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  • Articles  (77)
  • Rats  (77)
  • American Association for the Advancement of Science (AAAS)  (77)
  • American Institute of Physics
  • Elsevier
  • 2020-2022
  • 1985-1989  (77)
  • 1950-1954
  • 1945-1949
  • 1988  (77)
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  • Articles  (77)
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  • American Association for the Advancement of Science (AAAS)  (77)
  • American Institute of Physics
  • Elsevier
  • Springer  (1)
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  • 2020-2022
  • 1985-1989  (77)
  • 1950-1954
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  • 1
    Publication Date: 1988-07-15
    Description: Odorant-binding protein (OBP) is found in nasal epithelium, and it selectively binds odorants. Three complementary DNAs encoding rat odorant-binding protein have now been cloned and sequenced. One clone contains an open reading frame predicted to encode an 18,091-dalton protein. RNA blot analysis confirms the localization of OBP messenger RNA in the nasal epithelium. This OBP has 33 percent amino acid identity to alpha 2-microglobulin, a secreted plasma protein. Other members of an alpha 2-microglobulin superfamily bind and transport hydrophobic ligands. Thus, OBP probably binds and carries odorants within the nasal epithelium to putative olfactory receptors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pevsner, J -- Reed, R R -- Feinstein, P G -- Snyder, S H -- DA-00074/DA/NIDA NIH HHS/ -- GM-07626/GM/NIGMS NIH HHS/ -- P01 CA16519-13/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1988 Jul 15;241(4863):336-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3388043" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Carrier Proteins/*genetics ; Cloning, Molecular ; Ligands ; Membrane Proteins/*genetics ; Molecular Sequence Data ; Nasal Mucosa/*physiology ; Rats ; *Receptors, Odorant ; Smell/*physiology
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  • 2
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-10-21
    Description: Synthesis of a small group of highly conserved proteins in response to elevated temperature and other agents that induce stress is a universal feature of prokaryotic and eukaryotic cells. Although correlative evidence suggests that these proteins play a role in enhancing survival during and after stress, there is no direct evidence to support this in mammalian cells. To assess the role of the most highly conserved heat shock protein (hsp) family during heat shock, affinity-purified monoclonal antibodies to hsp70 were introduced into fibroblasts by needle microinjection. In addition to impairing the heat-induced translocation of hsp70 proteins into the nucleus after mild heat shock treatment, injected cells were unable to survive a brief incubation at 45 degrees C. Cells injected with control antibodies survived a similar heat shock. These results indicate that functional hsp70 is required for survival of these cells during and after thermal stress.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Riabowol, K T -- Mizzen, L A -- Welch, W J -- GM33551/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1988 Oct 21;242(4877):433-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cold Spring Harbor Laboratory, NY 11724.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3175665" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies/administration & dosage ; Antigen-Antibody Complex ; Cell Survival ; Fibroblasts/cytology ; Heat-Shock Proteins/immunology/*physiology ; *Hot Temperature ; Microinjections ; Rats
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  • 3
    Publication Date: 1988-12-16
    Description: Fibroblasts were genetically modified to secrete nerve growth factor (NGF) by infection with a retroviral vector and then implanted into the brains of rats that had surgical lesions of the fimbria-fornix. The grafted cells survived and produced sufficient NGF to prevent the degeneration of cholinergic neurons that would die without treatment. In addition, the protected cholinergic cells sprouted axons that projected in the direction of the cellular source of NGF. These results indicate that a combination of gene transfer and intracerebral grafting may provide an effective treatment for some disorders of the central nervous system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rosenberg, M B -- Friedmann, T -- Robertson, R C -- Tuszynski, M -- Wolff, J A -- Breakefield, X O -- Gage, F H -- AG06088/AG/NIA NIH HHS/ -- HD20034/HD/NICHD NIH HHS/ -- NS24279/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1988 Dec 16;242(4885):1575-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatrics, University of California School of Medicine, La Jolla 92093.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3201248" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcholinesterase/metabolism ; Animals ; Brain/cytology/enzymology/*pathology ; Cell Survival ; DNA/genetics ; Fibroblasts/metabolism/*transplantation ; Genetic Vectors ; Histocytochemistry ; Moloney murine leukemia virus/genetics ; Nerve Growth Factors/genetics/*physiology ; Rats
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  • 4
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-06-03
    Description: The proto-oncogene c-fos is expressed in neurons in response to direct stimulation by growth factors and neurotransmitters. In order to determine whether the c-fos protein (Fos) and Fos-related proteins can be induced in response to polysynaptic activation, rat hindlimb motor/sensory cortex was stimulated electrically and Fos expression examined immunohistochemically. Three hours after the onset of stimulation, focal nuclear Fos staining was seen in motor and sensory thalamus, pontine nuclei, globus pallidus, and cerebellum. Moreover, 24-hour water deprivation resulted in Fos expression in paraventricular and supraoptic nuclei. Fos immunohistochemistry therefore provides a cellular method to label polysynaptically activated neurons and thereby map functional pathways.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sagar, S M -- Sharp, F R -- Curran, T -- EY05721/EY/NEI NIH HHS/ -- NS24666/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1988 Jun 3;240(4857):1328-31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, University of California, San Francisco.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3131879" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*metabolism ; Cell Nucleus/metabolism ; Cerebellum/metabolism ; Cerebral Cortex/metabolism ; Electric Stimulation ; *Gene Expression Regulation ; Globus Pallidus/metabolism ; Hippocampus/metabolism ; Hypothalamus/metabolism ; Immunohistochemistry ; Motor Cortex/physiology ; Neurons/metabolism ; Pons/metabolism ; Proto-Oncogene Proteins/*genetics ; Proto-Oncogene Proteins c-fos ; Rats ; Thalamus/metabolism
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  • 5
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-01-01
    Description: Strong steric interactions among proteins on crowded living cell surfaces were revealed by measurements of the equilibrium spatial distributions of proteins in applied potential gradients. The fraction of accessible surface occupied by mobile surface proteins can be accurately represented by including steric exclusion in the statistical thermodynamic analysis of the data. The analyses revealed enhanced, concentration-dependent activity coefficients, implying unanticipated thermodynamic activity even at typical cell surface receptor concentrations.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ryan, T A -- Myers, J -- Holowka, D -- Baird, B -- Webb, W W -- AI18306/AI/NIAID NIH HHS/ -- AI22449/AI/NIAID NIH HHS/ -- GM33028/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1988 Jan 1;239(4835):61-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physics, Cornell University, Ithaca, NY 14853.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2962287" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Membrane/*physiology ; *Membrane Fluidity ; Membrane Proteins/*physiology ; Rats ; Receptors, Fc/physiology ; Receptors, IgE ; Thermodynamics ; Tumor Cells, Cultured
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  • 6
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-08-19
    Description: In mammalian cells, the glucocorticoid receptor binds specifically to glucocorticoid response element (GRE) DNA sequences and enhances transcription from linked promoters. It is shown here that derivatives of the glucocorticoid receptor also enhance transcription when expressed in yeast. Receptor-mediated enhancement in yeast was observed in fusions of GRE sequences to the yeast cytochrome c1 (CYC1) promoter; the CYC1 upstream activator sequences were not essential, since enhancement was observed in fusions of GREs to mutant CYC1 promoters retaining only the TATA region and transcription startpoints. It is concluded that the receptor operates by a common, highly conserved mechanism in yeast and mammalian cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schena, M -- Yamamoto, K R -- CA20535-12/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1988 Aug 19;241(4868):965-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Biophysics, University of California, San Francisco 94143.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3043665" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; DNA/metabolism ; *Enhancer Elements, Genetic ; Gene Expression Regulation ; Immunoassay ; Plasmids ; Promoter Regions, Genetic ; Rats ; Receptors, Glucocorticoid/*genetics ; Saccharomyces cerevisiae/*genetics ; *Transcription, Genetic
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  • 7
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-12-09
    Description: Cell types associated with angiotensinogen mRNA in rat brain were identified in individual brain sections by in situ hybridization with tritiated RNA probes or with a sulfur-35--labeled oligonucleotide combined with immunocytochemical detection of either glial fibrillary acidic protein (GFAP) for astrocytes or microtubule-associated protein (MAP-2) for neurons. Autoradiography revealed silver grains clustered primarily over GFAP-reactive soma and processes; most grain clusters were not associated with MAP-2--reactive cells. These results demonstrate that, in contrast to other known neuropeptide precursors, angiotensinogen is synthesized by glia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stornetta, R L -- Hawelu-Johnson, C L -- Guyenet, P G -- Lynch, K R -- R01 HL33513/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1988 Dec 9;242(4884):1444-6.〈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/3201232" target="_blank"〉PubMed〈/a〉
    Keywords: Angiotensinogen/*biosynthesis/genetics ; Animals ; Astrocytes/*metabolism ; Brain/*metabolism ; Glial Fibrillary Acidic Protein/analysis ; Histocytochemistry ; Microtubule-Associated Proteins/analysis ; Nucleic Acid Hybridization ; RNA, Messenger/analysis/genetics ; Rats
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  • 8
    Publication Date: 1988-03-04
    Description: Abnormal functional activity induces long-lasting physiological alterations in neural pathways that may play a role in the development of epilepsy. The cellular mechanisms of these alterations are not well understood. One hypothesis is that abnormal activity causes structural reorganization of neural pathways and promotes epileptogenesis. This report provides morphological evidence that synchronous perforant path activation and kindling of limbic pathways induce axonal growth and synaptic reorganization in the hippocampus, in the absence of overt morphological damage. The results show a previously unrecognized anatomic plasticity associated with synchronous activity and development of epileptic seizures in neural pathways.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sutula, T -- He, X X -- Cavazos, J -- Scott, G -- K07-NS00808/NS/NINDS NIH HHS/ -- R29-NS25020/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1988 Mar 4;239(4844):1147-50.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, University of Wisconsin, Madison 53792.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2449733" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/ultrastructure ; Cytoplasmic Granules/ultrastructure ; Electric Stimulation ; Electrophysiology ; Hippocampus/physiopathology/*ultrastructure ; Histocytochemistry ; Kindling, Neurologic ; Microscopy, Electron ; Neural Pathways/ultrastructure ; Neurons/ultrastructure ; Rats ; Seizures/*pathology/physiopathology ; Staining and Labeling ; Synapses/*ultrastructure
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  • 9
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-11-18
