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  • Articles  (1,447)
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  • 101
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    Activity-dependent decrease in NMDA receptor responses during development of the visual cortex (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-11-06
    Description: Plasticity of the developing visual system has been regarded as the best model for changes of neuronal connections under the influence of the environment. N-methyl-D-aspartate (NMDA) receptors are crucial for experience-dependent synaptic modifications that occur in the developing visual cortex. NMDA-mediated excitatory postsynaptic currents (EPSCs) in layer IV neurons of the visual cortex lasted longer in young rats than in adult rats, and the duration of the EPSCs became progressively shorter, in parallel with the developmental reduction in synaptic plasticity. This decrease in NMDA receptor-mediated EPSC duration is delayed when the animals are reared in the dark, a condition that prolongs developmental plasticity, and is prevented by treatment with tetrodotoxin, a procedure that inhibits neural activity. Application of L-glutamate to outside-out patches excised from layer IV neurons of young, but not of adult, rats activated prolonged bursts of NMDA channel openings. A modification of the NMDA receptor gating properties may therefore account for the age-dependent decline of visual cortical plasticity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Carmignoto, G -- Vicini, S -- P01 NS 28130-01/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1992 Nov 6;258(5084):1007-11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉FIDIA Georgetown Institute for the Neurosciences, Georgetown University School of Medicine, Washington, DC 20007.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1279803" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Aging/physiology ; Animals ; Electric Conductivity ; Glutamates/pharmacology ; Glutamic Acid ; Ion Channel Gating/physiology ; Ion Channels/physiology ; Neuronal Plasticity/physiology ; Neurons/drug effects/physiology ; Rats ; Receptors, N-Methyl-D-Aspartate/*physiology ; Synapses/physiology ; Tetrodotoxin/pharmacology ; Visual Cortex/*growth & development/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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  • 102
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    Interleukin-8 as a macrophage-derived mediator of angiogenesis (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-12-11
    Description: Angiogenic factors produced by monocytes-macrophages are involved in the pathogenesis of chronic inflammatory disorders characterized by persistent angiogenesis. The possibility was tested that interleukin-8 (IL-8), which is a cytokine that is chemotactic for lymphocytes and neutrophils, is also angiogenic. Human recombinant IL-8 was potently angiogenic when implanted in the rat cornea and induced proliferation and chemotaxis of human umbilical vein endothelial cells. Angiogenic activity present in the conditioned media of inflamed human rheumatoid synovial tissue macrophages or lipopolysaccharide-stimulated blood monocytes was equally blocked by antibodies to either IL-8 or tumor necrosis factor-alpha. An IL-8 antisense oligonucleotide specifically blocked the production of monocyte-induced angiogenic activity. These data suggest a function for macrophage-derived IL-8 in angiogenesis-dependent disorders such as rheumatoid arthritis, tumor growth, and wound repair.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koch, A E -- Polverini, P J -- Kunkel, S L -- Harlow, L A -- DiPietro, L A -- Elner, V M -- Elner, S G -- Strieter, R M -- AR30692/AR/NIAMS NIH HHS/ -- AR41492/AR/NIAMS NIH HHS/ -- HL39926/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1992 Dec 11;258(5089):1798-801.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Northwestern University Medical School, Chicago, IL 60611.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1281554" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arthritis, Rheumatoid/physiopathology ; Base Sequence ; Cell Division/drug effects ; Cells, Cultured ; Chemotaxis/*drug effects ; Cornea/*drug effects/physiology ; Dose-Response Relationship, Drug ; Endothelium, Vascular/drug effects/*physiology ; Fibroblast Growth Factor 2/pharmacology ; Humans ; Interleukin-8/genetics/*pharmacology ; Macrophages/*physiology ; Mice ; Molecular Sequence Data ; Monocytes/physiology ; *Neovascularization, Pathologic ; Oligonucleotides, Antisense/*pharmacology ; Rabbits ; Rats ; Recombinant Proteins/pharmacology ; Synovial Fluid/physiology ; Tumor Necrosis Factor-alpha/genetics ; Umbilical Veins
    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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  • 103
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    Dendritic spines: convergence of theory and experiment (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-05-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koch, C -- Zador, A -- Brown, T H -- New York, N.Y. -- Science. 1992 May 15;256(5059):973-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Computation and Neural Systems Program, California Institute of Technology, Pasadena 91125.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1589781" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/physiology/ultrastructure ; Calcium/metabolism ; Dendrites/physiology/*ultrastructure ; Electrophysiology ; Hippocampus/*ultrastructure ; Microscopy, Electron ; Rats ; Synapses/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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  • 104
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    Neutrophil recruitment by tumor necrosis factor from mast cells in immune complex peritonitis (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-12-18
    Description: During generalized immune complex-induced inflammation of the peritoneal cavity, two peaks of tumor necrosis factor (TNF) were observed in the peritoneal exudate of normal mice. In mast cell-deficient mice, the first peak was undetected, and the second peak of TNF and neutrophil influx were significantly reduced. Antibody to TNF significantly inhibited neutrophil infiltration in normal but not in mast cell-deficient mice. Mast cell repletion of the latter normalized TNF, neutrophil mobilization, and the effect of the antibody to TNF. Thus, in vivo, mast cells produce the TNF that augments neutrophil emigration.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Y -- Ramos, B F -- Jakschik, B A -- HL31922/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1992 Dec 18;258(5090):1957-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology and Pharmacology, 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/1470922" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen-Antibody Complex/*immunology ; Chickens ; Immunoglobulin G/immunology ; Inflammation ; Interleukin-1/pharmacology ; Leukotrienes/pharmacology ; Mast Cells/*physiology ; Mice ; Mice, Mutant Strains ; Neutrophils/drug effects/*physiology ; Ovalbumin/immunology ; Peritonitis/immunology/*physiopathology ; Rabbits ; Tumor Necrosis Factor-alpha/metabolism/pharmacology/*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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  • 105
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    Spontaneous hypercholesterolemia and arterial lesions in mice lacking apolipoprotein E (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-10-16
    Description: Apolipoprotein E (apoE) is a ligand for receptors that clear remnants of chylomicrons and very low density lipoproteins. Lack of apoE is, therefore, expected to cause accumulation in plasma of cholesterol-rich remnants whose prolonged circulation should be atherogenic. ApoE-deficient mice generated by gene targeting were used to test this hypothesis and to make a mouse model for spontaneous atherosclerosis. The mutant mice had five times normal plasma cholesterol, and developed foam cell-rich depositions in their proximal aortas by age 3 months. These spontaneous lesions progressed and caused severe occlusion of the coronary artery ostium by 8 months. The severe yet viable phenotype of the mutants should make them valuable for investigating genetic and environmental factors that modify the atherogenic process.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, S H -- Reddick, R L -- Piedrahita, J A -- Maeda, N -- HL42630/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1992 Oct 16;258(5081):468-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, University of North Carolina, Chapel Hill 27599-7525.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1411543" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apolipoproteins E/*deficiency/genetics ; Cholesterol/blood ; Disease Models, Animal ; Hypercholesterolemia/*genetics/pathology ; Lipoproteins/metabolism ; Mice ; Mice, Mutant Strains ; Mutagenesis, Insertional ; Triglycerides/blood
    Print ISSN: 0036-8075
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  • 106
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    Identification of a protein that binds to the SH3 region of Abl and is similar to Bcr and GAP-rho (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-08-07
    Description: A Src homology 3 (SH3) region is a sequence of approximately 50 amino acids found in many nonreceptor tyrosine kinases and other proteins. Deletion of the SH3 region from the protein encoded by the c-abl proto-oncogene activates the protein's transforming capacity, thereby suggesting the participation of the SH3 region in the negative regulation of transformation. A complementary DNA was isolated that encoded a protein, 3BP-1, to which the SH3 region of Abl bound with high specificity and to which SH3 regions from other proteins bound differentially. The sequence of the 3BP-1 protein is similar to that of a COOH-terminal segment of Bcr and to guanosine triphosphatase-activating protein (GAP)-rho, which suggests that it might have GAP activity for Ras-related proteins. The 3BP-1 protein may therefore be a mediator of SH3 function in transformation inhibition and may link tyrosine kinases to Ras-related proteins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cicchetti, P -- Mayer, B J -- Thiel, G -- Baltimore, D -- A107233/PHS HHS/ -- CA 08875/CA/NCI NIH HHS/ -- CA51462/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1992 Aug 7;257(5071):803-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Rockefeller University, New York, NY 10021.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1379745" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Amino Acid Sequence ; Animals ; Binding Sites ; Chimera ; Cloning, Molecular ; GTPase-Activating Proteins ; Gene Library ; *Genes, abl ; *Genes, src ; Glutathione Transferase/genetics/metabolism ; Mice ; Molecular Sequence Data ; Oncogene Proteins/genetics/*metabolism ; Plasmids ; Polymerase Chain Reaction/methods ; Prosencephalon/physiology ; Protein-Tyrosine Kinases/*metabolism ; Proteins/*metabolism ; *Proto-Oncogene Proteins ; Proto-Oncogene Proteins c-abl/genetics/*metabolism ; Proto-Oncogene Proteins c-bcr ; Proto-Oncogene Proteins pp60(c-src)/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Restriction Mapping ; Rho Factor/*metabolism ; Sequence Homology, Nucleic Acid ; ras GTPase-Activating Proteins
    Print ISSN: 0036-8075
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  • 107
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    Flow-dependent cytosolic acidification of vascular endothelial cells (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-10-23
    Description: Hemodynamic shear stress affects endothelial cell structure and function, but little is known about the signal transduction mechanisms involved in these processes. The effect of laminar shear stress on cytosolic pH (pHi) was examined in rat aortic endothelial cells cultured in glass capillary tubes. Shear stress forces led to a rapid decrease in pHi (maximal effect 0.09 pH unit at 13.4 dynes per square centimeter). Removal of specific ions or addition of exchange inhibitors suggests that in vascular endothelial cells shear stress forces activate both an alkali extruder, sodium ion-independent chloride-bicarbonate ion exchange, and an acid extruder, sodium-hydrogen ion exchange; the net effect in physiologic buffer with the bicarbonate ion is a decrease in pHi.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ziegelstein, R C -- Cheng, L -- Capogrossi, M C -- New York, N.Y. -- Science. 1992 Oct 23;258(5082):656-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Cardiovascular Science, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1329207" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bicarbonates/metabolism ; Carrier Proteins/physiology ; Cells, Cultured ; Chloride-Bicarbonate Antiporters ; Cytosol/*physiology ; Endothelium, Vascular/*physiology ; Hydrogen-Ion Concentration ; Membrane Proteins/physiology ; Rats ; Signal Transduction/physiology ; Sodium-Hydrogen Antiporter ; Stress, Mechanical
    Print ISSN: 0036-8075
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  • 108
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    The time course of glutamate in the synaptic cleft (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-11-27
    Description: The peak concentration and rate of clearance of neurotransmitter from the synaptic cleft are important determinants of synaptic function, yet the neurotransmitter concentration time course is unknown at synapses in the brain. The time course of free glutamate in the cleft was estimated by kinetic analysis of the displacement of a rapidly dissociating competitive antagonist from N-methyl-D-aspartate (NMDA) receptors during synaptic transmission. Glutamate peaked at 1.1 millimolar and decayed with a time constant of 1.2 milliseconds at cultured hippocampal synapses. This time course implies that transmitter saturates postsynaptic NMDA receptors. However, glutamate dissociates much more rapidly from alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors. Thus, the time course of free glutamate predicts that dissociation contributes to the decay of the AMPA receptor-mediated postsynaptic current.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Clements, J D -- Lester, R A -- Tong, G -- Jahr, C E -- Westbrook, G L -- MH46613/MH/NIMH NIH HHS/ -- NS21419/NS/NINDS NIH HHS/ -- NS26494/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1992 Nov 27;258(5087):1498-501.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Vollum Institute, Oregon Health Sciences University, Portland 97201.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1359647" target="_blank"〉PubMed〈/a〉
    Keywords: 2-Aminoadipic Acid/pharmacology ; Action Potentials/physiology ; Animals ; Cells, Cultured ; Glutamates/*metabolism ; Glutamic Acid ; Hippocampus/cytology/physiology ; Models, Neurological ; Neurons/physiology ; Neurotransmitter Agents/*metabolism ; Piperazines/pharmacology ; Rats ; Receptors, N-Methyl-D-Aspartate/drug effects/physiology ; Synapses/drug effects/*metabolism ; Time Factors
