotinic/drug effects/*isolation & purification/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    The Fc and not CD4 receptor mediates antibody enhancement of HIV infection in human cells (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-06-16
    Description: Antibodies that enhance human immunodeficiency virus (HIV) infectivity have been found in the blood of infected individuals and in infected or immunized animals. These findings raise serious concern for the development of a safe vaccine against acquired immunodeficiency syndrome. To address the in vivo relevance and mechanism of this phenomenon, antibody-dependent enhancement of HIV infectivity in peripheral blood macrophages, lymphocytes, and human fibroblastoid cells was studied. Neither Leu3a, a monoclonal antibody directed against the CD4 receptor, nor soluble recombinant CD4 even at high concentrations prevented this enhancement. The addition of monoclonal antibody to the Fc receptor III (anti-FcRIII), but not of antibodies that react with FcRI or FcRII, inhibited HIV type 1 and HIV type 2 enhancement in peripheral blood macrophages. Although enhancement of HIV infection in CD4+ lymphocytes could not be blocked by anti-FcRIII, it was inhibited by the addition of human immunoglobulin G aggregates. The results indicate that the FcRIII receptor on human macrophages and possibly another Fc receptor on human CD4+ lymphocytes mediate antibody-dependent enhancement of HIV infectivity and that this phenomenon proceeds through a mechanism independent of the CD4 protein.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Homsy, J -- Meyer, M -- Tateno, M -- Clarkson, S -- Levy, J A -- AI-26471/AI/NIAID NIH HHS/ -- R01-AI-24499/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1989 Jun 16;244(4910):1357-60.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, 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/2786647" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/*immunology ; Animals ; Antibodies, Monoclonal ; Antibody-Dependent Cell Cytotoxicity ; Guinea Pigs ; HIV Antibodies/biosynthesis/*immunology ; HIV-1/*immunology ; HIV-2/*immunology ; Humans ; In Vitro Techniques ; Pan troglodytes ; Receptors, Fc/*physiology ; Receptors, HIV ; Receptors, Virus/*physiology
    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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    Highly cooperative opening of calcium channels by inositol 1,4,5-trisphosphate (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-04-29
    Description: The kinetics of calcium release by inositol 1,4,5-trisphosphate (IP3) in permeabilized rat basophilic leukemia cells were studied to obtain insight into the molecular mechanism of action of this intracellular messenger of the phosphoinositide cascade. Calcium release from intracellular storage sites was monitored with fura-2, a fluorescent indicator. The dependence of the rate of calcium release on the concentration of added IP3 in the 4 to 40 nM range showed that channel opening requires the binding of at least three molecules of IP3. Channel opening occurred in the absence of added adenosine triphosphate, indicating that IP3 acts directly on the channel or on a protein that gates it. The channels were opened by IP3 in less than 4 seconds. The highly cooperative opening of calcium channels by nanomolar concentrations of IP3 enables cells to detect and amplify very small changes in the concentration of this messenger in response to hormonal, sensory, and growth control stimuli.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Meyer, T -- Holowka, D -- Stryer, L -- AI22449/AI/NIAID NIH HHS/ -- GM24032/GM/NIGMS NIH HHS/ -- GM30387/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1988 Apr 29;240(4852):653-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Sherman Fairchild Center, Stanford University School of Medicine, CA 94305.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2452482" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Basophils ; Benzofurans ; Calcimycin/pharmacology ; Calcium/*metabolism ; Cell Membrane Permeability ; Cytoplasm/metabolism ; Fluorescent Dyes ; Fura-2 ; Inositol 1,4,5-Trisphosphate ; Inositol Phosphates/metabolism/*pharmacology ; Ion Channels/drug effects/*metabolism ; Kinetics ; Leukemia, Experimental/metabolism ; Rats ; Spectrometry, Fluorescence ; Sugar Phosphates/*pharmacology ; Tumor Cells, Cultured
    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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  • 4
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    Long-term neuropathological and neurochemical effects of nucleus basalis lesions in the rat (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-11-13
    Description: The long-term effects of excitotoxic lesions in the nucleus basalis magnocellularis of the rat were found to mimic several neuropathological and chemical changes associated with Alzheimer's disease. Neuritic plaque-like structures, neurofibrillary changes, and neuronal atrophy or loss were observed in the frontoparietal cortex, hippocampus, amygdala, and entorhinal cortex 14 months after the lesions were made. Cholinergic markers in neocortex were reduced, while catecholamine and indoleamine metabolism was largely unaffected at this time. Bilateral lesions of the nucleus basalis magnocellularis increased somatostatin and neuropeptide Y in the cortex of the rat by at least 138 and 284 percent, respectively, suggesting a functional interaction between cholinergic and peptidergic neurons that may differ from that in Alzheimer's disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Arendash, G W -- Millard, W J -- Dunn, A J -- Meyer, E M -- HD 17933/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1987 Nov 13;238(4829):952-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, University of South Florida, Tampa 33620.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2890210" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcholinesterase/metabolism ; Animals ; Biogenic Amines/metabolism ; Brain/metabolism/*pathology ; Cerebral Cortex/metabolism/*pathology ; Choline/metabolism ; Choline O-Acetyltransferase/metabolism ; Male ; Neuropeptide Y/analysis ; Olivary Nucleus/*physiology ; Organ Specificity ; Rats ; Rats, Inbred Strains ; Somatostatin/analysis
    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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  • 5
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    Coupling of action potential activity between unmyelinated fibers in the peripheral nerve of monkey (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-01-11
    Description: Bidirectional coupling of action potential activity occurs between unmyelinated fibers in the normal peripheral nerve of monkey. The site of coupling is near the cutaneous nociceptive receptor associated with one of the fibers. This coupling could be due to an electrical synapse and could provide the basis for the flare associated with the axon reflex.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Meyer, R A -- Raja, S N -- Campbell, J N -- NS-00519/NS/NINDS NIH HHS/ -- NS-14447/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1985 Jan 11;227(4683):184-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3966152" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Electric Stimulation ; Macaca fascicularis ; Nerve Fibers/physiology ; Peripheral Nerves/*physiology ; Sensory Receptor Cells/physiology ; Skin/injuries
    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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  • 6
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    Corticotropin-releasing activity of monokines (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-11-29
    Description: Hepatocyte-stimulating factor and interleukin-1 are proteins produced by monocytes in response to inflammatory challenge. Neither of these monokines had direct effects on steroid production by cultured adrenocortical cells. Both monokines stimulated pituitary cells (AtT-20) to release adrenocorticotropic hormone; interleukin-1 was equipotent with a combination of corticotropin-releasing factor and arginine vasopressin, and hepatocyte-stimulating factor was at least three times as effective. The synthetic glucocorticoid, dexamethasone, inhibited production of hepatocyte-stimulating factor by cultured monocytes. These results indicate an axis between monocytes and pituitary and adrenocortical cells which may play a role in regulating host defense.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Woloski, B M -- Smith, E M -- Meyer, W J 3rd -- Fuller, G M -- Blalock, J E -- AI 18932/AI/NIAID NIH HHS/ -- IR01AM338-39-01A1/AM/NIADDK NIH HHS/ -- R01-H120201/PHS HHS/ -- New York, N.Y. -- Science. 1985 Nov 29;230(4729):1035-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2997929" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenal Glands/metabolism ; Adrenocorticotropic Hormone/*secretion ; Animals ; Interleukin-1/pharmacology ; Interleukin-6 ; Mice ; Monocytes/*physiology ; Monokines ; Pituitary-Adrenal System/*physiology ; Proteins/*pharmacology ; Secretory Rate/drug effects
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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