    Description: A rat kidney messenger RNA that induces a slowly activating, voltage-dependent potassium current on its expression in Xenopus oocytes was identified by combining molecular cloning with an electrophysiological assay. The cloned complementary DNA encodes a novel membrane protein that consists of 130 amino acids with a single putative transmembrane domain. This protein differs from the known ion channel proteins but is involved in the induction of selective permeation of potassium ions by membrane depolarization.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Takumi, T -- Ohkubo, H -- Nakanishi, S -- New York, N.Y. -- Science. 1988 Nov 18;242(4881):1042-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Immunology, Kyoto University Faculty of Medicine, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3194754" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Blotting, Northern ; Cloning, Molecular ; DNA/genetics ; Electric Conductivity ; Membrane Potentials ; Membrane Proteins/*genetics ; Molecular Sequence Data ; Molecular Weight ; Potassium Channels/*physiology ; Rats ; Xenopus laevis
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  • 10
    Publication Date: 1988-07-15
    Description: Daily variation has been found in the length of the polyadenylate tail attached to vasopressin messenger RNA in the suprachiasmatic nuclei, which is the location of an endogenous circadian pacemaker in mammals. No such variation was found in the supraoptic or paraventricular nuclei. This variation in the length of the polyadenylate tail may underlie the circadian rhythm of vasopressin peptide levels in cerebrospinal fluid and is a unique example of a daily rhythm in messenger RNA structure.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Robinson, B G -- Frim, D M -- Schwartz, W J -- Majzoub, J A -- 1P50HL36568/HL/NHLBI NIH HHS/ -- R01NS24542/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1988 Jul 15;241(4863):342-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3388044" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arginine Vasopressin/*physiology ; Biological Clocks ; Circadian Rhythm ; Gene Expression Regulation ; Poly A/*physiology ; RNA, Messenger/*physiology ; Rats ; Suprachiasmatic Nucleus/*physiology
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  • 11
    Publication Date: 1988-06-17
    Description: A technique, in situ transcription, is described, in which reverse transcription of mRNAs is achieved within fixed tissue sections. An oligonucleotide complementary to proopiomelanocortin (POMC) mRNA was used as a primer for the specific synthesis of radiolabeled POMC cDNA in fixed sections of rat pituitary, thus permitting the rapid anatomical localization of POMC mRNA by autoradiography. Intermediate lobe signal intensities were sensitive to dopaminergic drugs, demonstrating that the method can be used for studies of mRNA regulation. The transcripts may also be eluted from tissue sections for a variety of uses, including the identification and cloning of autoradiographically localized cDNAs from small amounts of tissue.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tecott, L H -- Barchas, J D -- Eberwine, J H -- DA-05010/DA/NIDA NIH HHS/ -- MH-23861/MH/NIMH NIH HHS/ -- MH09099/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1988 Jun 17;240(4859):1661-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Nancy Pritzker Laboratory of Behavioral Neurochemistry, Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, CA 94305.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2454508" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cloning, Molecular ; DNA/*biosynthesis ; Deoxycytidine/metabolism ; Electrophoresis, Polyacrylamide Gel ; Nucleic Acid Denaturation ; Nucleic Acid Hybridization ; Oligonucleotides/genetics ; Pituitary Gland/*metabolism ; Pro-Opiomelanocortin/*genetics ; RNA, Messenger/*metabolism ; RNA-Directed DNA Polymerase/metabolism ; Rats ; *Transcription, Genetic
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  • 12
    Publication Date: 1988-09-23
    Description: The imaging of phosphorescence provides a method for monitoring oxygen distribution within the vascular system of intact tissues. Isolated rat lives were perfused through the portal vein with media containing palladium coproporphyrin, which phosphoresced and was used to image the liver at various perfusion rates. Because oxygen is a powerful quenching agent for phosphors, the transition from well-perfused liver to anoxia (no flow of oxygen) resulted in large increases of phosphorescence. During stepwise restoration of oxygen flow, the phosphorescence images showed marked heterogeneous patterns of tissue reoxygenation, which indicated that there were regional inequalities in oxygen delivery.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rumsey, W L -- Vanderkooi, J M -- Wilson, D F -- GM 21524/GM/NIGMS NIH HHS/ -- GM 36393/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1988 Sep 23;241(4873):1649-51.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Biophysics, University of Pennsylvania School of Medicine, Philadelphia 19104.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3420417" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Coproporphyrins ; Liver Circulation ; *Luminescence ; Male ; Oxygen/*analysis ; Palladium ; Perfusion ; Rats ; Rats, Inbred Strains
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  • 13
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-09-02
    Description: When two different mammalian cell types are fused to generate a stable hybrid cell line, genes that are active in only one of the parents are frequently shut off, a phenomenon called extinction. In this study two distinct, complementary mechanisms for such extinction of growth hormone gene expression were identified. In hybrids formed by fusing fibroblasts to pituitary cells, pituitary-specific proteins that bind to the growth hormone promoter were absent. In addition, a negative regulatory element located near the rat growth hormone promoter was specifically activated.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tripputi, P -- Guerin, S L -- Moore, D D -- New York, N.Y. -- Science. 1988 Sep 2;241(4870):1205-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Massachusetts General Hospital, Boston.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2842865" target="_blank"〉PubMed〈/a〉
    Keywords: Acetyltransferases/genetics ; Animals ; Avian Sarcoma Viruses/genetics ; Chloramphenicol O-Acetyltransferase ; Enhancer Elements, Genetic ; Fibroblasts/metabolism ; *Gene Expression Regulation ; Growth Hormone/*genetics ; Herpesviridae/genetics ; Hybrid Cells/*metabolism ; Hypoxanthine Phosphoribosyltransferase/genetics ; L Cells (Cell Line) ; Mice ; Pituitary Gland/metabolism ; Plasmids ; Promoter Regions, Genetic ; Rats ; Thymidine Kinase/genetics ; Transfection
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  • 14
    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
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  • 15
    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
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  • 16
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-06-17
    Description: Biochemical and electrophysiological studies suggest that adenosine 3',5'-monophosphate (cAMP)-dependent phosphorylation of the nicotinic acetylcholine receptor channel is functionally significant because it modifies the receptor's rate of desensitization to acetylcholine. In studies that support this conclusion researchers have used forskolin to stimulate cAMP-dependent phosphorylation in intact muscle. It is now shown that although forskolin facilitated desensitization in voltage-clamped rat muscle, this effect was not correlated with the abilities of forskolin and forskolin analogs to activate adenylate cyclase or phosphorylate the receptor. Furthermore, elevation of intracellular cAMP or addition of the catalytic subunit of A-kinase failed to alter desensitization. Therefore, in intact skeletal muscle, cAMP-dependent phosphorylation does not modulate desensitization.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wagoner, P K -- Pallotta, B S -- GM32211/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1988 Jun 17;240(4859):1655-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Pharmacology, Glaxo Research Laboratories, Chapel Hill, NC 27599.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2454507" target="_blank"〉PubMed〈/a〉
    Keywords: 1-Methyl-3-isobutylxanthine/pharmacology ; Acetylcholine/pharmacology ; Adenylyl Cyclases/metabolism ; Animals ; Bucladesine/pharmacology ; Colforsin/*pharmacology ; Cyclic AMP/analogs & derivatives/*pharmacology ; Electric Conductivity ; Enzyme Activation/drug effects ; Kinetics ; Muscles/*metabolism ; Phosphorylation ; Rats ; Receptors, Cholinergic/drug effects/*physiology ; Torpedo/metabolism
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  • 17
    Publication Date: 1988-04-15
    Description: A new type of agonist-binding subunit of rat neuronal nicotinic acetylcholine receptors (nAChRs) was identified. Rat genomic DNA and complementary DNA encoding this subunit (alpha 2) were cloned and analyzed. Complementary DNA expression studies in Xenopus oocytes revealed that the injection of messenger RNAs (mRNAs) for alpha 2 and beta 2 (a neuronal nAChR subunit) led to the generation of a functional nAChR. In contrast to the other known neuronal nAChRs, the receptor produced by the injection of alpha 2 and beta 2 mRNAs was resistant to the alpha-neurotoxin Bgt3.1. In situ hybridization histochemistry showed that alpha 2 mRNA was expressed in a small number of regions, in contrast to the wide distribution of the other known agonist-binding subunits (alpha 3 and alpha 4) mRNAs. These results demonstrate that the alpha 2 subunit differs from other known agonist-binding alpha-subunits of nAChRs in its distribution in the brain and in its pharmacology.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wada, K -- Ballivet, M -- Boulter, J -- Connolly, J -- Wada, E -- Deneris, E S -- Swanson, L W -- Heinemann, S -- Patrick, J -- New York, N.Y. -- Science. 1988 Apr 15;240(4850):330-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Salk Institute for Biological Studies, San Diego, CA 92138.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2832952" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Brain/*metabolism ; DNA Restriction Enzymes ; Female ; *Genes ; Molecular Sequence Data ; Neurons/metabolism ; Nucleotide Mapping ; Oocytes/metabolism ; Rats ; Receptors, Nicotinic/*genetics/metabolism ; Transcription, Genetic ; Xenopus laevis
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  • 18
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-09-09
    Description: The mammalian cerebral cortex is organized into columns of cells with common functional properties. During embryogenesis, cortical neurons are formed deep, near the lateral ventricles, and migrate radially to their final position. This observation led to the suggestion that the cortex consists of radial, ontogenetic units of clonally related neurons. In the experiments reported here, this hypothesis was tested by studying cell lineage in the rat cortex with a retroviral vector carrying the Escherichia coli beta-galactosidase gene, which can be easily visualized. Labeled, clonally related cortical neurons did not occur in simple columnar arrays. Instead, clonally related neurons entered several different radial columns, apparently by migrating along different radial glial fibers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Walsh, C -- Cepko, C L -- EY07331-01/EY/NEI NIH HHS/ -- R01 NS 23021-01/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1988 Sep 9;241(4871):1342-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Harvard Medical School, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3137660" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Movement ; Cerebral Cortex/cytology/*embryology ; Clone Cells ; Neuroglia/physiology ; Rats ; Transfection ; beta-Galactosidase/metabolism
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  • 19
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    American Association for the Advancement of Science (AAAS)
    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
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  • 20
    Publication Date: 1988-05-20
    Description: A central hypothesis in transplantation biology is that resident leukocytes expressing class II histocompatibility antigens may determine the immunogenicity of an organ. By means of a novel method to deplete the kidney of resident leukocytes, essential fatty acid deficiency (EFAD), this hypothesis was tested in an intact, vascular organ. Kidneys subjected to EFAD and thus depleted of resident Ia-positive macrophages survived and functioned when transplanted across a major histocompatibility antigen barrier in the absence of immunosuppression of the recipient. Control allografts were rejected promptly. Allografts from donors subjected to EFAD normalized their lipid composition and were repopulated with host macrophages by 5 days. Administration of Ia-positive cells at the time of transplantation established that the resident leukocyte depletion induced by EFAD was responsible for the protective effect. These observations may provide insights into the mechanisms underlying tissue immunogenicity and the population of normal tissues with resident leukocytes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schreiner, G F -- Flye, W -- Brunt, E -- Korber, K -- Lefkowith, J B -- New York, N.Y. -- Science. 1988 May 20;240(4855):1032-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3285468" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Fatty Acids, Essential/*physiology ; *Graft Rejection ; Kidney/physiology ; *Kidney Transplantation ; Liver/analysis ; Macrophages/physiology ; Phospholipids/analysis ; Rats ; Rats, Inbred BUF ; Rats, Inbred Lew ; Transplantation, Homologous