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 109
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    Antisense and antigene properties of peptide nucleic acids (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-11-27
    Description: Peptide nucleic acids (PNAs) are polyamide oligomers that can strand invade duplex DNA, causing displacement of one DNA strand and formation of a D-loop. Binding of either a T10 PNA or a mixed sequence 15-mer PNA to the transcribed strand of a G-free transcription cassette caused 90 to 100 percent site-specific termination of pol II transcription elongation. When a T10 PNA was bound on the nontranscribed strand, site-specific inhibition never exceeded 50 percent. Binding of PNAs to RNA resulted in site-specific termination of both reverse transcription and in vitro translation, precisely at the position of the PNA.RNA heteroduplex. Nuclear microinjection of cells constitutively expressing SV40 large T antigen (T Ag) with either a 15-mer or 20-mer PNA targeted to the T Ag messenger RNA suppressed T Ag expression. This effect was specific in that there was no reduction in beta-galactosidase expression from a coinjected expression vector and no inhibition of T Ag expression after microinjection of a 10-mer PNA.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hanvey, J C -- Peffer, N J -- Bisi, J E -- Thomson, S A -- Cadilla, R -- Josey, J A -- Ricca, D J -- Hassman, C F -- Bonham, M A -- Au, K G -- New York, N.Y. -- Science. 1992 Nov 27;258(5087):1481-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Glaxo Inc. Research Institute, Research Triangle Park, NC 27709.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1279811" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Polyomavirus Transforming/genetics ; Base Sequence ; DNA/*metabolism ; Deoxyribonuclease HindIII/antagonists & inhibitors ; Gene Expression/drug effects ; HeLa Cells ; Humans ; In Vitro Techniques ; Molecular Sequence Data ; Oligodeoxyribonucleotides/*metabolism/pharmacology ; Oligonucleotides, Antisense/*metabolism/pharmacology ; *Peptide Nucleic Acids ; Plasmids ; Protein Biosynthesis/drug effects ; RNA/metabolism ; Rabbits ; Rats ; Transcription, Genetic/drug effects
    Print ISSN: 0036-8075
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  • 110
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    Correction of CD18-deficient lymphocytes by retrovirus-mediated gene transfer (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-06-15
    Description: Leukocyte adhesion deficiency (LAD) is an inherited disorder of leukocyte function caused by derangements in CD18 expression. The genetic and functional abnormalities in a lymphocyte cell line from a patient with LAD have been corrected by retrovirus-mediated transduction of a functional CD18 gene. Lymphocytes from patients with LAD were exposed to CD18-expressing retrovirus and enriched for cells that express CD11a and CD18 (LFA-1) on the cell surface. Molecular and functional analyses of these cells revealed (i) one copy of proviral sequence per cell, (ii) viral-directed CD18 RNA that exceeded normal endogenous levels, (iii) normal quantities of CD11a and CD18 protein on the cell surface, and (iv) reconstitution of LFA-1-dependent adhesive function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wilson, J M -- Ping, A J -- Krauss, J C -- Mayo-Bond, L -- Rogers, C E -- Anderson, D C -- Todd, R F -- R01 AI19031/AI/NIAID NIH HHS/ -- R01 AI23521/AI/NIAID NIH HHS/ -- R01 CA39064/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1990 Jun 15;248(4961):1413-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Internal Medicine, Ann Arbor, MI.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1972597" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD ; Antigens, CD18 ; Antigens, Differentiation/genetics/immunology ; Cell Aggregation ; Cell Line ; Cell Line, Transformed ; Gene Expression ; Genetic Therapy ; Genetic Vectors ; Herpesvirus 4, Human ; Humans ; *Leukocyte-Adhesion Deficiency Syndrome ; Lymphocyte Function-Associated Antigen-1 ; Lymphocytes/immunology ; Membrane Glycoproteins ; Mice ; Nucleic Acid Hybridization ; Receptors, Leukocyte-Adhesion/genetics/immunology ; Retroviridae/*genetics ; Tetradecanoylphorbol Acetate/pharmacology ; *Transfection
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  • 111
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    Regional variation of extracellular space in the hippocampus (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-08-10
    Description: The factors responsible for the unusual susceptibility of the hippocampus to seizures and ischemic cell damage are not well understood. The CA1 pyramidal subfield of the hippocampus is particularly vulnerable to seizure activity and damage after ischemia. The possibility was examined that regional differences exist in extracellular volume, which might influence neuronal excitability and response to injury in the hippocampus. CA1 stratum pyramidale exhibited an exceptionally low extracellular volume fraction (EVF) of 0.12, whereas the EVFs of CA3 and dentate were considerably higher--0.18 and 0.15, respectively. The EVF of CA1 stratum pyramidale was reversibly reduced by 30 percent when the extracellular potassium concentration was raised from 3.5 to 8.5 mM, a procedure that induced spontaneous electrographic seizures in CA1. Thus there are regional variations in the properties of the extracellular space in the hippocampus that might underlie the propensity of the CA1 region to develop seizures and to suffer damage after ischemia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McBain, C J -- Traynelis, S F -- Dingledine, R -- NS17771/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1990 Aug 10;249(4969):674-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of North Carolina, Chapel Hill 27599.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2382142" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Diffusion ; Extracellular Space/drug effects/*physiology ; Hippocampus/anatomy & histology/*physiology/physiopathology ; In Vitro Techniques ; Iontophoresis ; Organ Specificity ; Potassium/pharmacology ; Pyramidal Tracts/drug effects/*physiology ; Quaternary Ammonium Compounds/metabolism ; Rats ; Rats, Inbred Strains ; Seizures/physiopathology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 112
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    Autoimmune diseases: the failure of self tolerance (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-06-15
    Description: The ability to discriminate between self and nonself antigens is vital to the functioning of the immune system as a specific defense against invading microorganisms. Failure of the immune system to "tolerate" self tissues can result in pathological autoimmune states leading to debilitating illness and sometimes death. The induction of autoimmunity involves genetic and environmental factors that have focused the attention of researchers on the trimolecular complex formed by major histocompatibility complex molecules, antigen, and T cell receptors. Detailed molecular characterization of these components points to potential strategies for disease intervention.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sinha, A A -- Lopez, M T -- McDevitt, H O -- New York, N.Y. -- Science. 1990 Jun 15;248(4961):1380-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, Stanford University School of Medicine, CA 94305.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1972595" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autoantibodies/immunology ; Autoantigens/immunology ; Autoimmune Diseases/chemically induced/*immunology ; B-Lymphocytes/immunology ; Bacterial Infections/immunology ; Biological Factors/physiology ; CD4-Positive T-Lymphocytes/immunology ; Cytokines ; Gene Rearrangement, T-Lymphocyte ; Histocompatibility Antigens Class I/immunology ; Histocompatibility Antigens Class II/immunology ; Humans ; *Immune Tolerance ; Major Histocompatibility Complex ; Mice ; Polymorphism, Genetic ; Polymorphism, Restriction Fragment Length ; Receptors, Antigen, T-Cell/genetics/immunology ; T-Lymphocytes, Regulatory/immunology ; *Virus Diseases/immunology
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  • 113
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    Requirement for cotolerogenic gene products in the clonal deletion of I-E reactive T cells (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-02-23
    Description: T cells that express the T cell receptor V beta 5.2 domain react with the class II major histocompatibility complex (MHC) molecule I-E, and V beta 5.2+ T cells are deleted in mouse strains that express I-E glycoproteins. By examination of genetically defined recombinant inbred (RI) mouse strains, it was found that the deletion was dependent on the expression of I-E and one of a limited number of non-MHC gene products (cotolerogens). The gene encoding one of these cotolerogens maps to chromosome 12 and is linked to the endogenous provirus Mtv-9. These observations suggest that the I-E-mediated and minor lymphocyte-stimulating antigen (Mls)-mediated deletions of alpha beta T cells from the repertoire are similar; both require the expression of a class II MHC glycoprotein and a second non-MHC gene product.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Woodland, D -- Happ, M P -- Bill, J -- Palmer, E -- AI-22259/AI/NIAID NIH HHS/ -- AI-22295/AI/NIAID NIH HHS/ -- AR-37070/AR/NIAMS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1990 Feb 23;247(4945):964-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Basic Sciences, National Jewish Center for Immunology and Respiratory Medicine, Denver, CO 80206.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1968289" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CD4-Positive T-Lymphocytes/immunology ; Clone Cells ; Gene Expression ; Histocompatibility Antigens Class II/genetics/*immunology ; Hybridomas/immunology ; Immune Tolerance ; Mice ; Mice, Inbred C3H ; Mice, Inbred DBA ; Mice, Transgenic ; Phenotype ; Receptors, Antigen, T-Cell/*genetics/immunology ; Spleen/immunology ; T-Lymphocytes/*immunology ; T-Lymphocytes, Regulatory/immunology
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    Induction of chronic myelogenous leukemia in mice by the P210bcr/abl gene of the Philadelphia chromosome (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-02-16
    Description: In tumor cells from virtually all patients with chronic myelogenous leukemia, the Philadelphia chromosome, a fusion of chromosomes 9 and 22, directs the synthesis of the P210bcr/abl protein. The protein-tyrosine kinase activity and hybrid structure of P210bcr/abl are similar to the oncogene product of the Abelson murine leukemia virus, P160gag/v-abl, which induces acute lymphomas. To determine whether P210bcr/abl can induce chronic myelogenous leukemia, murine bone marrow was infected with a retrovirus encoding P210bcr/abl and transplanted into irradiated syngeneic recipients. Transplant recipients developed several hematologic malignancies; prominent among them was a myeloproliferative syndrome closely resembling the chronic phase of human chronic myelogenous leukemia. Tumor tissue from diseased mice harbored the provirus encoding P210bcr/abl. These results demonstrate that P210bcr/abl expression can induce chronic myelogenous leukemia. Retrovirus-mediated expression of the protein provides a murine model system for further analysis of the disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Daley, G Q -- Van Etten, R A -- Baltimore, D -- 2T 32 GM07753-07/GM/NIGMS NIH HHS/ -- CA38497/CA/NCI NIH HHS/ -- T32 GM007753/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1990 Feb 16;247(4944):824-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research, Massachusetts Institute of Technology, Cambridge 02142.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2406902" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bone Marrow/microbiology/pathology ; Cell Line ; DNA, Neoplasm/isolation & purification ; DNA, Viral/isolation & purification ; Fusion Proteins, bcr-abl/*genetics ; Humans ; Leukemia, Experimental/genetics/pathology ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/*genetics/pathology ; Mice ; Myeloproliferative Disorders/microbiology/pathology ; *Philadelphia Chromosome ; Retroviridae/genetics ; Spleen/microbiology ; Transduction, Genetic
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    HIV-1 coat protein neurotoxicity prevented by calcium channel antagonists (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-04-20
    Description: Coat protein gp120 from the human immunodeficiency virus type-1 (HIV-1) increased intracellular free calcium and injured rodent retinal ganglion cells and hippocampal neurons in culture. Highly purified recombinant gp120 envelope protein produced these effects in a dose-dependent fashion at picomolar concentrations. Immunoprecipitation with antibody to gp120, but not with control immunoglobulin-containing serum, depleted solutions of the viral envelope protein and also prevented both the rise in intracellular calcium and neuronal toxicity. The gp120-induced increase in intracellular calcium was abrogated by transiently lowering extracellular calcium or by adding the dihydropyridine calcium channel antagonist nimodipine (100 nM). Calcium channel antagonists also prevented gp120-induced neuronal injury. In addition, intracellular stores appeared to contribute substantially to the increase in calcium elicited by gp120. Since increases in intracellular calcium have been associated with neurotoxicity, it is possible that an injurious effect of gp120 on neurons might be related to this mechanism and that treatment with calcium channel antagonists may prove useful in mitigating HIV-1-related neuronal injury.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dreyer, E B -- Kaiser, P K -- Offermann, J T -- Lipton, S A -- EY 05477/EY/NEI NIH HHS/ -- NS 01395/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1990 Apr 20;248(4953):364-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, Children's Hospital, Boston, MA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2326646" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/*metabolism ; Calcium Channel Blockers/*pharmacology ; Cells, Cultured ; HIV Envelope Protein gp120/administration & dosage/antagonists & ; inhibitors/*physiology ; HIV-1/*analysis ; Hippocampus/cytology ; Neurons/*drug effects/metabolism ; Nimodipine/pharmacology ; Rats ; Recombinant Proteins/pharmacology ; Retinal Ganglion Cells/drug effects/metabolism
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    Olfactory recognition: a simple memory system (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-11-30
    Description: Mice have an olfactory (pheromone) recognition memory located at the first relay in the sensory system. It is acquired with one-trial learning, contingent upon norepinephrine activation at mating, and lasts for several weeks. The mechanism involves Hebbian (association-dependent) changes in synaptic efficacy at dendrodendritic synapses in the accessory olfactory bulb. As a result of this memory, males made familiar by mating are recognized by the females, thereby mitigating pregnancy block. Such a memory function is biologically important to the female, as it is required to sustain pregnancy in the presence of her stud male's odors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brennan, P -- Kaba, H -- Keverne, E B -- New York, N.Y. -- Science. 1990 Nov 30;250(4985):1223-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Sub-Department of Animal Behaviour, University of Cambridge, United Kingdom.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2147078" target="_blank"〉PubMed〈/a〉
    Keywords: Amygdala/drug effects/physiology ; Animals ; Female ; Hypothalamus/physiology ; Lidocaine/pharmacology ; Male ; Memory/*physiology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred CBA ; N-Methylaspartate/antagonists & inhibitors/physiology ; Norepinephrine/physiology ; Olfactory Bulb/drug effects/physiology ; Olfactory Pathways/drug effects/physiology ; *Pheromones/urine ; Pregnancy ; Pregnancy, Animal/*physiology ; Receptors, N-Methyl-D-Aspartate/physiology ; Reproduction/physiology ; Smell/*physiology ; Synapses/physiology
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    Autonomous developmental control of human embryonic globin gene switching in transgenic mice (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-11-23
    Description: The mechanisms by which expression of the beta-like globin genes are developmentally regulated are under intense investigation. The temporal control of human embryonic (epsilon) globin expression was analyzed. A 3.7-kilobase (kb) fragment that contained the entire human epsilon-globin gene was linked to a 2.5-kb cassette of the locus control region (LCR), and the developmental time of expression of this construct was studied in transgenic mice. The human epsilon-globin transgene was expressed in yolk sac-derived primitive erythroid cells, but not in fetal liver or bone marrow-derived definitive erythroid cells. The absence of epsilon gene expression in definitive erythroid cells suggests that the developmental regulation of the epsilon-globin gene depends only on the presence of the LCR and the epsilon-globin gene itself (that is, an autonomous negative control mechanism). The autonomy of epsilon-globin gene developmental control distinguishes it from the competitive mechanism of regulation of gamma and beta-globin genes, and therefore, suggests that at least two distinct mechanisms function in human hemoglobin switching.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Raich, N -- Enver, T -- Nakamoto, B -- Josephson, B -- Papayannopoulou, T -- Stamatoyannopoulos, G -- DK 3132/DK/NIDDK NIH HHS/ -- HL 20899/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1990 Nov 23;250(4984):1147-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Medical Genetics, University of Washington, Seattle 98195.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2251502" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bone Marrow/embryology ; Bone Marrow Cells ; Erythroid Precursor Cells/metabolism ; Erythropoiesis ; Fetus/*metabolism ; *Gene Expression Regulation ; Globins/*genetics ; Hemoglobins/biosynthesis ; Humans ; Liver/cytology/embryology ; Mice ; Mice, Transgenic ; Regulatory Sequences, Nucleic Acid ; Yolk Sac/cytology
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    Transcription factor interactions: selectors of positive or negative regulation from a single DNA element (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-09-14
    Description: The mechanism by which a single factor evokes opposite regulatory effects from a specific DNA sequence is not well understood. In this study, a 25-base pair element that resides upstream of the mouse proliferin gene was examined; it conferred on linked promoters either positive or negative glucocorticoid regulation, depending upon physiological context. This sequence, denoted a "composite" glucocorticoid response element (GRE), was bound selectively in vitro both by the glucocorticoid receptor and by c-Jun and c-Fos, components of the phorbol ester-activated AP-1 transcription factor. Indeed, c-Jun and c-Fos served as selectors of hormone responsiveness: the composite GRE was inactive in the absence of c-Jun, whereas it conferred a positive glucocorticoid effect in the presence of c-Jun, and a negative glucocorticoid effect in the presence of c-Jun and relatively high levels of c-Fos. The receptor also interacted selectively with c-Jun in vitro. A general model for composite GRE action is proposed that invokes both DNA binding and protein-protein interactions by receptor and nonreceptor factors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Diamond, M I -- Miner, J N -- Yoshinaga, S K -- Yamamoto, K R -- New York, N.Y. -- Science. 1990 Sep 14;249(4974):1266-72.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Biophysics, University of California, San Francisco 94143-0448.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2119054" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cross-Linking Reagents ; DNA-Binding Proteins/physiology ; Gene Expression Regulation/genetics/*physiology ; Glucocorticoids/physiology ; Glycoproteins/*genetics ; HeLa Cells ; Humans ; Intercellular Signaling Peptides and Proteins ; Mice ; Molecular Sequence Data ; Proto-Oncogene Proteins/physiology ; Proto-Oncogene Proteins c-fos ; Proto-Oncogene Proteins c-jun ; Receptors, Glucocorticoid/metabolism ; Regulatory Sequences, Nucleic Acid/genetics ; Tetradecanoylphorbol Acetate/pharmacology ; Transcription Factors/*physiology ; Transcription, Genetic/drug effects
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    Recognizing self from nonself (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-06-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koshland, D E Jr -- New York, N.Y. -- Science. 1990 Jun 15;248(4961):1273.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2356462" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/immunology ; Humans ; *Immune Tolerance ; Mice ; Mice, Transgenic ; T-Lymphocytes/immunology
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    Induction by antigen of intrathymic apoptosis of CD4+CD8+TCRlo thymocytes in vivo (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-12-21
    Description: In order to examine the mechanisms by which clonal deletion of autoreactive T cells occurs, a peptide antigen was used to induce deletion of antigen-reactive thymocytes in vivo. Mice transgenic for a T cell receptor (TCR) that reacts to this peptide contain thymocytes that progress from the immature to the mature phenotype. Intraperitoneal administration of the peptide antigen to transgenic mice results in a rapid deletion of the immature CD4+ CD8+ TCRlo thymocytes. Apoptosis of cortical thymocytes can be seen within 20 hours of treatment. These results provide direct evidence for the in vivo role of apoptosis in the development of antigen-induced tolerance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Murphy, K M -- Heimberger, A B -- Loh, D Y -- New York, N.Y. -- Science. 1990 Dec 21;250(4988):1720-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, 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/2125367" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antigens, CD4/*immunology ; Antigens, CD8 ; Antigens, Differentiation, T-Lymphocyte/*immunology ; Mice ; Mice, Transgenic ; Microscopy, Electron ; Molecular Sequence Data ; Ovalbumin/immunology ; Phagocytosis ; Phenotype ; Receptors, Antigen, T-Cell/genetics/*immunology ; T-Lymphocytes/cytology/*immunology/ultrastructure ; Thymus Gland/cytology/*immunology
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    Tolerance in transgenic mice expressing major histocompatibility molecules extrathymically on pancreatic cells (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-06-15
    Description: Transgenic mice with defined expression of major histocompatibility complex (MHC) proteins provide novel systems for understanding the fundamental question of T cell tolerance to nonlymphoid self components. The MHC class II I-E and I-A and class I H-2K molecules expressed specifically on pancreatic islet or acinar cells serve as model self antigens. In these systems, transgenic proteins are not detected in the thymus or other lymphoid tissues. Yet mice are tolerant to the pancreatic MHC products in vivo; this tolerance is not induced by clonal deletion. These studies have been aided by monoclonal antibodies specific for I-E-reactive T cells and indicate that clonal anergy may be an important mechanism of tolerance to peripheral proteins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Burkly, L C -- Lo, D -- Flavell, R A -- New York, N.Y. -- Science. 1990 Jun 15;248(4961):1364-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Biogen Incorporated, 14 Cambridge Center, MA 02142.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1694042" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen-Presenting Cells/immunology ; Autoantigens/immunology ; CD4-Positive T-Lymphocytes/immunology ; Clone Cells/immunology ; Epitopes/immunology ; H-2 Antigens/immunology ; Histocompatibility Antigens/*immunology ; Histocompatibility Antigens Class II/immunology ; *Immune Tolerance ; Islets of Langerhans/*immunology ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Receptors, Antigen, T-Cell/immunology ; T-Lymphocytes/*immunology ; T-Lymphocytes, Regulatory/immunology ; Thymus Gland/immunology
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    Different tumor-derived p53 mutants exhibit distinct biological activities (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-10-05
    Description: In its wild-type form, the protein p53 can interfere with neoplastic processes. Tumor-derived cells often express mutant p53. Full-length mutant forms of p53 isolated so far from transformed mouse cells exhibit three common properties in vitro: loss of transformation-suppressing activity, gain of pronounced transforming potential, and ability to bind the heat shock protein cognate hsc70. A tumor-derived mouse p53 variant is now described, whose site of mutation corresponds to a hot spot for p53 in human tumors. While absolutely nonsuppressing, it is only weakly transforming and exhibits no detectable hsc70 binding. The data suggest that the ability of a p53 mutant to bind endogenous p53 is not the sole determinant of its oncogenic potential. The data also support the existence of gain-of-function p53 mutants.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Halevy, O -- Michalovitz, D -- Oren, M -- R01 CA40099/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1990 Oct 5;250(4977):113-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemical Immunology, Weizmann Institute of Science, Rehovot, Israel.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2218501" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Transformation, Neoplastic ; Cloning, Molecular ; Humans ; Mice ; *Mutation ; Nuclear Proteins/*genetics ; Plasmids ; Polymerase Chain Reaction ; RNA, Messenger/genetics ; Rats ; Transfection ; Tumor Suppressor Protein p53/*genetics/physiology
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    Flunarizine protects neurons from death after axotomy or NGF deprivation (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-06-15
    Description: Systemically administered flunarizine enhanced neuronal survival in lumbar sensory ganglia in newborn rats after axotomy. Flunarizine-treated rats lost 71 percent fewer neurons than the untreated control rats at the end of 1 week. In cell culture, flunarizine at 30 to 40 microM also prevented neuronal death in nerve growth factor-dependent embryonic sensory and sympathetic neurons after the abrupt withdrawal of neurotrophic support. The drug may cause this effect by acting at an intracellular site, one distinct from its blockade of voltage-dependent calcium channels.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rich, K M -- Hollowell, J P -- HL20604/HL/NHLBI NIH HHS/ -- NS18071/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1990 Jun 15;248(4961):1419-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurosurgery, 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/2356470" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Cell Survival/drug effects ; Cells, Cultured ; Dose-Response Relationship, Drug ; Flunarizine/administration & dosage/*pharmacology ; Ganglia, Spinal/cytology/embryology ; Ganglia, Sympathetic/cytology/embryology ; Microscopy, Electron, Scanning ; Nerve Crush ; Nerve Growth Factors/administration & dosage/*pharmacology ; Neurons/*cytology/drug effects ; Rats ; Sciatic Nerve/physiology/surgery
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    Tumor resistance to alkylating agents conferred by mechanisms operative only in vivo (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-03-23
    Description: EMT-6 murine mammary tumors were made resistant to cis-diamminedichloroplatinum (II) (CDDP), carboplatin, cyclophosphamide (CTX), or thiotepa in vivo by treatment of tumor-bearing animals with the drug during a 6-month period. In spite of high levels of in vivo resistance, no significant resistance was observed when the cells from these tumors were exposed to the drugs in vitro. The pharmacokinetics of CDDP and CTX were altered in animals bearing the respective resistant tumors. The resistance of all tumor lines except for the EMT-6/thiotepa decreased during 3 to 6 months in vivo passage in the absence of drugs. These results indicate that very high levels of resistance to anticancer drugs can develop through mechanisms that are expressed only in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Teicher, B A -- Herman, T S -- Holden, S A -- Wang, Y Y -- Pfeffer, M R -- Crawford, J W -- Frei, E 3rd -- P01-CA38497/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1990 Mar 23;247(4949 Pt 1):1457-61.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Dana-Farber Cancer Institute, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2108497" target="_blank"〉PubMed〈/a〉
    Keywords: Alkylating Agents/pharmacokinetics/*therapeutic use ; Animals ; Antineoplastic Agents/pharmacokinetics/*therapeutic use ; Carboplatin ; Cisplatin/therapeutic use ; Cyclophosphamide/therapeutic use ; Drug Resistance ; Kidney/metabolism ; Liver/metabolism ; Mammary Neoplasms, Experimental/*drug therapy/metabolism ; Mice ; Mice, Inbred BALB C ; Organoplatinum Compounds/therapeutic use ; Sulfhydryl Compounds/analysis ; Thiotepa/therapeutic use ; Tissue Distribution ; Tumor Cells, Cultured
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    Erythropoietin retards DNA breakdown and prevents programmed death in erythroid progenitor cells (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-04-20