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  • 21
    Publication Date: 1988-07-08
    Description: The amyloid beta protein peptide is a major constituent of amyloid plaque cores in Alzheimer's disease and is apparently derived from a higher molecular weight precursor. It is now shown that the core protein of a heparan sulfate proteoglycan secreted from a nerve cell line (PC12) has an amino acid sequence and a size very similar to those of the amyloid beta protein precursor and that these molecules are antigenically related. This amyloid beta protein precursor-related protein is not found in the conditioned medium of a variant cell line (F3 PC12) that does not secrete heparan sulfate proteoglycan. The synaptic localization and metabolism of this class of proteoglycans are consistent with its potential involvement in central nervous system dysfunction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schubert, D -- Schroeder, R -- LaCorbiere, M -- Saitoh, T -- Cole, G -- AG 05131/AG/NIA NIH HHS/ -- F2 AG 05424A/AG/NIA NIH HHS/ -- NS 09658/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1988 Jul 8;241(4862):223-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Salk Institute for Biological Studies, San Diego, CA 92138.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2968652" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/*metabolism ; Amino Acid Sequence ; Amyloid/*metabolism ; Amyloid beta-Peptides ; Animals ; Cell Line ; Chondroitin Sulfate Proteoglycans/*metabolism ; Chromatography, High Pressure Liquid ; Glycosaminoglycans/*metabolism ; Heparan Sulfate Proteoglycans ; Heparitin Sulfate/*metabolism ; Immunologic Techniques ; Peptide Fragments ; Proteoglycans/*metabolism ; Rats ; Viral Core Proteins/*metabolism
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  • 22
    Publication Date: 1988-10-14
    Description: The signal sequence of simian virus 40 (SV40) large T-antigen for translocation into the nucleus is composed of positively charged amino acids Lys-Lys-Lys-Arg-Lys. Rabbit antibodies to a synthetic peptide containing the negatively charged amino acid sequence Asp-Asp-Asp-Glu-Asp were obtained. Indirect immunofluorescence of the antigens recognized by the antibody was punctate at the nuclear rim or the nuclear surface, depending on the plane of focus. The antibody blocked transport of nuclear proteins into the nucleus. The antigens recognized by the antibody were predominantly localized to the nuclear pores.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yoneda, Y -- Imamoto-Sonobe, N -- Matsuoka, Y -- Iwamoto, R -- Kiho, Y -- Uchida, T -- New York, N.Y. -- Science. 1988 Oct 14;242(4876):275-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Molecular and Cellular Biology, Osaka University, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3051382" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antigens/immunology ; Antigens, Polyomavirus Transforming ; Biological Transport ; Cell Line ; Cell Nucleus/*metabolism ; Fluorescent Antibody Technique ; Humans ; Molecular Sequence Data ; Nuclear Proteins/*metabolism ; Nucleoplasmins ; Oligopeptides/immunology/*physiology ; *Phosphoproteins ; Protein Sorting Signals/*physiology ; Rats
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  • 23
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-08-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roof, D J -- Heth, C A -- EY05790/EY/NEI NIH HHS/ -- EY06514/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 1988 Aug 12;241(4867):845-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Berman-Gund Laboratory, Harvard Medical School, Massachusetts Eye and Ear Infirmary, Boston 02114.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3136548" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Darkness ; GTP-Binding Proteins/*biosynthesis ; Light ; Membrane Proteins/*biosynthesis/isolation & purification ; Photoreceptor Cells/*metabolism ; Rats ; Rats, Inbred Strains ; Rod Cell Outer Segment/*metabolism/radiation effects ; Species Specificity ; Transducin
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  • 24
    Publication Date: 1988-04-22
    Description: These studies were set up to determine whether those oncogenes participating in the initiation of mammary carcinogenesis (for example, ras oncogenes) play a direct role in the outcome of events associated with the late stages of tumor development such as loss of hormone dependency. Mammary carcinomas induced by a single carcinogenic insult in pubescent rats was selected as an in vivo model system with direct relevance to human breast cancer. Acquisition of hormone-independent growth in these carcinogen-induced tumors was found to be independent of the activation of ras oncogenes during the early stages of carcinogenesis. In agreement with these observations, introduction of a human ras oncogene into human MCF-7 breast carcinoma cells did not abrogate their hormonal dependency for growth in vivo. These findings suggest that those events responsible for the critical stages of breast cancer development occur independently and in an uncoordinated manner.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sukumar, S -- Carney, W P -- Barbacid, M -- N01-CO-74101/CO/NCI NIH HHS/ -- New York, N.Y. -- Science. 1988 Apr 22;240(4851):524-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Developmental Oncology Section, Basic Research Program, Frederick Cancer Research Facility, MD 21701.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3282307" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Breast Neoplasms/*physiopathology ; Cell Line ; Estrogens/*physiology ; Gene Expression Regulation ; *Genes, ras ; Humans ; Mammary Neoplasms, Experimental/*physiopathology ; Methylnitrosourea ; Mice ; Mice, Nude ; Neoplasm Transplantation ; Rats ; Receptors, Estrogen/*physiology
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  • 25
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-08-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J L -- New York, N.Y. -- Science. 1988 Aug 19;241(4868):903-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3043664" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*metabolism ; Female ; Humans ; Male ; Menopause/*physiology ; Mice ; Pituitary Hormone-Releasing Hormones/*biosynthesis ; Puberty/*physiology ; Rats ; Sexual Maturation
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  • 26
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-09-09
    Description: A karyotypic analysis was performed on seven independently derived clones of primary rat embryo cells transformed by the ras oncogene plus the cooperating oncogene myc. The transfected oncogenes were sometimes present in amplified copy number, with heterogeneity in the levels of amplification. Some chromosomal features, such as aberrantly banding regions and double-minute chromosomes, typical of cells carrying amplified genes, were also seen in three of the seven cell lines. Underlying this heterogeneity there was an unexpected finding. All seven lines showed a common integration site for ras on the q arm of rat chromosome 3 (3q12), though some lines also had other sites of integration. In four of the lines integration of ras was accompanied by deletion of the p arm of chromosome 3 or its possible translocation to chromosome 12.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McKenna, W G -- Nakahara, K -- Muschel, R J -- New York, N.Y. -- Science. 1988 Sep 9;241(4871):1325-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Radiation Oncology, University of Pennsylvania School of Medicine, Philadelphia 19104.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3045971" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromosome Mapping ; Gene Amplification ; *Genes, ras ; Oncogenes ; Rats ; Recombination, Genetic ; Transformation, Genetic ; Translocation, Genetic
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  • 27
    Publication Date: 1988-10-14
    Description: Suspensions of thymocytes from young rats were incubated with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), which resulted in a sustained increase in cytosolic free Ca2+ concentration followed by DNA fragmentation and loss of cell viability. Both the Ca2+ increase and DNA fragmentation were prevented in cells treated with the inhibitor of protein synthesis, cycloheximide, and DNA fragmentation and cell killing were not detected when cells were incubated in a "Ca2+-free" medium or pretreated with high concentrations of the calcium probe, quin-2 tetraacetoxymethyl ester. These results indicate that TCDD can kill immature thymocytes by initiating a suicide process similar to that previously described for glucocorticoid hormones.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McConkey, D J -- Hartzell, P -- Duddy, S K -- Hakansson, H -- Orrenius, S -- New York, N.Y. -- Science. 1988 Oct 14;242(4876):256-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Toxicology, Karolinska Institutet, Stockholm, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3262923" target="_blank"〉PubMed〈/a〉
    Keywords: Aminoquinolines ; Animals ; Calcium/metabolism/*pharmacology ; Cell Survival/drug effects ; Cycloheximide/pharmacology ; Cytosol/metabolism ; DNA/metabolism ; Deoxyribonuclease I/*metabolism ; Dioxins/*pharmacology ; Enzyme Activation/drug effects ; Fluorescent Dyes ; Glucocorticoids/pharmacology ; Kinetics ; Rats ; T-Lymphocytes/drug effects ; Tetrachlorodibenzodioxin/*pharmacology ; Thymus Gland/*drug effects/metabolism
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  • 28
    Publication Date: 1988-02-12
    Description: In rats, an environmental manipulation occurring early in life resulted in changes in the adrenocortical axis that persisted throughout the entire life of the animals and attenuated certain deficits associated with aging. Rats handled during infancy had a permanent increase in concentrations of receptors for glucocorticoids in the hippocampus, a critical region in the negative-feedback inhibition of adrenocortical activity. Increased receptor concentrations led to greater hippocampal sensitivity to glucocorticoids and enhanced negative-feedback efficacy in the handled rats. Thus, at all ages tested, rats that were not handled secreted more glucocorticoids in response to stress than did handled rats. At later ages, nonhandled rats also showed elevated basal glucocorticoid levels, with the result that there was a greater cumulative exposure to glucocorticoids in nonhandled rats. Increased exposure to adrenal glucocorticoids can accelerate hippocampal neuron loss and cognitive impairments in aging. Hippocampal cell loss and pronounced spatial memory deficits emerged with age in the nonhandled rats, but were almost absent in the handled rats. Previous work showed that glucocorticoid hypersecretion, hippocampal neuron death, and cognitive impairments form a complex degenerative cascade of aging in the rat. The present study shows that a subtle manipulation early in life can retard the emergence of this cascade.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Meaney, M J -- Aitken, D H -- van Berkel, C -- Bhatnagar, S -- Sapolsky, R M -- AG-06633/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 1988 Feb 12;239(4841 Pt 1):766-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychiatry, Faculty of Medicine, McGill University, Montreal, Quebec, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3340858" target="_blank"〉PubMed〈/a〉
    Keywords: Aging ; Animals ; Animals, Newborn ; Dexamethasone/metabolism ; *Handling (Psychology) ; Hippocampus/*growth & development/physiology/physiopathology ; Learning ; Memory ; Rats ; Receptors, Glucocorticoid/metabolism
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  • 29
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    American Association for the Advancement of Science (AAAS)
    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
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  • 30
    Publication Date: 1988-06-17
    Description: The specificity of complex formation between cytochrome b5 (cyt b5) and cytochrome c (cyt c) is believed to involve the formation of salt linkages between specific carboxylic acid residues of cyt b5 with lysine residues on cyt c. Site-directed mutagenesis was used to alter the specified acidic residues of cyt b5 to the corresponding amide analogues, which resulted in a lower affinity for complex formation with cyt c. The dissociation of the complex under high pressure resulted in specific volume changes, the magnitude of which reflected the degree of solvation of the acidic residues in the proposed protein-protein interface.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rodgers, K K -- Pochapsky, T C -- Sligar, S G -- GM 31756/GM/NIGMS NIH HHS/ -- GM 33775/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1988 Jun 17;240(4859):1657-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, University of Illinois, Urbana 61801.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2837825" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cytochrome b Group/genetics/*metabolism ; Cytochrome c Group/*metabolism ; Cytochromes b5 ; Hydrogen Bonding ; Hydrogen-Ion Concentration ; Hydrostatic Pressure ; Macromolecular Substances ; Mutation ; Protein Conformation ; Rats ; Solubility ; Thermodynamics