    Description: The mechanism by which erythropoietin controls mammalian erythrocyte production is unknown. Labeling experiments in vitro with [3H]thymidine demonstrated DNA cleavage in erythroid progenitor cells that was accompanied by DNA repair and synthesis. Erythropoietin reduced DNA cleavage by a factor of 2.6. In the absence of erythropoietin, erythroid progenitor cells accumulated DNA cleavage fragments characteristic of those found in programmed cell death (apoptosis) by 2 to 4 hours and began dying by 16 hours. In the presence of erythropoietin, the progenitor cells survived and differentiated into reticulocytes. Thus, apoptosis is a major component of normal erythropoiesis, and erythropoietin controls erythrocyte production by retarding DNA breakdown and preventing apoptosis in erythroid progenitor cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koury, M J -- Bondurant, M C -- DK 31513/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1990 Apr 20;248(4953):378-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Hematology, Vanderbilt University Medical Center, Nashville, TN.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2326648" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; DNA/biosynthesis/*drug effects/metabolism ; DNA Repair ; Erythrocyte Aging/drug effects ; Erythroid Precursor Cells/cytology/drug effects/*metabolism ; Erythropoietin/*pharmacology ; Friend murine leukemia virus ; Leukemia, Erythroblastic, Acute ; Mice ; Molecular Weight
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    An insulin-stimulated protein kinase similar to yeast kinases involved in cell cycle control (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-07-06
    Description: A protein kinase characterized by its ability to phosphorylate microtubule-associated protein-2 (MAP2), is thought to be an early intermediate in an insulin-stimulated phosphorylation cascade and in a variety of other mammalian cell responses to extracellular signals. A complementary DNA that encodes this protein serine-threonine kinase has been cloned, and the protein designated extracellular signal-regulated kinase 1 (ERK1). ERK1 has striking similarity to two protein kinases, KSS1 and FUS3, from yeast. The yeast kinases function in an antagonistic manner to regulate the cell cycle in response to mating factors. Thus, ERK1 and the two yeast kinases constitute a family of evolutionarily conserved enzymes involved in regulating the response of eukaryotic cells to extracellular signals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Boulton, T G -- Yancopoulos, G D -- Gregory, J S -- Slaughter, C -- Moomaw, C -- Hsu, J -- Cobb, M H -- DK 01918/DK/NIDDK NIH HHS/ -- DK 34128/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1990 Jul 6;249(4964):64-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of Texas Southwestern Graduate School of Biomedical Sciences, Dallas 75235.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2164259" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Calcium-Calmodulin-Dependent Protein Kinases ; Cell Cycle/*physiology ; Cell Line ; Central Nervous System/*enzymology ; DNA/*genetics ; Fibroblasts/enzymology ; Humans ; Insulin/pharmacology ; Mitogen-Activated Protein Kinase 3 ; *Mitogen-Activated Protein Kinases ; Molecular Sequence Data ; Phosphorylation ; Protein Kinases/genetics/*metabolism ; Rats ; Receptor, Insulin/metabolism ; Yeasts/enzymology
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    Target control of collateral extension and directional axon growth in the mammalian brain (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-01-12
    Description: Individual neurons in the brain send their axons over considerable distances to multiple targets, but the mechanisms governing this process are unresolved. An amenable system for studying axon outgrowth, branching, and target selection is the mammalian corticopontine projection. This major connection develops from parent corticospinal axons that have already grown past the pons, by a delayed interstitial budding of collateral branches that then grow directly into their target, the basilar pons. When cocultured with explants of developing cortex in three-dimensional collagen matrices, the basilar pons elicits the formation and directional growth of cortical axon collaterals across the intervening matrix. This effect appears to be target-specific and selectively influences neurons in the appropriate cortical layer. These in vitro findings provide evidence that the basilar pons becomes innervated by controlling at a distance the budding and directed ingrowth of cortical axon collaterals through the release of a diffusible, chemotropic molecule.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Heffner, C D -- Lumsden, A G -- O'Leary, D D -- EY07025/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 1990 Jan 12;247(4939):217-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy and Neurobiology, Washington University School of Medicine, St. Louis, MO 63110.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2294603" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/*physiology/ultrastructure ; Cerebral Cortex/growth & development/*ultrastructure ; Culture Techniques ; Fluorescent Dyes ; Motor Cortex/ultrastructure ; Nerve Growth Factors/physiology ; Neural Pathways/growth & development/ultrastructure ; Pons/*physiology/ultrastructure ; Rats ; Spinal Cord/ultrastructure ; Visual Cortex/ultrastructure
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    Alteration of alpha 1 Na+,K(+)-ATPase 86Rb+ influx by a single amino acid substitution (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-08-31
    Description: The sodium- and potassium-dependent adenosine triphosphatase (Na+,K(+)-ATPase) maintains the transmembrane Na+ gradient to which is coupled all active cellular transport systems. The R and S alleles of the gene encoding the Na+,K(+)-ATPase alpha 1 subunit isoform were identified in Dahl salt-resistant (DR) and Dahl salt-sensitive (DS) rats, respectively. Characterization of the S allele-specific Na+,K(+)-ATPase alpha 1 complementary DNA identified a leucine substitution of glutamine at position 276. This mutation alters the hydropathy profile of a region in proximity to T3(Na), the trypsin-sensitive site that is only detected in the presence of Na+. This mutation causes a decrease in the rubidium-86 influx of S allele-specific sodium pumps, thus marking a domain in the Na+,K(+)-ATPase alpha subunit important for K+ transport, and supporting the hypothesis of a putative role of these pumps in hypertension.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Herrera, V L -- Ruiz-Opazo, N -- HL 01967/HL/NHLBI NIH HHS/ -- HL 18318/HL/NHLBI NIH HHS/ -- HL 39267/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1990 Aug 31;249(4972):1023-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Molecular Genetics, Whitaker Cardiovascular Institute, Boston University School of Medicine, MA 02118.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1975705" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cell Membrane/enzymology ; Kidney/enzymology ; Kinetics ; Molecular Sequence Data ; *Mutation ; Polymorphism, Restriction Fragment Length ; Protein Conformation ; Rats ; Rats, Inbred Strains ; Rubidium/*metabolism ; Rubidium Radioisotopes ; Sodium-Potassium-Exchanging ATPase/*genetics/metabolism
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    Molecular characterization of a functional cDNA encoding the rat substance P receptor (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-02-23
    Description: Substance P is a member of the tachykinin peptide family and participates in the regulation of diverse biological processes. The polymerase chain reaction and conventional library screening were used to isolate a complementary DNA (cDNA) encoding the rat substance P receptor from brain and submandibular gland. By homology analysis, this receptor belongs to the G protein-coupled receptor superfamily. The receptor cDNA was expressed in a mammalian cell line and the ligand binding properties of the encoded receptor were pharmacologically defined by Scatchard analysis and tachykinin peptide displacement as those of a substance P receptor. The distribution of the messenger RNA for this receptor is highest in urinary bladder, submandibular gland, striatum, and spinal cord, which is consistent with the known distribution of substance P receptor binding sites. Thus, this receptor appears to mediate the primary actions of substance P in various brain regions and peripheral tissues.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hershey, A D -- Krause, J E -- NS21937/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1990 Feb 23;247(4945):958-62.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy and Neurobiology, Washington University School of Medicine, St. Louis, MO 63110.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2154852" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Brain Chemistry ; Cloning, Molecular ; DNA/*genetics/isolation & purification ; GTP-Binding Proteins/metabolism ; Gene Expression ; Intestine, Small/analysis ; Molecular Sequence Data ; Nucleic Acid Hybridization ; Polymerase Chain Reaction ; RNA, Messenger/analysis ; Rats ; Receptors, Neurokinin-1 ; Receptors, Neurotransmitter/*genetics ; Sequence Homology, Nucleic Acid ; Submandibular Gland/analysis ; Tissue Distribution ; Urinary Bladder/analysis
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    A cytoplasmic protein inhibits the GTPase activity of H-Ras in a phospholipid-dependent manner (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-11-16
    Description: A cytoplasmic protein has been identified that inhibits the guanosine triphosphatase (GTPase) activity of bacterially synthesized, cellular H-Ras protein. This GTPase inhibiting protein is able to counteract the activity of GTPase activating protein (GAP), which has been postulated to function as a negative regulator of Ras activity. The potential biological importance of the GTPase inhibiting protein is further supported by its interaction with lipids. Phospholipids produced in cells as a consequence of mitogenic stimulation increase the activity of the GTPase inhibiting protein, as well as inhibit the activity of GAP. The interaction of such lipids with each of these two regulatory proteins would, therefore, tend to increase the biological activity of Ras and stimulate cell proliferation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tsai, M H -- Yu, C L -- Stacey, D W -- CA 48662/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1990 Nov 16;250(4983):982-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Cleveland Clinic Foundation 44195.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2237442" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Division ; Dose-Response Relationship, Drug ; GTP Phosphohydrolases/*antagonists & inhibitors ; GTPase-Activating Proteins ; Mice ; Phospholipids/*pharmacology ; Proteins/antagonists & inhibitors ; Proto-Oncogene Proteins p21(ras)/*antagonists & inhibitors ; ras GTPase-Activating Proteins
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    Increased activity of calcium leak channels in myotubes of Duchenne human and mdx mouse origin (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-11-02
    Description: Elevated free Ca2+ concentrations found in adult dystrophic muscle fibers result in enhanced protein degradation. Since the difference in concentrations may reflect differences in entry, Ca2+ leak channels in cultures of normal and Duchenne human myotubes, and normal and mdx murine myotubes, have been identified and characterized. The open probability of leak channels is markedly increased in dystrophic myotubes. Other channel properties, such as mean open times, single channel conductance, ion selectivity, and behavior in the presence of pharmacological agents, were similar among myotube types. Compared to the Ca2+ concentrations in normal human and normal mouse myotubes, intracellular resting free Ca2+ concentrations ([Ca2+]i) in myotubes of Duchenne and mdx origin were significantly higher at a time when dystrophin is first expressed in normal tissue. Taken together, these findings suggest that the increased open probability of Ca2+ leak channels contributes to the elevated free intracellular Ca2+ concentration in Duchenne human and mdx mouse myotubes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fong, P Y -- Turner, P R -- Denetclaw, W F -- Steinhardt, R A -- New York, N.Y. -- Science. 1990 Nov 2;250(4981):673-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cell Biology, University of California, Berkeley 94720.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2173137" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/*metabolism ; Calcium Channels/drug effects/*physiology ; Dystrophin/genetics ; Humans ; Membrane Potentials ; Mice ; Muscles/metabolism ; Muscular Dystrophies/*metabolism ; Muscular Dystrophy, Animal/*metabolism ; Nifedipine/pharmacology
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    Tumorigenicity in human melanoma cell lines controlled by introduction of human chromosome 6 (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-02-02
    Description: Chromosome banding analysis of human malignant melanoma has documented the nonrandom alteration of chromosome 6. To determine the relevance of chromosome 6 abnormalities in melanoma, a normal chromosome 6 was directly introduced into melanoma cell lines. The resulting (+6) microcell hybrids were significantly altered in their phenotypic properties in culture and lost their ability to form tumors in nude mice. The loss of the chromosome 6 from melanoma microcell hybrids resulted in the reversion to tumorigenicity of these cells in mice. The introduction of the selectable marker (psv2neo) alone into melanoma cell lines had no effect on tumorigenicity. These results support the idea that one or more genes on chromosome 6 may control the malignant expression of human melanoma.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Trent, J M -- Stanbridge, E J -- McBride, H L -- Meese, E U -- Casey, G -- Araujo, D E -- Witkowski, C M -- Nagle, R B -- CA-19104/CA/NCI NIH HHS/ -- CA-23074/CA/NCI NIH HHS/ -- R37-CA-29476/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1990 Feb 2;247(4942):568-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of Arizona, Arizona Cancer Center, Tucson 85724.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2300817" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Division ; Cell Line ; Chromosome Aberrations ; Chromosome Banding ; *Chromosomes, Human, Pair 6 ; Humans ; Hybrid Cells/cytology ; Karyotyping ; Melanoma/*genetics/pathology ; Mice ; Phenotype ; Transplantation, Heterologous
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    Light-evoked changes in the interphotoreceptor matrix (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-06-29