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  • 31
    Publication Date: 1988-10-14
    Description: A survey of rat tissues by RNA analysis, aimed at uncovering the physiological function of the parathyroid hormone-like peptide (PTH-LP) associated with hypercalcemia of malignancy, revealed the presence of a 1.5-kilobase messenger RNA encoding this peptide in lactating mammary glands. PTH-LP messenger RNA is expressed in mammary tissue only during lactation; it appears and disappears rapidly (2 to 4 hours) as a function of the sucking stimulus. The identity of this messenger RNA was confirmed by cloning the rat PTH-LP complementary DNA, which predicts a peptide with strong similarity to the human homolog. Moreover, extracts from lactating mammary tissue stimulated parathyroid hormone-dependent adenylate cyclase. These findings suggest that PTH-LP plays a physiological role in lactation, possibly as a hormone for the mobilization or transfer (or both) of calcium to the milk.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thiede, M A -- Rodan, G A -- New York, N.Y. -- Science. 1988 Oct 14;242(4876):278-80.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Bone Biology and Osteoporosis Research, Merck Sharp & Dohme Research Laboratories, West Point, PA 19486.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3175653" target="_blank"〉PubMed〈/a〉
    Keywords: Adenylyl Cyclases/metabolism ; Amino Acid Sequence ; Animals ; Base Sequence ; Calcium/*metabolism ; Cloning, Molecular ; DNA/genetics ; Female ; *Gene Expression Regulation ; Humans ; Lactation/*metabolism ; Mammary Glands, Animal/*metabolism ; Molecular Sequence Data ; Neoplasm Proteins/*genetics/physiology ; Parathyroid Hormone-Related Protein ; Pregnancy ; RNA, Messenger/genetics/*metabolism ; Rats ; Sequence Homology, Nucleic Acid ; Tissue Distribution
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  • 32
    Publication Date: 1988-03-18
    Description: In the anterior pituitary gland, there are five phenotypically distinct cell types, including cells that produce either prolactin (lactotrophs) or growth hormone (somatotrophs). Multiple, related cis-active elements that exhibit synergistic interactions appear to be the critical determinants of the transcriptional activation of the rat prolactin and growth hormone genes. A common positive tissue-specific transcription factor, referred to as Pit-1, appears to bind to all the cell-specific elements in each gene and to be required for the activation of both the prolactin and growth hormone genes. The data suggest that, in the course of development, a single tissue-specific factor activates sets of genes that ultimately exhibit restricted cell-specific expression and define cellular phenotype.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nelson, C -- Albert, V R -- Elsholtz, H P -- Lu, L I -- Rosenfeld, M G -- New York, N.Y. -- Science. 1988 Mar 18;239(4846):1400-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Eukaryotic Regulatory Biology Program, University of California, San Diego, School of Medicine 92093.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2831625" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Avian Sarcoma Viruses/genetics ; Binding, Competitive ; Cell Line ; DNA, Recombinant ; Enhancer Elements, Genetic ; *Gene Expression Regulation ; Growth Hormone/*genetics ; Phenotype ; Photochemistry ; Pituitary Gland, Anterior/metabolism ; Prolactin/*genetics ; Promoter Regions, Genetic ; Rats ; Regulatory Sequences, Nucleic Acid ; Transcription Factors/*physiology ; Transcription, Genetic
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  • 33
    Publication Date: 1988-09-09
    Description: Angiogenesis is an important component of organogenesis and wound repair and occurs during the pathology of oncogenesis, atherogenesis, and other disease processes. Thus, it is important to understand the physiological mechanisms that control neovascularization, especially with methods that permit the molecular dissection of the phenomenon in vivo. Heparin-binding growth factor-1 was shown to bind to collagen type I and type IV. When complexed with gelatin, heparin-binding growth factor-1 can induce neovascularization at polypeptide concentrations that are consistent with the biological activity of the mitogen in vitro. The adsorption strategy induces rapid blood vessel formation at and between organ- and tissue-specific sites and permits recovery of the site-specific implant for examination and manipulation by molecular methods.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thompson, J A -- Anderson, K D -- DiPietro, J M -- Zwiebel, J A -- Zametta, M -- Anderson, W F -- Maciag, T -- HL32348/HL/NHLBI NIH HHS/ -- HL35627/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1988 Sep 9;241(4871):1349-52.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Hematology, National Heart, Lung and Blood Institute, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2457952" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Vessels/cytology ; Collagen/metabolism ; Extracellular Matrix ; Fibroblast Growth Factor 1 ; Gelatin/metabolism ; Growth Substances/*pharmacology ; Heparin/*pharmacology ; *Neovascularization, Pathologic ; Rats ; Tampons, Surgical
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  • 34
    Publication Date: 1988-12-16
    Description: Human T cell leukemia viruses (HTLV-I and HTLV-II) can infect many cell types in vitro. HTLV-I and HTLV-II use the same cell surface receptor, as shown by interference with syncytium formation and with infection by vesicular stomatitis virus (VSV) pseudotypes bearing the HTLV envelope glycoproteins. Human-mouse somatic cell hybrids were used to determine which human chromosome was required to confer susceptibility to VSV(HTLV) infection. The only human chromosome common to all susceptible cell hybrids was chromosome 17, and the receptor gene was localized to 17cen-qter. Antibodies to surface antigens known to be determined by genes on 17q did not block the HTLV receptor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sommerfelt, M A -- Williams, B P -- Clapham, P R -- Solomon, E -- Goodfellow, P N -- Weiss, R A -- New York, N.Y. -- Science. 1988 Dec 16;242(4885):1557-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Chester Beatty Laboratories, Institute of Cancer Research, London, U.K.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3201246" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cattle ; Cell Line ; Chromosome Mapping ; *Chromosomes, Human, Pair 17 ; Cricetinae ; *Genes ; Human T-lymphotropic virus 1/*physiology ; Human T-lymphotropic virus 2/*physiology ; Humans ; Hybrid Cells/cytology/microbiology ; Mice ; Rats ; Receptors, Virus/*genetics
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  • 35
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-01-15
    Description: Immunocytochemical and electrophysiological evidence suggests that somatostatin may be a transmitter in the hippocampus. To characterize the ionic mechanisms underlying somatostatin effects, voltage-clamp and current-clamp studies on single CA1 pyramidal neurons in the hippocampal slice preparation were performed. Both somatostatin-28 and somatostatin-14 elicited a steady outward current and selectively augmented the noninactivating, voltage-dependent outward potassium current known as the M-current. Since the muscarinic cholinergic agonists carbachol and muscarine antagonized this current, these results suggest a reciprocal regulation of the M-current by somatostatin and acetylcholine.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Moore, S D -- Madamba, S G -- Joels, M -- Siggins, G R -- AA-06420/AA/NIAAA NIH HHS/ -- AA-07456/AA/NIAAA NIH HHS/ -- DK-26741/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1988 Jan 15;239(4837):278-80.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Research Institute of Scripps Clinic, La Jolla, CA 92037.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2892268" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcholine/pharmacology ; Action Potentials/drug effects ; Animals ; Carbachol/pharmacology ; Cesium/pharmacology ; Electric Conductivity ; Hippocampus/drug effects/*physiology ; Membrane Potentials ; Muscarine/pharmacology ; Neurons/drug effects/*physiology ; Potassium/*metabolism ; Rats ; Somatostatin/*pharmacology ; Somatostatin-28
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  • 36
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-12-23
    Description: The contributions of two subclasses of excitatory amino acid transmitter receptors to the induction and expression of long-term potentiation (LTP) were analyzed in hippocampal slices. The quisqualate/kainate receptor antagonist DNQX (6,7-dinitro-quinoxaline-2,3-dione) blocked 85% of the evoked field potential, leaving a small response that was sensitive to D-AP5 (D-2-amino-5-phosphonopentanoate), an N-methyl-D-aspartate (NMDA) receptor blocker. This residual D-AP5-sensitive response was of comparable size in control and previously potentiated inputs. High-frequency stimulation in the presence of DNQX did not result in the development of robust LTP. Washout of the drug, however, revealed the potentiation effect. Thus NMDA-mediated responses can induce, but are not greatly affected by, LTP; non-NMDA receptors, conversely, mediate responses that are not needed to elicit LTP but that are required for its expression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Muller, D -- Joly, M -- Lynch, G -- New York, N.Y. -- Science. 1988 Dec 23;242(4886):1694-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for the Neurobiology of Learning and Memory, University of California, Irvine 92717.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2904701" target="_blank"〉PubMed〈/a〉
    Keywords: 2-Amino-5-phosphonovalerate ; Animals ; Electric Conductivity ; Electric Stimulation ; Evoked Potentials/drug effects ; Hippocampus/*physiology ; Magnesium/pharmacology ; Male ; Membrane Potentials/drug effects ; Quinoxalines/pharmacology ; Rats ; Rats, Inbred Strains ; Receptors, AMPA ; Receptors, N-Methyl-D-Aspartate ; Receptors, Neurotransmitter/drug effects/*physiology ; Synapses/*physiology ; Valine/analogs & derivatives/pharmacology
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  • 37
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-06-03
    Description: The present study was undertaken to examine the possibility that cerebral energy metabolism can be fueled by lactate. As a sole energy substrate, lactate supported normal synaptic function in rat hippocampal slices for hours without any sign of deterioration. Slices that were synaptically silent as a result of glucose depletion could be reactivated with lactate to show normal synaptic function. When slices were exposed to the glycolytic inhibitor iodoacetic acid, lactate-supported synaptic function was unaffected, whereas that supported by glucose was completely abolished. This indicated that lactate was metabolized directly via pyruvate to enter the tricarboxylic acid cycle. Thus, under conditions that lead to lactate accumulation (cerebral ischemia) this "end product" may be a useful alternative as a substrate for energy metabolism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schurr, A -- West, C A -- Rigor, B M -- New York, N.Y. -- Science. 1988 Jun 3;240(4857):1326-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anesthesiology, University of Louisville School of Medicine, KY 40292.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3375817" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Energy Metabolism ; Evoked Potentials/drug effects ; Glucose/pharmacology ; Glycolysis/drug effects ; Hippocampus/*physiology ; Iodoacetates/pharmacology ; Iodoacetic Acid ; Lactates/metabolism/*pharmacology ; Lactic Acid ; Rats ; Synapses/*physiology
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  • 38
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-06-24
    Description: Epidermal growth factor (EGF) is a well-characterized polypeptide hormone with diverse biological activities, including stimulation of astrocyte division. A soluble astrocyte mitogen inhibitor, immunologically related to the EGF receptor, is present in rat brain. Injury to the brain causes a time-dependent reduction in the levels of this inhibitor and the concomitant appearance of EGF receptor on the astrocyte surface. Intracerebral injection of antibody capable of binding the inhibitor caused the appearance of numerous reactive astrocytes. EGF receptor-related inhibitors may play a key role in the control of glial cell division in both normal and injured brain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nieto-Sampedro, M -- AG 00538-09A/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 1988 Jun 24;240(4860):1784-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychobiology, University of California, Irvine 92717.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3289118" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Astrocytes/*physiology ; Brain Injuries/*physiopathology ; Cell Division ; Cross Reactions ; Immunologic Techniques ; Rats ; Receptor, Epidermal Growth Factor/*antagonists & inhibitors/immunology ; Receptors, Mitogen/*antagonists & inhibitors ; Structure-Activity Relationship ; Time Factors
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  • 39
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-06-17
    Description: Angiotensin II (Ang II) is present in high concentrations in preovulatory follicular fluid, and ovarian follicular cells have specific Ang II receptors. To investigate the possible direct involvement of Ang II in ovulation the specific receptor antagonist of Ang II, saralasin, was administered by intraperitoneal injection to immature rats in which follide development and ovulation had been induced with pregnant mare serum gonadotrophin (PMSG) and human chorionic gonadotrophin (hCG), respectively. Saralasin halved the number of oocytes found in the fallopian tubes 17 to 20 hours after administration of hCG. The antiovulatory effect was observed when saralasin was given 1 hour before hCG or 1 or 3 hours after hCG but not when given 5 hours after hCG. Simultaneous administration of Ang II reversed the saralasin blockage of ovulation. These results indicate a direct, obligate role for Ang II in ovulation and raise the possibility of contraceptive and profertility applications for agonists or antagonists of the renin-angiotensin system that are aimed at the ovulatory process.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pellicer, A -- Palumbo, A -- DeCherney, A H -- Naftolin, F -- HD22970/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1988 Jun 17;240(4859):1660-1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Obstetrics and Gynecology, Yale University School of Medicine, New Haven, CT 06510.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3381087" target="_blank"〉PubMed〈/a〉
    Keywords: Angiotensin II/antagonists & inhibitors/*physiology ; Animals ; Cell Count ; Chorionic Gonadotropin/pharmacology ; Fallopian Tubes/cytology ; Female ; Gonadotropins, Equine/pharmacology ; Oocytes/cytology ; Ovulation/*drug effects ; Rats ; Rats, Inbred Strains ; Saralasin/*pharmacology
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  • 40
    Publication Date: 1988-08-26
    Description: Several complementary DNAs (cDNAs) coding for sphingolipid activator protein-2 (SAP-2) were isolated from a lambda gt-11 human hepatoma library by means of polyclonal antibodies. The nucleotide sequence of the largest cDNA was colinear with the derived amino acid sequence of SAP-2 and with the nucleotide sequence of the cDNA coding for the 70-kilodalton precursor of SAP-1 (SAP precursor cDNA). The coding sequence for mature SAP-2 was located 3' to that coding for SAP-1 in the SAP precursor cDNA. Both SAP-1 and SAP-2 appeared to be derived by proteolytic processing from a common precursor that is coded by a genetic locus on human chromosome 10. Two other domains similar to SAP-1 and SAP-2 were also identified in SAP precursor protein. Each of the four domains was approximately 80 amino acid residues long, had nearly identical placement of cysteine residues, potential glycosylation sites, and proline residues. Each domain also contained internal amino acid sequences capable of forming amphipathic helices separated by helix breakers to give a cylindrical hydrophobic domain that is probably stabilized by disulfide bridges. Protein immunoblotting experiments indicated that SAP precursor protein (70 kilodaltons) as well as immunoreactive SAP-like proteins of intermediate sizes (65, 50, and 31 kilodaltons) are present in most human tissues.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉O'Brien, J S -- Kretz, K A -- Dewji, N -- Wenger, D A -- Esch, F -- Fluharty, A L -- DK 38795/DK/NIDDK NIH HHS/ -- HD 18983/HD/NICHD NIH HHS/ -- NS 08682/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1988 Aug 26;241(4869):1098-101.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurosciences, University of California, San Diego, La Jolla 92093.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2842863" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Carcinoma, Hepatocellular/analysis ; Chromosome Mapping ; Chromosomes, Human, Pair 10 ; DNA/genetics/isolation & purification ; Glycoproteins/analysis/*genetics ; Humans ; Liver Neoplasms/analysis ; Male ; Mice ; Mice, Nude ; Molecular Sequence Data ; Nucleic Acid Hybridization ; Protein Conformation ; Protein Precursors/analysis/genetics ; Protein Processing, Post-Translational ; Rats ; Saposins ; Sphingolipid Activator Proteins ; Tissue Distribution
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  • 41
    Publication Date: 1988-11-11
    Description: Manganous superoxide dismutase (MnSOD) scavenges potentially toxic superoxide radicals produced in the mitochondria. Tumor necrosis factor-alpha (TNF-alpha) was found to induce the messenger RNA for MnSOD, but not the mRNAs for other antioxidant or mitochondrial enzymes tested. The increase in MnSOD mRNA occurred rapidly and was blocked by actinomycin D, but not by cycloheximide. Induction of MnSOD mRNA was also observed with TNF-beta, interleukin-1 alpha (IL-1 alpha), and IL-1 beta but not with other cytokines or agents tested. TNF-alpha induced MnSOD mRNA in all cell lines and normal cells examined in vitro and in various organs of mice in vivo. These effects of TNF-alpha and IL-1 on target cells may contribute to their reported protective activity against radiation as well as their ability to induce resistance to cell killing induced by the combination of TNF-alpha and cycloheximide.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wong, G H -- Goeddel, D V -- New York, N.Y. -- Science. 1988 Nov 11;242(4880):941-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Genentech, San Francisco, CA 94080.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3263703" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Catalase/metabolism ; Cell Line ; Cycloheximide/pharmacology ; Dactinomycin/pharmacology ; Enzyme Induction/drug effects ; Humans ; Interleukin-1/pharmacology ; Kinetics ; Mice ; Mitochondria/enzymology ; RNA, Messenger/biosynthesis ; Rats ; Superoxide Dismutase/*biosynthesis/genetics/metabolism ; Tissue Distribution ; Tumor Necrosis Factor-alpha/*pharmacology
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  • 42
    Publication Date: 1988-03-11
    Description: The alterations in morphology and function of the ovarian follicle as it matures, ovulates, and becomes a corpus luteum are dramatic. A variety of steroid and polypeptide hormones influence these processes, and the ovary in turn produces specific hormonal signals for endocrine regulation. One such signal is inhibin, a heterodimeric protein that suppresses the secretion of follicle-stimulating hormone from pituitary gonadotrophs. Rat inhibin complementary DNA probes have been used to examine the levels and distribution of inhibin alpha-and beta A-subunit messenger RNAs in the ovaries of cycling animals. Striking, dynamic changes have been found in inhibin messenger RNA accumulation during the developmental maturation of the ovarian follicle.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Woodruff, T K -- D'Agostino, J -- Schwartz, N B -- Mayo, K E -- HD07504/HD/NICHD NIH HHS/ -- HD21921/HD/NICHD NIH HHS/ -- P01 HD021921/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1988 Mar 11;239(4845):1296-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, Molecular Biology and Cell Biology, Northwestern University, Evanston, IL 60208.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3125611" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Estrus ; Female ; Follicle Stimulating Hormone/blood ; Inhibins/*genetics ; Luteinizing Hormone/blood ; Macromolecular Substances ; Nucleic Acid Hybridization ; Ovarian Follicle/*physiology ; Ovary/physiology ; RNA, Messenger/*genetics/metabolism ; Rats
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  • 43
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-10-14
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barnes, D M -- New York, N.Y. -- Science. 1988 Oct 14;242(4876):193-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3175650" target="_blank"〉PubMed〈/a〉
    Keywords: Aging ; Amphibians ; Animals ; Cell Division ; DNA/biosynthesis ; Heart/*growth & development ; Heart Atria/cytology ; Humans ; Myocardium/*cytology ; Rats ; Ussr ; United States
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  • 44
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-04-15
    Description: Complementary DNAs (cDNAs) encoding androgen receptors were obtained from human testis and rat ventral prostate cDNA libraries. The amino acid sequence deduced from the nucleotide sequences of the cDNAs indicated the presence of a cysteine-rich DNA-binding domain that is highly conserved in all steroid receptors. The human cDNA was transcribed and the RNA product was translated in cell-free systems to yield a 76-kilodalton protein. The protein was immunoprecipitable by human autoimmune antibodies to the androgen receptor. The protein bound androgens specifically and with high affinity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chang, C S -- Kokontis, J -- Liao, S T -- DK-09461/DK/NIDDK NIH HHS/ -- DK-37694/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1988 Apr 15;240(4850):324-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Ben May Institute, University of Chicago, IL 60637.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3353726" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Binding, Competitive ; *Cloning, Molecular ; DNA/genetics ; *Genes ; Humans ; Male ; Molecular Sequence Data ; Molecular Weight ; Rats ; Receptors, Androgen/*genetics/metabolism ; Sequence Homology, Nucleic Acid ; Species Specificity ; Testis/metabolism
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  • 45
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-01-15
    Description: A crucial question in the study of immunological reactions in the central nervous system (CNS) concerns the identity of the parenchymal cells that function as the antigen-presenting cells in that organ. Rat bone marrow chimeras and encephalitogenic, major histocompatability--restricted T-helper lymphocytes were used to show that a subset of endogenous CNS cells, commonly termed "perivascular microglial cells," is bone marrow-derived. In addition, these perivascular cells are fully competent to present antigen to lymphocytes in an appropriately restricted manner. These findings are important for bone marrow transplantation and for neuroimmunological diseases such as multiple sclerosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hickey, W F -- Kimura, H -- KO7-NS0087/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1988 Jan 15;239(4837):290-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia, PA 19104-6079.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3276004" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen-Presenting Cells/*immunology ; Astrocytes/immunology ; Bone Marrow/*immunology ; Bone Marrow Transplantation ; Central Nervous System/blood supply/*immunology/pathology ; Chimera ; Encephalomyelitis, Autoimmune, Experimental/immunology/pathology ; Endothelium/immunology ; Graft vs Host Disease/immunology ; Histocompatibility Antigens/analysis/immunology ; Immunohistochemistry ; Multiple Sclerosis/immunology/pathology ; Neuroglia/*immunology ; Rats ; Rats, Inbred Lew ; T-Lymphocytes/immunology
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  • 46
    Publication Date: 1988-09-16
    Description: Hormone-sensitive lipase, a key enzyme in fatty acid mobilization, overall energy homeostasis, and possibly steroidogenesis, is acutely controlled through reversible phosphorylation by catecholamines and insulin. The 757-amino acid sequence predicted from a cloned rat adipocyte complementary DNA showed no homology with any other known lipase or protein. The activity-controlling phosphorylation site was localized to Ser563 in a markedly hydrophilic domain, and a lipid-binding consensus site was tentatively identified. One or several messenger RNA species (3.3, 3.5, or 3.9 kilobases) were expressed in adipose and steroidogenic tissues and heart and skeletal muscle. The human hormone-sensitive lipase gene mapped to chromosome 19 cent-q13.3.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Holm, C -- Kirchgessner, T G -- Svenson, K L -- Fredrikson, G -- Nilsson, S -- Miller, C G -- Shively, J E -- Heinzmann, C -- Sparkes, R S -- Mohandas, T -- New York, N.Y. -- Science. 1988 Sep 16;241(4872):1503-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical and Physiological Chemistry, University of Lund, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3420405" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Chromosome Mapping ; *Chromosomes, Human, Pair 19 ; Cloning, Molecular ; DNA/genetics ; Gene Expression Regulation ; Humans ; Molecular Sequence Data ; Rats ; Sterol Esterase/*genetics
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  • 47