    Description: The normal function of vertebrate photoreceptor cells depends on multiple interactions and transfer of substances between the photoreceptors and the retinal pigment epithelium (RPE), but the mechanisms of these interactions are poorly understood. Many are thought to be mediated by the interphotoreceptor matrix (IPM), a complex extracellular matrix that surrounds the photoreceptors and lies between them and the RPE. Histochemical, immunocytochemical, and lectin probes for several IPM constituents revealed that components of the IPM in the rat undergo a major shift in distribution or molecular conformation after the transition between light and dark. In the light, various IPM constituents concentrated in bands at the apical and basal regions of the outer segment zone; in the dark, they distributed much more uniformly throughout the zone. The change in IPM distribution was triggered by the light-dark transition; it was not a circadian event, and it was not driven by a systemic factor. The light-evoked change in IPM distribution may facilitate the transfer of substances between the photoreceptors and the RPE.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Uehara, F -- Matthes, M T -- Yasumura, D -- LaVail, M M -- EYO1919/EY/NEI NIH HHS/ -- EYO2162/EY/NEI NIH HHS/ -- EYO6842/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 1990 Jun 29;248(4963):1633-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy, University of California, San Francisco 94143.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2194288" target="_blank"〉PubMed〈/a〉
    Keywords: Albinism ; Animals ; Darkness ; Extracellular Matrix/physiology ; *Fluorescein-5-isothiocyanate/*analogs & derivatives ; Fluoresceins ; Glycoconjugates/analysis ; Immunoenzyme Techniques ; Immunohistochemistry ; In Vitro Techniques ; Light ; Photoreceptor Cells/*physiology/radiation effects ; Pigment Epithelium of Eye/cytology/*physiology ; Rats ; Rats, Inbred F344 ; Retina/cytology/*physiology/radiation effects ; Rod Cell Outer Segment/physiology ; Sialic Acids/analysis ; Wheat Germ Agglutinins
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    Inhibition of leishmanias but not host macrophages by the antitubulin herbicide trifluralin (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-08-24
    Description: The dinitroaniline herbicide trifluralin (alpha, alpha, alpha-trifluoro-2,6-dinitro-N, N-dipropyl-p-toluidine), at micromolar concentrations, selectively inhibited both proliferation and differentiation of the parasitic protozoan Leishmania mexicana amazonensis. In vitro, radioactive trifluralin showed specific binding to leishmania tubulin but not to mammalian tubulin. Because herbicides such as trifluralin are economical and are considered safe for man and domesticated animals, they may serve as useful sources of potential antiparasitic agents.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chan, M M -- Fong, D -- AI 21364/AI/NIAID NIH HHS/ -- CA 49359/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1990 Aug 24;249(4971):924-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, Rutgers, State University of New Jersey, Piscataway 08855.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2392684" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Division/drug effects ; Cell Line ; Leishmania mexicana/drug effects/*growth & development ; Macrophages/drug effects/*physiology ; Protein Binding ; Rats ; Species Specificity ; Toluidines/*pharmacology ; Trifluralin/metabolism/*pharmacology ; Tubulin/metabolism ; *Tubulin Modulators ; Tumor Cells, Cultured/cytology/drug effects
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    Cloning and expression of a developmentally regulated protein that induces mitogenic and neurite outgrowth activity (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-12-21
    Description: A heparin binding mitogenic protein isolated from bovine uterus shares NH2-terminal amino acid sequence with a protein isolated from newborn rat brain. The cDNA's of the bovine, human, and rat genes have been isolated and encode extraordinarily conserved proteins unrelated to known growth or neurotrophic factors, although identity of nearly 50 percent has been found with the predicted sequence of a retinoic acid induced transcript in differentiating mouse embryonal carcinoma cells. Lysates of COS-7 cells transiently expressing this protein were mitogenic for NRK cells and initiated neurite outgrowth from mixed cultures of embryonic rat brain cells. RNA transcripts encoding this protein were widely distributed in tissues and were developmentally regulated. This protein, previously designated as heparin binding growth factor (HBGF)-8, is now renamed pleiotrophin (PTN) to reflect its diverse activities. PTN may be the first member of a family of developmentally regulated cytokines.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Y S -- Milner, P G -- Chauhan, A K -- Watson, M A -- Hoffman, R M -- Kodner, C M -- Milbrandt, J -- Deuel, T F -- CA49712/CA/NCI NIH HHS/ -- HL14147/HL/NHLBI NIH HHS/ -- HL31102/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1990 Dec 21;250(4988):1690-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Jewish Hospital, Washington University Medical Center, St. Louis, MO 63110.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2270483" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Axons/*physiology/ultrastructure ; Base Sequence ; Brain/*metabolism ; *Carrier Proteins ; Cattle ; Cell Division ; Cell Line ; Cloning, Molecular ; Cytokines/*genetics ; Humans ; Mitogens/*genetics ; Molecular Sequence Data ; Organ Specificity ; Rats ; Sequence Homology, Nucleic Acid ; Transfection
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    Structural mutations of the T cell receptor zeta chain and its role in T cell activation (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-07-13
    Description: T cell hybridomas that express zeta zeta, but not zeta eta, dimers in their T cell receptors (TCRs) produce interleukin-2 (IL-2) and undergo an inhibition of spontaneous growth when activated by antigen, antibodies to the receptor, or antibodies to Thy-1. Hybridomas without zeta and eta were reconstituted with mutated zeta chains. Cytoplasmic truncations of up to 40% of the zeta molecule reconstituted normal surface assembly of TCRs, but antigen-induced IL-2 secretion and growth inhibition were lost. In contrast, cross-linking antibodies to the TCR activated these cells. A point mutation conferred the same signaling phenotype as did the truncations and caused defective antigen-induced tyrosine kinase activation. Thus zeta allows the binding of antigen/major histocompatibility complex (MHC) to alpha beta to effect TCR signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Frank, S J -- Niklinska, B B -- Orloff, D G -- Mercep, M -- Ashwell, J D -- Klausner, R D -- New York, N.Y. -- Science. 1990 Jul 13;249(4965):174-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cell Biology and Metabolism Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2371564" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cross-Linking Reagents ; Dose-Response Relationship, Immunologic ; Hybridomas ; Immunity, Cellular ; Immunoblotting ; Interleukin-2/*biosynthesis ; Ligands ; *Lymphocyte Activation ; Major Histocompatibility Complex ; Mice ; Molecular Sequence Data ; Mutation ; Peptide Fragments/genetics/*immunology ; Precipitin Tests ; Receptors, Antigen, T-Cell/genetics/*immunology ; Signal Transduction ; T-Lymphocytes/*immunology ; Transfection
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    Fetal brain grafts and Parkinson's disease (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-12-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉New York, N.Y. -- Science. 1990 Dec 7;250(4986):1434-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2255915" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenal Medulla/transplantation ; Animals ; Brain Tissue Transplantation/*physiology ; Disease Models, Animal ; Fetal Tissue Transplantation/*physiology ; Humans ; Parkinson Disease/physiopathology/*surgery ; Rats
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    Cell proliferation in carcinogenesis (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-08-31
    Description: Chemicals that induce cancer at high doses in animal bioassays often fail to fit the traditional characterization of genotoxins. Many of these nongenotoxic compounds (such as sodium saccharin) have in common the property that they increase cell proliferation in the target organ. A biologically based, computerized description of carcinogenesis was used to show that the increase in cell proliferation can account for the carcinogenicity of nongenotoxic compounds. The carcinogenic dose-response relationship for genotoxic chemicals (such as 2-acetylaminofluorene) was also due in part to increased cell proliferation. Mechanistic information is required for determination of the existence of a threshold for the proliferative (and carcinogenic) response of nongenotoxic chemicals and the estimation of risk for human exposure.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, S M -- Ellwein, L B -- CA28015/CA/NCI NIH HHS/ -- CA32513/CA/NCI NIH HHS/ -- CA36727/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1990 Aug 31;249(4972):1007-11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha 68198.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2204108" target="_blank"〉PubMed〈/a〉
    Keywords: 2-Acetylaminofluorene/metabolism/toxicity ; Animals ; Carcinogens/pharmacology/*toxicity ; Cell Division/*drug effects ; Humans ; Liver/metabolism ; Liver Neoplasms/chemically induced ; Mice ; Mitotic Index/drug effects ; Rats ; Saccharin/toxicity ; Urinary Bladder Neoplasms/chemically induced
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  • 139
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    Secretion of neurotoxins by mononuclear phagocytes infected with HIV-1 (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-12-14
    Description: Mononuclear phagocytes (microglia, macrophages, and macrophage-like giant cells) are the principal cellular targets for human immunodeficiency virus-1 (HIV-1) in the central nervous system (CNS). Since HIV-1 does not directly infect neurons, the causes for CNS dysfunction in acquired immunodeficiency syndrome (AIDS) remain uncertain. HIV-1-infected human monocytoid cells, but not infected human lymphoid cells, released toxic agents that destroy chick and rat neurons in culture. These neurotoxins were small, heat-stable, protease-resistant molecules that act by way of N-methyl-D-aspartate receptors. Macrophages and microglia infected with HIV-1 may produce neurologic disease through chronic secretion of neurotoxic factors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Giulian, D -- Vaca, K -- Noonan, C A -- NS 25637/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1990 Dec 14;250(4987):1593-6.〈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/2148832" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Assay ; Cell Line ; Cell Survival/*drug effects ; Chick Embryo ; Culture Media/analysis ; HIV-1/*physiology ; Humans ; Intermediate Filaments ; Lymphocytes/microbiology/physiology ; Macrophages/microbiology/physiology ; Monocytes/microbiology/physiology ; N-Methylaspartate/*analogs & derivatives ; Neuroglia/microbiology/physiology ; Neurons/cytology/drug effects/*physiology ; Phagocytes/microbiology/*physiology ; Rats ; Receptors, N-Methyl-D-Aspartate/*physiology ; Spinal Cord/cytology
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  • 140
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    Behavioral effects of progesterone associated with rapid modulation of oxytocin receptors (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-11-02
    Description: The ventromedial nuclei of the hypothalamus (VMN) are important for the control of feminine mating behavior, and hormone action within these nuclei has been causally related to behavior. Estradiol induces receptors for oxytocin in the VMN and in the area lateral to these nuclei over the course of 1 to 2 days, and progesterone causes, within 30 minutes of its application, a further increase in receptor binding and an expansion of the area covered by these receptors lateral to the VMN. The rapid progesterone effect appears to be a direct and specific effect of this steroid on the receptor or membrane, because it was produced in vitro as well as in vivo and was not mimicked by a variety of other steroids. The effect of progesterone occurred in the posterior part of the VMN, where oxytocin infusion facilitated feminine mating behavior; it did not take place in the anterior part of the VMN, where oxytocin infusion had no effect on mating behavior.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schumacher, M -- Coirini, H -- Pfaff, D W -- McEwen, B S -- HD-05751/HD/NICHD NIH HHS/ -- NS-07080/NS/NINDS NIH HHS/ -- TWO4103/TW/FIC NIH HHS/ -- New York, N.Y. -- Science. 1990 Nov 2;250(4981):691-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Neuroendocrinology, Rockefeller University, New York, NY 10021.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2173139" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Estradiol/pharmacology ; Female ; Oxytocin/pharmacology ; Progesterone/*pharmacology ; Rats ; Receptors, Angiotensin/*drug effects/metabolism ; Receptors, Oxytocin ; Sexual Behavior, Animal/*drug effects ; Ventromedial Hypothalamic Nucleus/*drug effects
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  • 141
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    Soluble human complement receptor type 1: in vivo inhibitor of complement suppressing post-ischemic myocardial inflammation and necrosis (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-07-13
    Description: The complement system is an important mediator of the acute inflammatory response, and an effective inhibitor would suppress tissue damage in many autoimmune and inflammatory diseases. Such an inhibitor might be found among the endogenous regulatory proteins of complement that block the enzymes that activate C3 and C5. Of these proteins, complement receptor type 1 (CR1; CD35) has the most inhibitory potential, but its restriction to a few cell types limits its function in vivo. This limitation was overcome by the recombinant, soluble human CR1, sCR1, which lacks the transmembrane and cytoplasmic domains. The sCR1 bivalently bound dimeric forms of its ligands, C3b and methylamine-treated C4 (C4-ma), and promoted their inactivation by factor I. In nanomolar concentrations, sCR1 blocked complement activation in human serum by the two pathways. The sCR1 had complement inhibitory and anti-inflammatory activities in a rat model of reperfusion injury of ischemic myocardium, reducing myocardial infarction size by 44 percent. These findings identify sCR1 as a potential agent for the suppression of complement-dependent tissue injury in autoimmune and inflammatory diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weisman, H F -- Bartow, T -- Leppo, M K -- Marsh, H C Jr -- Carson, G R -- Concino, M F -- Boyle, M P -- Roux, K H -- Weisfeldt, M L -- Fearon, D T -- New York, N.Y. -- Science. 1990 Jul 13;249(4965):146-51.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, The 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/2371562" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autoimmune Diseases/*immunology/pathology ; Complement Activation ; Complement C3/antagonists & inhibitors ; Complement C3b Inactivator Proteins/pharmacology ; Complement C4b/antagonists & inhibitors ; Complement C5/antagonists & inhibitors ; Complement Inactivator Proteins/*pharmacology/ultrastructure ; Disease Models, Animal ; Myocardial Reperfusion Injury/*immunology/pathology/prevention & control ; Myocardium/*pathology ; Necrosis ; Rats ; Receptors, Complement/*pharmacology/ultrastructure ; Recombinant Proteins/pharmacology