    Publication Date: 1988-08-05
    Description: The N-methyl-D-aspartate (NMDA)-subtype of glutamate receptors has been well described as a result of the early appearance of NMDA antagonists, but no potent antagonist for the "non-NMDA" glutamate receptors has been available. Quinoxalinediones have now been found to be potent and competitive antagonists at non-NMDA glutamate receptors. These compounds will be useful in the determination of the structure-activity relations of quisqualate and kainate receptors and the role of such receptors in synaptic transmission in the mammalian brain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Honore, T -- Davies, S N -- Drejer, J -- Fletcher, E J -- Jacobsen, P -- Lodge, D -- Nielsen, F E -- New York, N.Y. -- Science. 1988 Aug 5;241(4866):701-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Ferroson Research Division, Soeborg, Denmark.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2899909" target="_blank"〉PubMed〈/a〉
    Keywords: 6-Cyano-7-nitroquinoxaline-2,3-dione ; Action Potentials/drug effects ; Animals ; Aspartic Acid/analogs & derivatives/pharmacology ; Binding, Competitive ; Cell Membrane/metabolism ; Cerebral Cortex/metabolism ; Ibotenic Acid/analogs & derivatives/metabolism ; Kainic Acid/metabolism ; Ketamine/pharmacology ; N-Methylaspartate ; Neurons/physiology ; Piperazines/metabolism ; Quinoxalines/*pharmacology ; Rats ; Receptors, AMPA ; Receptors, Drug/drug effects/metabolism ; Receptors, Glutamate ; Receptors, Kainic Acid ; Receptors, N-Methyl-D-Aspartate ; Receptors, Neurotransmitter/*drug effects/metabolism ; Spinal Cord/physiology ; alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid
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  • 48
    Publication Date: 1988-07-29
    Description: Neurons that release serotonin as a neurotransmitter project to most regions of the central and peripheral nervous system and mediate diverse neural functions. The physiological effects of serotonin are initiated by the activation of multiple, distinct receptor subtypes. Cloning in RNA expression vectors was combined with a sensitive electrophysiological assay in Xenopus oocytes in order to isolate a functional cDNA clone encoding the 5HTlc serotonin receptor. Injection of RNA transcribed in vitro from this clone into Xenopus oocytes elicits serotonin sensitivity. Mouse fibroblasts transformed with this clone bind serotonin agonists and antagonists and exhibit an increase in intracellular Ca2+ concentrations in response to serotonin. The sequence of the 5HTlc receptor reveals that it belongs to the family of G protein-coupled receptors, which are thought to traverse the cytoplasmic membrane seven times. Moreover, in situ hybridization and RNA blot analysis indicate that the 5HTlc receptor is expressed in neurons in many regions of the central nervous system and suggest that this subclass of receptor may mediate many of the central actions of serotonin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Julius, D -- MacDermott, A B -- Axel, R -- Jessell, T M -- New York, N.Y. -- Science. 1988 Jul 29;241(4865):558-64.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Biophysics, 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/3399891" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cloning, Molecular ; DNA/genetics ; Fibroblasts/physiology ; Gene Expression Regulation ; Membrane Glycoproteins/genetics ; Molecular Sequence Data ; Oocytes/physiology ; Phosphoproteins/physiology ; Rats ; Receptors, Serotonin/*genetics ; Serotonin/*physiology ; Xenopus laevis
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  • 49
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-08-12
    Description: Receptors for N-methyl-D-aspartate (NMDA) are involved in many plastic and pathological processes in the brain. Glycine has been reported to potentiate NMDA responses in neurons and in Xenopus oocytes injected with rat brain messenger RNA. Glycine is now shown to be absolutely required for activation of NMDA receptors in oocytes. In voltage-clamped oocytes, neither perfusion nor rapid pressure application of NMDA onto messenger RNA-injected oocytes caused a distinct ionic current without added glycine. When glycine was added, however, NMDA evoked large inward currents. The concentration of glycine required to produce a half-maximal response was 670 nanomolar, and the glycine dose-response curve extrapolated to zero in the absence of glycine. Several analogs of glycine could substitute for glycine, among which D-serine and D-alanine were the most effective. The observation that D-amino acids are effective will be important in developing drugs targeted at the glycine site.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kleckner, N W -- Dingledine, R -- NS17771/NS/NINDS NIH HHS/ -- NS22249/NS/NINDS NIH HHS/ -- NS23804/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1988 Aug 12;241(4867):835-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of North Carolina, Chapel Hill 27599-7365.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2841759" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acids/pharmacology ; Animals ; Brain/metabolism ; Female ; Glycine/*analogs & derivatives/*pharmacology ; Kinetics ; Oocytes/drug effects/*metabolism ; RNA, Messenger/genetics ; Rats ; Receptors, N-Methyl-D-Aspartate ; Receptors, Neurotransmitter/drug effects/genetics/*metabolism ; Xenopus
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  • 50
    Publication Date: 1988-10-14
    Description: Sarafotoxins, a group of 21-residue cardiotoxic peptides from snake venom that induce coronary vasoconstriction, show high-affinity binding to rat atrial and brain membranes and activate the hydrolysis of phosphoinositides. Neither their binding nor their activity is affected by blockers or activators of known receptors and ion channels, suggesting that sarafotoxins act either directly on the phosphoinositide phosphodiesterase system or on a novel receptor. Their amino acid sequence shows a high degree of homology with that of endothelin, a recently described 21-residue vasoconstrictor peptide found in porcine aortic endothelium. This is remarkable, since endothelin is a natural compound of the mammalian vascular system while sarafotoxins are highly toxic components of snake venom.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kloog, Y -- Ambar, I -- Sokolovsky, M -- Kochva, E -- Wollberg, Z -- Bdolah, A -- New York, N.Y. -- Science. 1988 Oct 14;242(4876):268-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, George S. Wise Faculty of Life Sciences, Tel Aviv University, Israel.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2845579" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Brain/*metabolism ; Calcium/metabolism ; Cell Membrane/metabolism ; Endothelins ; Enzyme Activation ; Heart Atria/metabolism ; Hydrolysis ; Inositol/metabolism ; Molecular Sequence Data ; Myocardium/*metabolism ; Peptides ; Phosphatidylinositol Diacylglycerol-Lyase ; Phosphatidylinositols/*metabolism ; Phosphoric Diester Hydrolases/metabolism ; Rats ; Sequence Homology, Nucleic Acid ; Vasoconstriction ; Viper Venoms/*metabolism
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  • 51
    Publication Date: 1988-01-08
    Description: In a study of the mechanism of resistance to autoimmune disease induced by T cell vaccination, rats were vaccinated against experimental autoimmune encephalomyelitis (EAE) by injecting them once in the hind footpads with a subencephalitogenic dose (10(4)) of a clone of T lymphocytes specific for myelin basic protein (BP). The response to vaccination was assayed by challenging the rats with an encephalitogenic dose (3 X 10(6)) of T lymphocytes of this BP-specific clone. Five to six days after vaccination, the cells responsible for mediating resistance to adoptively transferred EAE were concentrated in the popliteal lymph nodes draining the vaccination site. Transfer of the draining lymph node cells to unvaccinated rats led to loss of resistance in the donor rats and acquisition of resistance by the recipient rats. Limiting-dilution cultures of the draining lymph node cells were established with irradiated cells of the BP-specific clone as stimulators. Two sets of T lymphocytes specifically responsive to the BP-specific T cells from the clone were isolated: CD4+CD8- helper and CD4-CD8+ suppressor cells. The helper T cells, like the BP antigen, specifically stimulated the BP-specific vaccinating clone. In contrast, the suppressor T cells specifically suppressed the response of the BP-specific vaccinating clone to its BP antigen. These results suggest that T cell vaccination induces resistance to autoimmune disease by activating an antiidiotypic network.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lider, O -- Reshef, T -- Beraud, E -- Ben-Nun, A -- Cohen, I R -- AM32192/AM/NIADDK NIH HHS/ -- NS23372/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1988 Jan 8;239(4836):181-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Weizmann Institute of Science, Rehovot, Israel.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2447648" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Differentiation, T-Lymphocyte/analysis ; Dose-Response Relationship, Immunologic ; Encephalomyelitis, Autoimmune, Experimental/*immunology ; Immunization, Passive ; Immunoglobulin Idiotypes/*immunology ; Immunosuppression ; Lymph Nodes/cytology ; Lymphocyte Activation ; Myelin Basic Protein/*immunology ; Rats ; Rats, Inbred Lew ; T-Lymphocytes/classification/*immunology ; Vaccination
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  • 52
    Publication Date: 1988-03-11
    Description: Functional nicotinic cholinergic receptors are found on mammalian retinal ganglion cell neurons in culture. The neurotransmitter acetylcholine (ACh) can be detected in the medium of many of these retinal cultures, after release presumably from the choline acetyltransferase-positive amacrine cells. The postsynaptic effect of endogenous or applied ACh on the ganglion cells can be blocked with specific nicotinic antagonists. Here it is shown that within 24 hours of producing such a pharmacologic blockade, the retinal ganglion cells begin to sprout or regenerate neuronal processes. Thus, the growth-enhancing effect of nicotinic antagonists may be due to the removal of inhibition to growth by tonic levels of ACh present in the culture medium. Since there is a spontaneous leak of ACh in the intact retina, the effects of nicotinic cholinergic drugs on process outgrowth in culture may reflect a normal control mechanism for growth or regeneration of retinal ganglion cell processes that is exerted by ACh in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lipton, S A -- Frosch, M P -- Phillips, M D -- Tauck, D L -- Aizenman, E -- EY05477/EY/NEI NIH HHS/ -- EY06087/EY/NEI NIH HHS/ -- NS00879/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1988 Mar 11;239(4845):1293-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Neuroscience, Children's Hospital, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3344435" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Atropine/*pharmacology ; Cells, Cultured ; Mecamylamine/*pharmacology ; Picrotoxin/pharmacology ; Rats ; Receptors, Nicotinic/drug effects/*physiology ; Retina/*cytology ; Retinal Ganglion Cells/*cytology/drug effects ; Tubocurarine/*pharmacology
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  • 53
    Publication Date: 1988-03-04
    Description: Amino acid sequences deduced from rat complementary DNA clones encoding the insulin-like growth factor II (IGF-II) receptor closely resemble those of the bovine cation-independent mannose-6-phosphate receptor (Man-6-P receptorCI), suggesting they are identical structures. It is also shown that IGF-II receptors are adsorbed by immobilized pentamannosyl-6-phosphate and are specifically eluted with Man-6-P. Furthermore, Man-6-P specifically increases by about two times the apparent affinity of the purified rat placental receptor for 125I-labeled IGF-II. These results indicate that the type II IGF receptor contains cooperative, high-affinity binding sites for both IGF-II and Man-6-P-containing proteins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉MacDonald, R G -- Pfeffer, S R -- Coussens, L -- Tepper, M A -- Brocklebank, C M -- Mole, J E -- Anderson, J K -- Chen, E -- Czech, M P -- Ullrich, A -- CA 39240/CA/NCI NIH HHS/ -- DK 30648/DK/NIDDK NIH HHS/ -- DK 34063/DK/NIDDK NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1988 Mar 4;239(4844):1134-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, University of Massachusetts Medical Center, Worcester 01655.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2964083" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Carrier Proteins/genetics/*metabolism ; Cell Membrane/analysis/metabolism ; Chromatography, Affinity ; DNA/genetics ; Female ; Hexosephosphates/*metabolism ; Insulin-Like Growth Factor II/*metabolism ; Mannosephosphates/*metabolism ; Molecular Sequence Data ; Placenta/analysis ; Pregnancy ; Rats ; Receptor, IGF Type 2 ; Receptor, Insulin/genetics/*metabolism ; Receptors, Somatomedin ; Sequence Homology, Nucleic Acid ; Somatomedins/*metabolism
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  • 54
    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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  • 55
    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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  • 56
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-02-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barnes, D M -- New York, N.Y. -- Science. 1988 Feb 19;239(4842):864-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2893452" target="_blank"〉PubMed〈/a〉
    Keywords: *3,4-Methylenedioxyamphetamine/adverse effects/analogs & derivatives/therapeutic ; use/toxicity ; *Amphetamines/adverse effects/therapeutic use/toxicity ; Animals ; Brain/pathology ; Haplorhini ; Humans ; Legislation, Drug ; N-Methyl-3,4-methylenedioxyamphetamine ; Nervous System Diseases/*chemically induced/pathology ; Neurons/metabolism/pathology ; Psychotherapy ; Rats ; Serotonin/metabolism ; *Substance-Related Disorders
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  • 57
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-07-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Broadwell, R D -- New York, N.Y. -- Science. 1988 Jul 22;241(4864):473-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Neurological Surgery, University of Maryland School of Medicine, Baltimore.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3393914" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Blood-Brain Barrier ; *Brain Tissue Transplantation ; Rats
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  • 58
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-02-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Britton, K T -- Ehlers, C L -- Koob, G F -- AA 06420/AA/NIAAA NIH HHS/ -- New York, N.Y. -- Science. 1988 Feb 5;239(4840):648-50.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3340849" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Azides/*pharmacology ; Benzodiazepines/*pharmacology ; Brain/drug effects/*physiology ; Conditioning (Psychology)/*drug effects ; Electroshock ; Ethanol/*antagonists & inhibitors/pharmacology ; Rats
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  • 59
    Publication Date: 1988-09-23
    Description: A defective herpes simplex virus 1 (HSV-1) vector, pHSVlac, has been developed that contains a transcription unit that places the Escherichia coli lacZ gene under the control of the HSV-1 immediate early 4/5 promoter. The vector pHSVlac was propagated with the HSV-1 temperature-sensitive mutant ts K as helper virus. Infection of neurons from rat superior cervical ganglia and dorsal root ganglia in primary culture resulted in stable expression of high levels of beta-galactosidase without cell death. These HSV-1 vectors should be useful for introducing genes into postmitotic cells, such as neurons, in vitro and in vivo.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2581874/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2581874/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Geller, A I -- Breakefield, X O -- DK39836/DK/NIDDK NIH HHS/ -- NS24279/NS/NINDS NIH HHS/ -- R01 NS034025/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1988 Sep 23;241(4873):1667-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, Massachusetts General Hospital, Boston 02114.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2843986" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; DNA, Viral/metabolism ; Defective Viruses/*genetics ; Escherichia coli/enzymology/*genetics ; Fluorescent Antibody Technique ; Galactosidases/*genetics ; *Genetic Vectors ; Helper Viruses ; Neurons/*microbiology ; Rats ; Recombinant Fusion Proteins/biosynthesis ; Simplexvirus/genetics ; Transfection ; beta-Galactosidase/biosynthesis/*genetics
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  • 60
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-10-07
    Description: The existence of spontaneous neural activity in mammalian retinal ganglion cells during prenatal life has long been suspected. This activity could play a key role in the refinement of retinal projections during development. Recordings in vivo from the retinas of rat fetuses between embryonic day 17 and 21 found action potentials in spontaneously active ganglion cells at all the ages studied.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Galli, L -- Maffei, L -- New York, N.Y. -- Science. 1988 Oct 7;242(4875):90-1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Istituto di Neurofisiologia Consiglio Nazionale Delle Richerche via San Zeno, Pisa, Italy.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3175637" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Electric Conductivity ; Female ; Fetus/physiology ; Pregnancy ; Rats ; Retina/*embryology/*physiology ; Retinal Ganglion Cells/*physiology
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  • 61
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-03-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Arimura, A -- New York, N.Y. -- Science. 1988 Mar 11;239(4845):1313.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2830676" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenocorticotropic Hormone/*secretion ; Animals ; Female ; Interleukin-1/*pharmacology ; Male ; Pituitary Gland, Anterior/drug effects/*secretion ; Rats
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  • 62
    Publication Date: 1988-11-18
    Description: The sense of taste permits animals to discriminate between foods that are safe and those that are toxic. Because most poisonous plant alkaloids are intensely bitter, bitter taste warns animals of potentially hazardous foods. To investigate the mechanism of bitter taste transduction, a preparation of dissociated rat taste cells was developed that can be studied with techniques designed for single-cell measurements. Denatonium, a very bitter substance, caused a rise in the intracellular calcium concentration due to release from internal stores in a small subpopulation of taste cells. Thus, the transduction of bitter taste may occur via a receptor-second messenger mechanism leading to neurotransmitter release and may not involve depolarization-mediated calcium entry.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Akabas, M H -- Dodd, J -- Al-Awqati, Q -- DK 20999/DK/NIDDK NIH HHS/ -- DK 34742/DK/NIDDK NIH HHS/ -- NS22993/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1988 Nov 18;242(4881):1047-50.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, 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/3194756" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/immunology ; Calcium/*physiology ; Cell Separation ; Cytoplasm/physiology ; Extracellular Space/physiology ; Membrane Potentials ; Quaternary Ammonium Compounds/*pharmacology ; Rats ; Sensory Receptor Cells/physiology ; Taste/*physiology ; Taste Buds/cytology/immunology/*physiology
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  • 63
    Publication Date: 1988-08-19
    Description: Previous studies have shown that adrenalectomy augments arginine vasopressin (AVP) messenger RNA levels in the adult paraventricular nucleus. It is now demonstrated that unilateral lesions in the lateral septal nucleus enhance the adrenalectomy-induced expression of AVP mRNA. This effect was entirely ipsilateral to the lesion and most prominent in the rostral paraventricular nucleus and related nuclei. Moreover, AVP and AVP mRNA were found to be colocalized with oxytocin in a few neurons. These results indicate that mRNA expression is modulated by synaptic influences and raise the possibility that synaptically mediated selection of neuronal phenotypes is a dynamic feature of the mature central nervous system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Baldino, F Jr -- O'Kane, T M -- Fitzpatrick-McElligott, S -- Wolfson, B -- New York, N.Y. -- Science. 1988 Aug 19;241(4868):978-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Products Department, E. I. du Pont de Nemours & Company, Wilmington, DE 19898.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3406747" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenalectomy ; Animals ; Gene Expression Regulation ; Male ; Neurons/analysis/*physiology ; Oxytocin/analysis ; Paraventricular Hypothalamic Nucleus/*physiology ; Phenotype ; RNA, Messenger/analysis/*biosynthesis ; Rats ; Rats, Inbred Strains ; Synapses/*physiology ; Vasopressins/analysis/*genetics
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  • 64
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    American Association for the Advancement of Science (AAAS)
    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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  • 65
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-10-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barnes, D M -- New York, N.Y. -- Science. 1988 Oct 21;242(4877):376-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3175661" target="_blank"〉PubMed〈/a〉
    Keywords: AIDS-Related Complex/complications/physiopathology ; Acquired Immunodeficiency Syndrome/*complications/physiopathology ; Animals ; Humans ; Rats ; Sarcoma, Kaposi/*etiology
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  • 66
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    American Association for the Advancement of Science (AAAS)
    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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  • 67
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-11-25
    Description: Inositol 1,4,5-trisphosphate [I(1,4,5)P3] is a second messenger generated along with diacylglycerol upon the binding of various physiological agents with their cell surface receptors. I(1,4,5)P3 mobilizes Ca2+ from intracellular storage sites through a receptor-coupled mechanism, and the subsequent increased intracellular free calcium ion concentration [( Ca2+]i) activates a multitude of cellular responses. Electropermeabilized neoplastic rat liver epithelial (261B) cells were used to study Ca2+ sequestration, a process that reverses the elevated [Ca2+]i to resting levels and replenishes intracellular Ca2+ pools. Although I (1,4,5)P3-mobilized Ca2+ is readily sequestered into storage pools by the action of Ca2+-adenosine triphosphatases, Ca2+ mobilized by addition of the nonmetabolized inositol trisphosphate isomer I(2,4,5)P3 is not sequestered, suggesting that metabolism is necessary to eliminate the stimulus for Ca2+ release. Several inositol phosphate compounds were examined for their ability to lower the buffer [Ca2+] to determine if a specific I(1,4,5)P3 metabolite might be involved in stimulating Ca2+ sequestration; of these, I(1,3,4,5)P4 alone was found to induce Ca2+ sequestration, demonstrating a physiological role for this inositol trisphosphate metabolite.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hill, T D -- Dean, N M -- Boynton, A L -- CA 39745/CA/NCI NIH HHS/ -- CA 42942/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1988 Nov 25;242(4882):1176-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Research Center of Hawaii, University of Hawaii, Honolulu 96813.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2847317" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/*metabolism ; *Calcium Channels ; Calcium-Transporting ATPases/metabolism ; Cell Membrane Permeability ; Epithelium/metabolism ; Inositol 1,4,5-Trisphosphate ; Inositol 1,4,5-Trisphosphate Receptors ; Inositol Phosphates/metabolism/*pharmacology ; Liver/drug effects/*metabolism ; Liver Neoplasms, Experimental/metabolism ; Rats ; Receptors, Cell Surface/metabolism ; *Receptors, Cytoplasmic and Nuclear ; Sugar Phosphates/*pharmacology ; Tumor Cells, Cultured
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  • 68
    Publication Date: 1988-07-08
    Description: Sodium, potassium-adenosine triphosphatase (Na+, K+-ATPase) is hypothesized to be involved in systemic vascular hypertension through its effects on smooth muscle reactivity and myocardial contractility. By means of RNA blot analyses of cardiac, aortic, and skeletal muscle RNAs in two rat hypertensive models, Na+,K+-ATPase alpha-subunit messenger RNA isoforms (alpha 2 and alpha 3) were shown to be deinduced in response to increased intravascular pressure. The changes were observed after 48 hours or more of experimental hypertension. Under these conditions, there is coordinate induction of another alpha isoform (alpha 1) and of beta-subunit messenger RNAs, probably in response to alterations in sodium flux rather than to elevated blood pressure.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Herrera, V L -- Chobanian, A V -- Ruiz-Opazo, N -- HL01967/HL/NHLBI NIH HHS/ -- HL18318/HL/NHLBI NIH HHS/ -- HL39267/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1988 Jul 8;241(4862):221-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Molecular Genetics, Boston University Medical Center, MA 02118.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2838907" target="_blank"〉PubMed〈/a〉
    Keywords: Angiotensin II ; Animals ; Cardiomegaly/enzymology/genetics ; Desoxycorticosterone ; Heart Ventricles/enzymology ; Hypertension/enzymology/*genetics ; Isoenzymes/genetics ; RNA, Messenger/genetics ; Rats ; Sodium-Potassium-Exchanging ATPase/*genetics