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  • 142
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    Transmission between pairs of hippocampal slice neurons: quantal levels, oscillations, and LTP (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-05-03
    Description: Long-term potentiation (LTP) of synaptic transmission after coincident pre- and postsynaptic activity is considered a cellular model of changes underlying learning and memory. In intact tissue, LTP has been observed only between populations of neurons, making analysis of mechanisms difficult. Transmission between individual pre- and postsynaptic hippocampal cells was studied, suggesting quantal amplitude distributions with little variability in quantal size. LTP between such pairs is manifested by large, persistent, and synapse-specific potentiation with a shift in amplitude distribution that suggests presynaptic changes. Oscillations in amplitude of transmission, apparently of presynaptic origin, are common and can be triggered by LTP.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Malinow, R -- New York, N.Y. -- Science. 1991 May 3;252(5006):722-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Physiology, Stanford University, CA 94305.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1850871" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Electric Conductivity ; Electrophysiology ; Hippocampus/*cytology ; Kinetics ; Membrane Potentials ; Neurons/*physiology ; Rats ; Statistics as Topic ; Synapses/*physiology ; Synaptic Transmission/*physiology
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  • 143
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    Atomic structure of adenosine deaminase complexed with a transition-state analog: understanding catalysis and immunodeficiency mutations (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-05-31
    Description: The crystal structure of a murine adenosine deaminase complexed with 6-hydroxyl-1,6-dihydropurine ribonucleoside, a nearly ideal transition-state analog, has been determined and refined at 2.4 angstrom resolution. The structure is folded as an eight-stranded parallel alpha/beta barrel with a deep pocket at the beta-barrel COOH-terminal end wherein the inhibitor and a zinc are bound and completely sequestered. The presence of the zinc cofactor and the precise structure of the bound analog were not previously known. The 6R isomer of the analog is very tightly held in place by the coordination of the 6-hydroxyl to the zinc and the formation of nine hydrogen bonds. On the basis of the structure of the complex a stereoselective addition-elimination or SN2 mechanism of the enzyme is proposed with the zinc atom and the Glu and Asp residues playing key roles. A molecular explanation of a hereditary disease caused by several point mutations of an enzyme is also presented.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wilson, D K -- Rudolph, F B -- Quiocho, F A -- CA14030/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1991 May 31;252(5010):1278-84.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Baylor College of Medicine, Houston, TX 77030.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1925539" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Deaminase/*chemistry/deficiency/metabolism ; Amino Acid Sequence ; Animals ; Binding Sites ; Catalysis ; Crystallization ; Immunologic Deficiency Syndromes/*enzymology/genetics ; Mice ; Models, Molecular ; Molecular Structure ; Mutation ; Protein Conformation ; Purine Nucleosides/chemistry/*metabolism ; Ribonucleosides/chemistry/*metabolism ; Zinc/metabolism
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  • 144
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    Primary structure and functional expression of the 5HT3 receptor, a serotonin-gated ion channel (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-10-18
    Description: The neurotransmitter serotonin (5HT) activates a variety of second messenger signaling systems and through them indirectly regulates the function of ion channels. Serotonin also activates ion channels directly, suggesting that it may also mediate rapid, excitatory responses. A complementary DNA clone containing the coding sequence of one of these rapidly responding channels, a 5HT3 subtype of the serotonin receptor, has been isolated by screening a neuroblastoma expression library for functional expression of serotonin-gated currents in Xenopus oocytes. The predicted protein product has many of the features shared by other members of the ligand-gated ion channel family. The pharmacological and electrophysiological characteristics of the cloned receptor are largely consistent with the properties of native 5HT3 receptors. Messenger RNA encoding this receptor is found in the brain, spinal cord, and heart. This receptor defines a new class of excitatory ligand-gated channels.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Maricq, A V -- Peterson, A S -- Brake, A J -- Myers, R M -- Julius, D -- GM44298/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1991 Oct 18;254(5030):432-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of California, San Francisco 94143-0450.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1718042" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Binding, Competitive ; Cell Line ; Ion Channels/*chemistry/drug effects/physiology ; Mice ; Molecular Sequence Data ; Oocytes/metabolism ; Poly A ; RNA, Messenger ; Radioligand Assay ; Receptors, Serotonin/*chemistry/drug effects/physiology ; Xenopus
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  • 145
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    The trk proto-oncogene product: a signal transducing receptor for nerve growth factor (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-04-26
    Description: The trk proto-oncogene encodes a 140-kilodalton, membrane-spanning protein tyrosine kinase (p140prototrk) that is expressed only in neural tissues. Nerve growth factor (NGF) stimulates phosphorylation of p140prototrk in neural cell lines and in embryonic dorsal root ganglia. Affinity cross-linking and equilibrium binding experiments with 125I-labeled NGF indicate that p140prototrk binds NGF specifically in cultured cells with a dissociation constant of 10(-9) molar. The identification of p140prototrk as an NGF receptor indicates that this protein participates in the primary signal transduction mechanism of NGF.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaplan, D R -- Hempstead, B L -- Martin-Zanca, D -- Chao, M V -- Parada, L F -- N01-CO-74101/CO/NCI NIH HHS/ -- New York, N.Y. -- Science. 1991 Apr 26;252(5005):554-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Eukaryotic Signal Transduction Group, National Cancer Institute-Frederick Cancer Research and Development Center, MD 21702.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1850549" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cell Membrane/physiology ; Cross-Linking Reagents ; Embryo, Mammalian ; Ganglia, Spinal/*metabolism ; Humans ; Kinetics ; Mice ; Nerve Growth Factors/metabolism/*physiology ; Neuroblastoma ; Protein-Tyrosine Kinases/*metabolism ; Proto-Oncogene Proteins/*metabolism ; *Proto-Oncogenes ; Receptor, trkA ; Receptors, Cell Surface/metabolism/*physiology ; Receptors, Nerve Growth Factor ; *Signal Transduction
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  • 146
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    Oscillations of cytosolic sodium during calcium oscillations in exocrine acinar cells (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-11-15
    Description: In acinar cells from rat salivary glands, cholinergic agonists cause oscillations in cytoplasmic free calcium concentration, which then drive oscillations of cell volume that reflect oscillating cell solute content and fluid secretion. By quantitative fluorescence ratio microscopy of an intracellular indicator dye for sodium, it has now been shown that large amplitude oscillations of sodium concentration were associated with the calcium and cell volume oscillations. Both calcium and sodium oscillations were dependent on the continued presence of calcium in the extracellular medium and were abolished by the specific sodium-potassium adenosine triphosphatase inhibitor ouabain. Thus, calcium oscillations in salivary acinar cells, by modulating the activities of ion transport pathways in the plasma membrane, can cause significant oscillations of monovalent ions that may in turn feed back to regulate calcium oscillations and fluid secretion.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wong, M M -- Foskett, J K -- New York, N.Y. -- Science. 1991 Nov 15;254(5034):1014-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Cell Biology, Research Institute, Hospital for Sick Children, Toronto, Ontario, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1948071" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/*physiology ; Chlorides/physiology ; Cytosol/physiology ; In Vitro Techniques ; Male ; Ouabain/pharmacology ; Parotid Gland/*physiology ; Periodicity ; Potassium/physiology ; Rats ; Rats, Inbred Strains ; Sodium/*physiology ; Water-Electrolyte Balance
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  • 147
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    Effect of light chain V region duplication on IgG oligomerization and in vivo efficacy (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-05-03
    Description: A human immunoglobulin G1 (IgG1) antibody oligomer was isolated from a transfected myeloma cell line that produced a monoclonal antibody to group B streptococci. Compared to the IgG1 monomer, the oligomer was significantly more effective at protecting neonatal rats from infection in vivo. The oligomer was also shown to cross the placenta and to be stable in neonatal rats. Immunochemical analysis and complementary DNA sequencing showed that the transfected cell line produced two distinct kappa light chains: a normal light chain (Ln) with a molecular mass of 25 kilodaltons and a 37-kilodalton species (L37), the domain composition of which was variable-variable-constant (V-V-C). Cotransfection of vectors encoding the heavy chain and L37 resulted in production of oligomeric IgG.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shuford, W -- Raff, H V -- Finley, J W -- Esselstyn, J -- Harris, L J -- New York, N.Y. -- Science. 1991 May 3;252(5006):724-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immune Sciences, Bristol-Myers Squibb Pharmaceutical Research Institute-Seattle, WA 98121.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1902593" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Antibodies, Bacterial/biosynthesis/immunology/pharmacokinetics ; Antibodies, Monoclonal/biosynthesis/immunology/pharmacokinetics ; Cell Line ; Female ; Humans ; Immunization, Passive ; Immunoglobulin G/*biosynthesis/genetics/immunology ; Immunoglobulin M/genetics ; Immunoglobulin Variable Region/*biosynthesis/genetics/immunology ; Immunoglobulin kappa-Chains/*biosynthesis/genetics/immunology ; Macromolecular Substances ; Maternal-Fetal Exchange ; Multiple Myeloma ; Pregnancy ; Rats ; Streptococcal Infections/prevention & control ; Streptococcus agalactiae/immunology ; Transfection
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  • 148
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    Carcinogenesis models (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-01-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉New York, N.Y. -- Science. 1991 Jan 11;251(4990):142-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1987635" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Carcinogenicity Tests ; Cell Division ; Mathematics ; Mice ; Mitosis
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    OPC-21268, an orally effective, nonpeptide vasopressin V1 receptor antagonist (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-04-26
    Description: An orally effective, nonpeptide, vasopressin V1 receptor antagonist, OPC-21268, has been identified. This compound selectively antagonized binding to the V1 subtype of the vasopressin receptor in a competitive manner. In vivo, the compound acted as a specific antagonist of arginine vasopressin (AVP)-induced vasoconstriction. After oral administration in conscious rats, the compound also antagonized pressor responses to AVP. OPC-21268 can be used to study the physiological role of AVP and may be therapeutically useful in the treatment of hypertension and congestive heart failure.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yamamura, Y -- Ogawa, H -- Chihara, T -- Kondo, K -- Onogawa, T -- Nakamura, S -- Mori, T -- Tominaga, M -- Yabuuchi, Y -- New York, N.Y. -- Science. 1991 Apr 26;252(5005):572-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Second Tokushima Institute of New Drug Research, Otsuka Pharmaceutical Co., Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1850553" target="_blank"〉PubMed〈/a〉
    Keywords: Administration, Oral ; Angiotensin II/pharmacology ; Animals ; Arginine Vasopressin/antagonists & inhibitors/metabolism/*pharmacology ; Binding, Competitive ; Blood Pressure/*drug effects ; Cell Membrane/metabolism ; Kidney/metabolism ; Kinetics ; Liver/metabolism ; Norepinephrine/pharmacology ; Piperidines/administration & dosage/*pharmacology ; Quinolones/administration & dosage/*pharmacology ; Rats ; Receptors, Angiotensin/*drug effects/metabolism ; Receptors, Vasopressin ; Time Factors
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  • 150
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    The anion paradox in sodium taste reception: resolution by voltage-clamp studies (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-11-01
    Description: Sodium salts are potent taste stimuli, but their effectiveness is markedly dependent on the anion, with chloride yielding the greatest response. The cellular mechanisms that mediate this phenomenon are not known. This "anion paradox" has been resolved by considering the field potential that is generated by restricted electrodiffusion of the anion through paracellular shunts between taste-bud cells. Neural responses to sodium chloride, sodium acetate, and sodium gluconate were studied while the field potential was voltage-clamped. Clamping at electronegative values eliminated the anion effect, whereas clamping at electropositive potentials exaggerated it. Thus, field potentials across the lingual epithelium modulate taste reception, indicating that the functional unit of taste reception includes the taste cell and its paracellular microenvironment.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ye, Q -- Heck, G L -- DeSimone, J A -- DC00122/DC/NIDCD NIH HHS/ -- New York, N.Y. -- Science. 1991 Nov 1;254(5032):724-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, Virginia Commonwealth University, Richmond 23298-0551.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1948054" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anions ; Chemoreceptor Cells/physiology ; Epithelium/physiology ; Evoked Potentials ; Female ; Models, Biological ; Mouth Mucosa/innervation/*physiology ; Neurons/physiology ; Rats ; Rats, Inbred Strains ; *Sodium ; *Sodium Chloride ; Taste/*physiology ; Tongue/*innervation