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  • 69
    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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  • 70
    Publication Date: 1988-12-02
    Description: Band 3 multigene family consists of several distinct but structurally related polypeptides which are probably involved in the transport of anions across the plasma membrane of both erythrocytes and nonerythroid cells. A novel member of this family of polypeptides that resides in the Golgi complex was identified with antibodies to Band 3. The Golgi antigen had a larger molecular size and was antigenically distinct from Band 3 in the amino-terminal domain. It was expressed most prominently in cells that secrete large amounts of sulfated proteins and proteoglycans. This polypeptide may participate in sulfate transport across Golgi membranes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kellokumpu, S -- Neff, L -- Jamsa-Kellokumpu, S -- Kopito, R -- Baron, R -- DE-04724/DE/NIDCR NIH HHS/ -- New York, N.Y. -- Science. 1988 Dec 2;242(4883):1308-11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Yale University School of Medicine, New Haven, CT 06510.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2461589" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anion Exchange Protein 1, Erythrocyte/*immunology ; Cloning, Molecular ; Golgi Apparatus/*ultrastructure ; Immunoenzyme Techniques ; Intracellular Membranes/*ultrastructure ; Ion Channels/*ultrastructure ; Molecular Weight ; Rats
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  • 71
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-02-19
    Description: Autocrine activation of platelet-derived growth factor (PDGF) receptors is the mechanism of transformation by the v-sis oncogene. Since the addition of PDGF does not transform normal cells, autocrine mechanisms may involve unique pathways of receptor activation. In this study autocrine stimulation of the PDGF receptor was observed in v-sis-transformed normal rat kidney (NRK) cells. In contrast to receptor activation in normal cells, autocrine activation of PDGF receptors in v-sis-transformed cells occurred in intracellular compartments, disrupting receptor processing and diverting receptors and their precursors to a chloroquine-sensitive degradation pathway. These findings show that intracellular activation of receptors by autocrine mechanisms may play a role in cell transformation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Keating, M T -- Williams, L T -- 5 K11 HL01556-02/HL/NHLBI NIH HHS/ -- R01 HL32898-04/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1988 Feb 19;239(4842):914-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, San Francisco, CA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2829358" target="_blank"〉PubMed〈/a〉
    Keywords: Ammonium Chloride/pharmacology ; Animals ; Cell Line, Transformed ; Cell Membrane/metabolism ; Chloroquine/pharmacology ; Half-Life ; Hexosaminidases/pharmacology ; Immunosorbent Techniques ; Molecular Weight ; *Oncogenes ; Phosphorylation ; Platelet-Derived Growth Factor/pharmacology ; Protein Precursors/metabolism ; Rats ; Receptors, Cell Surface/drug effects/*metabolism ; Receptors, Platelet-Derived Growth Factor ; Trypsin/metabolism
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  • 72
    Publication Date: 1988-07-01
    Description: High specific activity estradiol labeled with iodine-125 was used to detect approximately 200 saturable, high-affinity (dissociation constant approximately equal to 1.0 nM) nuclear binding sites in rat (ROS 17/2.8) and human (HOS TE85) clonal osteoblast-like osteosarcoma cells. Of the steroids tested, only testosterone exhibited significant cross-reactivity with estrogen binding. RNA blot analysis with a complementary DNA probe to the human estrogen receptor revealed putative receptor transcripts of 6 to 6.2 kilobases in both rat and human osteosarcoma cells. Type I procollagen and transforming growth factor-beta messenger RNA levels were enhanced in cultured human osteoblast-like cells treated with 1 nM estradiol. Thus, estrogen can act directly on osteoblasts by a receptor-mediated mechanism and thereby modulate the extracellular matrix and other proteins involved in the maintenance of skeletal mineralization and remodeling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Komm, B S -- Terpening, C M -- Benz, D J -- Graeme, K A -- Gallegos, A -- Korc, M -- Greene, G L -- O'Malley, B W -- Haussler, M R -- New York, N.Y. -- Science. 1988 Jul 1;241(4861):81-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, University of Arizona College of Medicine, Tucson 85724.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3164526" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding, Competitive ; Cell Nucleus/metabolism ; DNA/genetics ; Estradiol/*metabolism/pharmacology ; Humans ; Iodine Radioisotopes ; Nucleic Acid Hybridization ; Osteoblasts/drug effects/*metabolism ; Osteosarcoma/*metabolism ; Peptides/genetics ; Procollagen/genetics ; RNA, Messenger/*metabolism ; Rats ; Receptors, Estrogen/genetics/*metabolism ; Transcription, Genetic ; Transforming Growth Factors ; Tumor Cells, Cultured
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  • 73
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-10-14
    Description: Messenger RNAs isolated from adult or newborn rat spinal cord were fractionated in a sucrose gradient. The fractions were injected into Xenopus oocytes to determine their potencies for expression of glycine receptors (GlyRs), which were then examined electrophysiologically. The sedimentation profiles disclosed two classes of GlyR mRNAs, one heavy and the other light. The adult spinal cord was rich in heavy GlyR mRNA, whereas the light GlyR mRNA was more abundant in neonatal spinal cord and in adult cerebral cortex. Glycine receptors encoded by heavy and light mRNAs of adult spinal cord showed some electrophysiological differences. Thus there are two types of GlyRs encoded by mRNAs of different sizes, and the expression of these mRNAs is developmentally regulated. A tissue- and age-dependent distribution of heterogeneous GlyR mRNAs may imply diverse roles of the GlyRs in neuronal function in the central nervous system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Akagi, H -- Miledi, R -- R01-NS23284/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1988 Oct 14;242(4876):270-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychobiology, University of California, Irvine 92717.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2845580" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Cell Membrane/physiology ; Centrifugation, Density Gradient ; Cerebral Cortex/*analysis ; DNA/genetics ; Electric Conductivity ; Glycine/pharmacology ; Nucleic Acid Hybridization ; Oocytes/drug effects/physiology ; RNA, Messenger/*genetics/isolation & purification ; Rats ; Receptors, Glycine ; Receptors, Neurotransmitter/*genetics/physiology ; Spinal Cord/*analysis ; Transcription, Genetic ; Xenopus laevis
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  • 74
    Publication Date: 1988-06-03
    Description: In situ hybridization with complementary DNA probes for nerve growth factor (NGF) was used to identify cells containing NGF messenger RNA in rat and mouse brain. The most intense labeling occurred in hippocampus, where hybridizing neurons were found in the dentate gyrus and the pyramidal cell layer. The neuronal identity of NGF mRNA-containing cells was further assessed by a loss of NGF-hybridizing mRNA in hippocampal areas where neurons had been destroyed by kainic acid or colchicine. RNA blot analysis also revealed a considerable decrease in the level of NGF mRNA in rat dentate gyrus after a lesion was produced by colchicine. This lesion also caused a decrease in the level of Thy-1 mRNA and an increase in the level of glial fibrillary acidic protein mRNA. Neuronal death was thus associated with the disappearance of NGF mRNA. These results suggest a synthesis of NGF by neurons in the brain and imply that, in hippocampus, NGF influences NGF-sensitive neurons through neuron-to-neuron interactions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ayer-LeLievre, C -- Olson, L -- Ebendal, T -- Seiger, A -- Persson, H -- New York, N.Y. -- Science. 1988 Jun 3;240(4857):1339-41.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Chemistry, Karolinska Institutet, Stockholm, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2897715" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Surface/genetics ; Antigens, Thy-1 ; Colchicine/pharmacology ; Dna ; *Gene Expression Regulation ; Glial Fibrillary Acidic Protein/genetics ; Hippocampus/drug effects/*metabolism ; Kainic Acid/pharmacology ; Nerve Growth Factors/*genetics ; Neurons/*metabolism ; Nucleic Acid Hybridization ; RNA, Messenger/*metabolism ; Rats
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  • 75
    Publication Date: 1988-02-05
    Description: Gold-filled Sendai virus envelopes were fused with cell suspensions from the basal forebrain of fetal rat donors, and the resulting gold-labeled cells were transplanted into the neocortex of adult rat recipients. Not only did large numbers of labeled cells remain intact through 3 months in the neocortex, but sizable numbers migrated subcortically to the recipient's lesioned nucleus basalis region (a distance of 4 to 5 millimeters). Since this technique is capable of labeling most transplanted cells for long periods of time, it may be useful in determining the survival, migration, and connectivity of intracerebrally transplanted tissues.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ardizzoni, S C -- Michaels, A -- Arendash, G W -- HD 17933/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1988 Feb 5;239(4840):635-7.〈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/2829355" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/cytology/embryology ; Fetus ; Gold ; Nerve Tissue/*transplantation ; Neurons/cytology/*transplantation ; Parainfluenza Virus 1, Human ; Rats ; *Viral Envelope Proteins
    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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  • 76
    Publication Date: 1988-10-28
    Description: Mineralocorticoid receptors, both when in tissue extracts and when recombinant-derived, have equal affinity for the physiological mineralocorticoid aldosterone and for the glucocorticoids cortisol and corticosterone, which circulate at much higher concentrations than aldosterone. Such receptors are found in physiological mineralocorticoid target tissues (kidney, parotid, and colon) and in nontarget tissues such as hippocampus and heart. In mineralocorticoid target tissues the receptors are selective for aldosterone in vivo because of the presence of the enzyme 11 beta-hydroxy-steroid dehydrogenase, which converts cortisol and corticosterone, but not aldosterone, to their 11-keto analogs. These analogs cannot bind to mineralocorticoid receptors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Funder, J W -- Pearce, P T -- Smith, R -- Smith, A I -- New York, N.Y. -- Science. 1988 Oct 28;242(4878):583-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Centre, Prince Henry's Hospital, Melbourne, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2845584" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenalectomy ; Aldosterone/*physiology ; Animals ; Carbenoxolone/pharmacology ; Colon/physiology ; Corticosterone/metabolism ; Heart/physiology ; Hippocampus/physiology ; Hydrocortisone/metabolism ; Hydroxysteroid Dehydrogenases/*metabolism ; Kidney/physiology ; Parotid Gland/physiology ; Rats ; Receptors, Mineralocorticoid ; Receptors, Steroid/*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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  • 77
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-09-30
    Description: Restriction of maternal dietary sodium on or before embryonic day 8 reduced taste responses of the chorda tympani nerve to sodium chloride in the offspring. The response attenuation was substantial; responses to sodium chloride in the offspring of deprived rats were approximately 40 percent of those in control animals. Instituting the low sodium diet at embryonic day 10 or later did not produce functional changes. Thus, a sensitive period for the gustatory system exists, and the abrupt transition from maximal environmental susceptibility to no susceptibility occurs during a 2-day prenatal period. Moreover, events important in determining the developmental fate of taste membrane components occur before the initial formation of taste buds.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hill, D L -- Przekop, P R Jr -- NS01215/NS/NINDS NIH HHS/ -- NS24741/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1988 Sep 30;241(4874):1826-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychology, University of Virginia, Charlottesville 22903.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3175625" target="_blank"〉PubMed〈/a〉
    Keywords: Amiloride/pharmacology ; Animals ; Neurons/physiology ; Rats ; Sensory Receptor Cells/*physiology ; Sodium/deficiency/*physiology ; Taste/*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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