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    The effect of anti-neoplastic drugs on murine acquired immunodeficiency syndrome (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-01-18
    Description: The murine acquired immunodeficiency syndrome (MAIDS) is associated with proliferation of target cells that have been infected by a defective retrovirus. To control the growth of this primary neoplasia, virus-inoculated mice were treated with anti-neoplastic drugs. Paradoxically, cyclophosphamide, which is also immunosuppressive, was very effective in preventing the appearance and progression of the disease, in restoring a normal T cell function, and in depleting the number of infected target cells. This result suggests that the proliferating infected target cells were responsible for the immunodeficiency.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Simard, C -- Jolicoeur, P -- New York, N.Y. -- Science. 1991 Jan 18;251(4991):305-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Biology, Clinical Research Institute of Montreal, Quebec, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1987646" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antineoplastic Agents/*therapeutic use ; Blotting, Northern ; Blotting, Southern ; Cell Division ; Cyclophosphamide/therapeutic use ; Lymphocyte Activation ; Mice ; Mice, Inbred BALB C ; Murine Acquired Immunodeficiency Syndrome/*drug therapy/pathology ; RNA, Viral/analysis ; Spleen/pathology ; Virus Replication
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 152
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    Prevention of xenograft rejection by masking donor HLA class I antigens (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-06-21
    Description: Destruction of target cells by cytotoxic T lymphocytes requires the presence of HLA (human lymphocyte antigen) class I antigens on the target cells for adhesion as well as for triggering of the antigen-specific T cell receptor. Rejection of xenogeneic human pancreatic islets and liver was circumvented by masking, before transplantation, donor antigens with F(ab')2 antibody fragments to HLA class I or tissue-specific epitopes. This strategy eliminated the need for recipient immunosuppression and allowed islet xenograft survival beyond 200 days, as demonstrated functionally by C peptide secretion as well as by histology. These in vivo observations are consistent with the importance of donor HLA class I in eliciting graft rejection and have potential applicability to the successful transplantation of other HLA class I-bearing donor tissues.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Faustman, D -- Coe, C -- New York, N.Y. -- Science. 1991 Jun 21;252(5013):1700-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Diabetes Unit, Massachusetts General Hospital, Harvard Medical School, Boston 02129.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1710828" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/immunology ; Antigen-Antibody Complex ; Antigens, CD/immunology ; Antigens, CD29 ; C-Peptide/blood ; *Graft Rejection ; Histocompatibility Antigens Class I/*immunology ; Humans ; Immunoglobulin Fab Fragments/immunology ; Islets of Langerhans/*immunology ; Islets of Langerhans Transplantation/*immunology ; Mice ; Mice, Inbred BALB C ; T-Lymphocytes/*immunology ; Transplantation, Heterologous
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 153
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    Dynamic organization of developing Purkinje cells revealed by transgene expression (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-11-01
    Description: The cerebellum has many properties that make it a useful model for investigating neural development. Purkinje cells, the major output neurons of the cerebellar cortex, have drawn special attention because of the availability of biochemical markers and mutants that affect their development. The spatial expression of L7, a protein specific for Purkinje cells, and L7 beta Gal, a gene expressed in transgenic mice that was constructed from the L7 promoter and the marker beta-galactosidase, delineated bands of Purkinje cells that increased in number during early postnatal development. Expression of the transgene in adult reeler mutant mice, which show inverted cortical lamination, and in primary culture showed that the initial expression of L7 is intrinsic to Purkinje cells and does not depend on extracellular signals. This may reflect an underlying developmental map in cerebellum.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Smeyne, R J -- Oberdick, J -- Schilling, K -- Berrebi, A S -- Mugnaini, E -- Morgan, J I -- NRSA 08-08601/NR/NINR NIH HHS/ -- NS-09904/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1991 Nov 1;254(5032):719-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurosciences, Roche Institute of Molecular Biology, Roche Research Center, Nutley, NJ 07110.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1948052" target="_blank"〉PubMed〈/a〉
    Keywords: Aging ; Animals ; Cerebellum/cytology/embryology/*growth & development ; Embryonic and Fetal Development ; Mice ; Mice, Neurologic Mutants ; Mice, Transgenic ; Purkinje Cells/cytology/*physiology ; Recombinant Proteins/metabolism ; beta-Galactosidase/*genetics/metabolism
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  • 154
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    Zinc finger-DNA recognition: crystal structure of a Zif268-DNA complex at 2.1 A (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-05-10
    Description: The zinc finger DNA-binding motif occurs in many proteins that regulate eukaryotic gene expression. The crystal structure of a complex containing the three zinc fingers from Zif268 (a mouse immediate early protein) and a consensus DNA-binding site has been determined at 2.1 angstroms resolution and refined to a crystallographic R factor of 18.2 percent. In this complex, the zinc fingers bind in the major groove of B-DNA and wrap part way around the double helix. Each finger has a similar relation to the DNA and makes its primary contacts in a three-base pair subsite. Residues from the amino-terminal portion of an alpha helix contact the bases, and most of the contracts are made with the guanine-rich strand of the DNA. This structure provides a framework for understanding how zinc fingers recognize DNA and suggests that this motif may provide a useful basis for the design of novel DNA-binding proteins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pavletich, N P -- Pabo, C O -- GM-31471/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1991 May 10;252(5007):809-17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology and Genetics, 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/2028256" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Crystallography ; DNA/*metabolism ; DNA-Binding Proteins/*chemistry/isolation & purification/physiology ; Early Growth Response Protein 1 ; *Immediate-Early Proteins ; Mice ; Models, Molecular ; Molecular Sequence Data ; Molecular Structure ; Transcription Factors/*chemistry/isolation & purification/physiology ; Zinc Fingers/*physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 155
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    Identification of a gene located at chromosome 5q21 that is mutated in colorectal cancers (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-03-15
    Description: Recent studies have suggested the existence of a tumor suppressor gene located at chromosome region 5q21. DNA probes from this region were used to study a panel of sporadic colorectal carcinomas. One of these probes, cosmid 5.71, detected a somatically rearranged restriction fragment in the DNA from a single tumor. Further analysis of the 5.71 cosmid revealed two regions that were highly conserved in rodent DNA. These sequences were used to identify a gene, MCC (mutated in colorectal cancer), which encodes an 829-amino acid protein with a short region of similarity to the G protein-coupled m3 muscarinic acetylcholine receptor. The rearrangement in the tumor disrupted the coding region of the MCC gene. Moreover, two colorectal tumors were found with somatically acquired point mutations in MCC that resulted in amino acid substitutions. MCC is thus a candidate for the putative colorectal tumor suppressor gene located at 5q21. Further studies will be required to determine whether the gene is mutated in other sporadic tumors or in the germ line of patients with an inherited predisposition to colonic tumorigenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kinzler, K W -- Nilbert, M C -- Vogelstein, B -- Bryan, T M -- Levy, D B -- Smith, K J -- Preisinger, A C -- Hamilton, S R -- Hedge, P -- Markham, A -- 6M 07184/PHS HHS/ -- CA 06973/CA/NCI NIH HHS/ -- CA 09243/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1991 Mar 15;251(4999):1366-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Genetics Laboratory, Johns Hopkins Oncology Center, Baltimore, MD 21231.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1848370" target="_blank"〉PubMed〈/a〉
    Keywords: Adenomatous Polyposis Coli/*genetics ; Amino Acid Sequence ; Animals ; Base Sequence ; *Chromosomes, Human, Pair 5 ; Colorectal Neoplasms/*genetics ; Exons ; GTP-Binding Proteins/metabolism ; Gene Expression ; *Genes, Tumor Suppressor ; Humans ; Molecular Sequence Data ; Mutation ; Oligonucleotides/chemistry ; Polymerase Chain Reaction ; Proteins/*genetics/metabolism ; Rats ; Sequence Homology, Nucleic Acid ; *Tumor Suppressor Proteins
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  • 156
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    Anti-HIV and anti-anti-MHC antibodies in alloimmune and autoimmune mice (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-09-06
    Description: Alloimmune mice (mice that have been exposed to cells from another murine strain) were shown to make antibodies against gp120 and p24 of human immunodeficiency virus (HIV), and mice of the autoimmune strains MRL-lpr/lpr and MRL-(+)/+ made antibodies against gp120. This is surprising because the mice were not exposed to HIV. Furthermore, anti-anti-MHC antibodies (molecules that have shapes similar to those of major histocompatibility complex molecules) were detected in both alloimmune sera and MRL mice. These results are discussed in the context of a possible role for allogeneic stimuli in the pathogenesis of acquired immunodeficiency syndrome, as suggested by an idiotypic network model.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kion, T A -- Hoffmann, G W -- New York, N.Y. -- Science. 1991 Sep 6;253(5024):1138-40.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, University of British Columbia, Vancouver, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1909456" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal ; *Antibody Formation ; Autoimmune Diseases/genetics/*immunology/microbiology ; Enzyme-Linked Immunosorbent Assay ; Gene Products, gag/*immunology ; HIV Antibodies/*biosynthesis ; HIV Antigens/*immunology ; HIV Core Protein p24 ; HIV Envelope Protein gp120/*immunology ; Histocompatibility Antigens Class II/*immunology ; Isoantibodies/*biosynthesis ; *Major Histocompatibility Complex ; Mice ; Mice, Inbred BALB C ; Mice, Inbred CBA ; Mice, Mutant Strains ; T-Lymphocytes/immunology ; Viral Core Proteins/*immunology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Human hemoglobin switching (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-04-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stamatoyannopoulos, G -- New York, N.Y. -- Science. 1991 Apr 19;252(5004):383.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of Washington, Seattle 98195.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2017679" target="_blank"〉PubMed〈/a〉
    Keywords: Anemia, Sickle Cell/genetics ; Animals ; Fetus/metabolism ; *Gene Expression Regulation ; Globins/*genetics ; Humans ; Mice ; Mice, Transgenic ; Regulatory Sequences, Nucleic Acid ; Thalassemia/genetics
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    GPI-anchored cell-surface molecules complexed to protein tyrosine kinases (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-11-15
    Description: Binding of ligand or antibody to certain cell-surface proteins that are anchored to the membrane by glycophosphatidylinositol (GPI) can cause activation of leukocytes. However, it is not known how these molecules, which lack intracellular domains, can transduce signals. The GPI-linked human molecules CD59, CD55, CD48, CD24, and CD14 as well as the mouse molecules Thy-1 and Ly-6 were found to associate with protein tyrosine kinases, key regulators of cell activation and signal transduction. A protein tyrosine kinase associated with the GPI-linked proteins CD59, CD55, and CD48 in human T cells, and with Thy-1 in mouse T cells was identified as p56lck, a protein tyrosine kinase related to Src. This interaction of GPI-linked molecules with protein tyrosine kinases suggests a potential mechanism of signal transduction in cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stefanova, I -- Horejsi, V -- Ansotegui, I J -- Knapp, W -- Stockinger, H -- New York, N.Y. -- Science. 1991 Nov 15;254(5034):1016-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Immunology-Vienna International Research Cooperation Center, University of Vienna, Austria.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1719635" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD/*physiology ; Antigens, Differentiation/physiology ; Cell Adhesion Molecules/physiology ; Glycolipids/physiology ; Glycosylphosphatidylinositols ; Humans ; Membrane Glycoproteins/physiology ; Membrane Proteins/*physiology ; Mice ; Phosphatidylinositols/physiology ; Phosphorylation ; Phosphotyrosine ; Protein-Tyrosine Kinases/*physiology ; Receptor Aggregation ; Receptors, Cell Surface/*physiology ; Signal Transduction ; Tyrosine/analogs & derivatives/metabolism
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  • 159
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    Suppression of the immune response by a soluble complement receptor of B lymphocytes (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-10-04
    Description: The CD19-CR2 complex of B lymphocytes contains proteins that participate in two host-defense systems, the immune and complement systems. The ligand for the subunit of the immune system, CD19, is not known, but the complement receptor subunit, CR2 (CD21), binds activation fragments of the C3 component of the complement system and may mediate immunopotentiating effects of complement. A recombinant, soluble CR2 was prepared by fusing the C3-binding region of the receptor to immunoglobulin G1 (IgG1). The (CR2)2-IgG1 chimera competed with cellular CR2 for C3 binding and suppressed the antibody response to a T cell-dependent antigen when administered to mice at the time of immunization. This inhibitory effect of (CR2)2-IgG1 demonstrates the B cell-activating function of the CD19-CR2 complex and suggests a new method for humoral immunosuppression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hebell, T -- Ahearn, J M -- Fearon, D T -- AI-22833/AI/NIAID NIH HHS/ -- AI-28191/AI/NIAID NIH HHS/ -- GM-43803/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1991 Oct 4;254(5028):102-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, 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/1718035" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; *Antibody Formation ; Antigens, CD/*physiology ; Antigens, CD19 ; Antigens, Differentiation, B-Lymphocyte/chemistry/*physiology ; B-Lymphocytes/*physiology ; Base Sequence ; Binding, Competitive ; Cloning, Molecular ; Immunosuppression ; In Vitro Techniques ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C3H ; Molecular Sequence Data ; Receptors, Complement/chemistry/*physiology ; Receptors, Complement 3d ; Recombinant Fusion Proteins ; Signal Transduction ; Solubility
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    Characterization of a cofactor that regulates dimerization of a mammalian homeodomain protein (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-12-20
    Description: Dimerization among transcription factors has become a recurrent theme in the regulation of eukaryotic gene expression. Hepatocyte nuclear factor-1 alpha (HNF-1 alpha) is a homeodomain-containing protein that functions as a dimer. A dimerization cofactor of HNF-1 alpha (DCoH) was identified that displayed a restricted tissue distribution and did not bind to DNA, but, rather, selectively stabilized HNF-1 alpha dimers. The formation of a stable tetrameric DCoH-HNF-1 alpha complex, which required the dimerization domain of HNF-1 alpha, did not change the DNA binding characteristics of HNF-1 alpha, but enhanced its transcriptional activity. However, DCoH did not confer transcriptional activation to the GAL4 DNA binding domain. These results indicate that DCoH regulates formation of transcriptionally active tetrameric complexes and may contribute to the developmental specificity of the complex.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mendel, D B -- Khavari, P A -- Conley, P B -- Graves, M K -- Hansen, L P -- Admon, A -- Crabtree, G R -- CA 09302/CA/NCI NIH HHS/ -- HD 07201/HD/NICHD NIH HHS/ -- HL 33942/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1991 Dec 20;254(5039):1762-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Stanford University, CA 94305.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1763325" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cell Nucleus/physiology ; Chromosome Deletion ; DNA-Binding Proteins/*metabolism ; Gene Library ; Hepatocyte Nuclear Factor 1 ; Hepatocyte Nuclear Factor 1-alpha ; Hepatocyte Nuclear Factor 1-beta ; Humans ; *Hydro-Lyases ; Liver/physiology ; Macromolecular Substances ; Mice ; Molecular Sequence Data ; *Nuclear Proteins ; Protein Biosynthesis ; RNA, Messenger/genetics ; Rabbits ; Rats ; Reticulocytes/metabolism ; Transcription Factors/genetics/*metabolism ; Transcription, Genetic
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  • 161
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    Control of granulocytes and macrophages: molecular, cellular, and clinical aspects (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-10-25
    Description: The production and functional activity of two important white blood cells, the granulocytes and macrophages, are regulated mainly by a group of glycoprotein colony-stimulating factors. The colony-stimulating factors have been mass-produced with recombinant technology and are now proving of value in preventing or suppressing infections in a variety of individuals with subnormal or defective formation of blood cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Metcalf, D -- New York, N.Y. -- Science. 1991 Oct 25;254(5031):529-33.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Walter and Eliza Hall Institute of Medical Research, Post Office Royal Melbourne Hospital, Victoria, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1948028" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/therapy ; Anemia, Aplastic/therapy ; Animals ; Colony-Stimulating Factors/genetics/*physiology/therapeutic use ; Granulocytes/cytology/*physiology ; Hematopoiesis ; Hematopoietic Stem Cells/cytology/*physiology ; Humans ; Macrophages/cytology/*physiology ; Mice ; Neoplasms/therapy ; Neutropenia/therapy ; Recombinant Proteins/therapeutic use
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    Of genes and genomes (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-10-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hillis, D M -- Bull, J J -- New York, N.Y. -- Science. 1991 Oct 25;254(5031):528.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Zoology, University of Texas, Austin 78712.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1948027" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Genes ; *Genome ; Mice ; Mice, Inbred Strains/*genetics ; *Phylogeny ; Polymorphism, Genetic
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 163
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    Energy transfer between two peptides bound to one MHC class II molecule (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-10-04
    Description: The 17-amino acid peptide from chicken ovalbumin, Ova(323-339), was labeled at the amino terminus with fluorescein [FOva(323-339)] and near the carboxyl terminus with Texas Red [AcOva(323-338)KTR]. Fluorescence spectroscopy was carried out on resolved electrophoretic bands on nonreducing polyacrylamide gels derived from incubation mixtures containing major histocompatibility complex (MHC) class II molecules IAd and the FOva(323-339)- and AcOva(323-338)KTR-labeled peptides. Energy transfer between fluorescein and Texas Red was observed in the "floppy" alpha beta heterodimer band, but not in the "compact" alpha beta heterodimer band. Energy transfer was detected between the truncated peptides FOva(323-328)CONH2 and AcOva(331-338)KTR in both the compact alpha beta and floppy alpha beta gel bands. The energy-transfer data suggest that the two binding sites of floppy alpha beta arise from splitting apart a putative large, single binding site region in compact alpha beta.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tampe, R -- Clark, B R -- McConnell, H M -- 2R37 AI 13587-16/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1991 Oct 4;254(5028):87-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Stauffer Laboratory for Physical Chemistry, Stanford University, CA 94305.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1656526" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Binding Sites ; Energy Transfer ; Histocompatibility Antigens Class II/chemistry/*metabolism ; In Vitro Techniques ; Mice ; Molecular Sequence Data ; Ovalbumin/chemistry ; Peptides/chemistry/*metabolism ; Spectrometry, Fluorescence ; Structure-Activity Relationship
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    Generation and analysis of interleukin-4 deficient mice (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-11-01
    Description: Interleukin-4 (IL-4) promotes the growth and differentiation of many hematopoietic cells in vitro; in particular, it directs the immunoglobulin (Ig) class switch to IgG1 and IgE. Mice homozygous for a mutation that inactivates the IL-4 gene were generated to test the requirement for IL-4 in vivo. In the mutant mice T and B cell development was normal, but the serum levels of IgG1 and IgE were strongly reduced. The IgG1 dominance in a T cell-dependent immune response was lost, and IgE was not detectable upon nematode infection. Thus, some but not all of the in vitro properties of IL-4 are critical for the physiology of the immune system in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kuhn, R -- Rajewsky, K -- Muller, W -- New York, N.Y. -- Science. 1991 Nov 1;254(5032):707-10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Genetics, University of Cologne, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1948049" target="_blank"〉PubMed〈/a〉
    Keywords: Aging ; Alleles ; Animals ; B-Lymphocytes/immunology ; Blotting, Southern ; Chromosome Deletion ; Concanavalin A ; DNA/genetics/isolation & purification ; Female ; Interleukin-4/deficiency/*genetics ; Lymph Nodes/growth & development/immunology ; Lymphocyte Activation ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Mutant Strains ; Restriction Mapping ; Spleen/growth & development/immunology ; T-Lymphocytes/immunology ; Thymus Gland/growth & development/immunology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Cloning of a serotonin transporter affected by antidepressants (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-10-25
    Description: A complementary DNA clone for a serotonin (5HT) transporter has been isolated from rat basophilic leukemia cells. The complementary DNA sequence predicts a 653-amino acid protein with 12 to 13 putative transmembrane domains. The 5HT transporter has significant homology to the gamma-aminobutyric acid, dopamine, and norepinephrine transporters. Uptake by CV-1 cells expressing the transporter complementary DNA resembles 5HT uptake by platelets and brain synaptosomes; it is sensitive to antidepressants, amphetamine derivatives, and cocaine.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hoffman, B J -- Mezey, E -- Brownstein, M J -- New York, N.Y. -- Science. 1991 Oct 25;254(5031):579-80.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Cell Biology, National Institute of Mental Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1948036" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antidepressive Agents/*pharmacology ; Base Sequence ; Carrier Proteins/drug effects/*genetics/metabolism ; Cell Line ; Cloning, Molecular ; Kinetics ; Leukemia, Basophilic, Acute ; Molecular Sequence Data ; Oligonucleotide Probes ; Rats ; Serotonin/*metabolism ; Transfection
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Genes for epilepsy mapped in the mouse (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-08-09
    Description: The neurological mutant mouse strain E1 is a model for complex partial seizures in humans. The inheritance of epileptic seizures with seven conventional chromosomal markers and over 60 endogenous proviral markers was studied by means of back-crosses of E1 with two seizure-resistant strains, DBA/2J and ABP/LeJ. The major gene responsible for this epileptic phenotype (El-1) was localized to a region distal with respect to the centromere on chromosome 9. At least one other gene, El-2, linked to proviral markers on chromosome 2, also influences the seizure phenotype. In addition, a potential modifier of seizures was detected in the DBA/2J background. The location of El-1 on distal chromosome 9 may allow identification of an epilepsy candidate gene in humans on the basis of conserved synteny with human chromosome 3.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rise, M L -- Frankel, W N -- Coffin, J M -- Seyfried, T N -- NS 23355/NS/NINDS NIH HHS/ -- R35CA44385/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1991 Aug 9;253(5020):669-73.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Boston College, Chestnut Hill 02167.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1871601" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromosome Mapping ; Crosses, Genetic ; Epilepsy/*genetics ; Female ; Genetic Predisposition to Disease ; Male ; Mice ; Mice, Inbred Strains ; Mice, Neurologic Mutants/*genetics ; Recombination, Genetic ; Seizures/genetics ; Software
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 167
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    Peripheral selection of the T cell repertoire (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-03-08
    Description: T lymphocytes undergo selection events not only in the thymus, but also after they leave the thymus and reside in the periphery. Peripheral selection was found to be dependent on T cell receptor (TCR)-ligand interactions but to differ from thymic selection with regard to specificity and mechanism. Unlike thymic selection, peripheral selection required binding of antigen to the TCR, and it induced expansion of T cell clones. Tolerance to self antigens that are restricted to the periphery occurred through the elimination of self-reactive T cells and by the clonal anergy, which was associated with down-regulation of the alpha beta TCR and CD8.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rocha, B -- von Boehmer, H -- New York, N.Y. -- Science. 1991 Mar 8;251(4998):1225-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Unite INSERM U-25 CNRS UA-122, Hopital Necker, Paris, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1900951" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD4/immunology ; Antigens, CD8 ; Antigens, Differentiation, T-Lymphocyte/immunology ; Cells, Cultured ; Down-Regulation ; Female ; Histocompatibility Antigens Class I/immunology ; Immunotherapy, Adoptive ; Male ; Mice ; Mice, Nude ; Receptors, Antigen, T-Cell/*physiology ; T-Lymphocytes/*immunology ; Thymectomy ; Thymus Gland/*immunology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 168
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    A dominant negative form of transcription activator mTFE3 created by differential splicing (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-10-04
    Description: Transcription factor E3 (mTFE3) is a murine transcription activator that binds to the intronic enhancer of the immunoglobulin heavy chain gene. A naturally occurring splice product of mTFE3 messenger RNA (mRNA) lacked 105 nucleotides that encode an activation domain; both absolute and relative amounts of long and truncated mRNAs varied in different tissues. Cells were cotransfected with complementary DNAs that encoded the two mRNA forms in amounts that corresponded to the amounts of each mRNA found in different cells. Small changes in substoichiometric amounts of the truncated form of mRNA effected trans-dominant negative modulation of mTFE3 activity. These findings identify a function for differential splicing in the regulation of transcription factor activity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roman, C -- Cohn, L -- Calame, K -- R01CA38571/CA/NCI NIH HHS/ -- R01GM28361/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1991 Oct 4;254(5028):94-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Chemistry, University of California, Los Angeles 90024.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1840705" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors ; DNA-Binding Proteins/*genetics ; *Gene Expression Regulation ; Mice ; Molecular Sequence Data ; RNA Splicing ; RNA, Messenger/genetics ; Regulatory Sequences, Nucleic Acid ; Structure-Activity Relationship ; Transcription Factors/*genetics ; *Transcription, Genetic
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    Oct-3 and the beginning of mammalian development (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-07-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rosner, M H -- Vigano, M A -- Rigby, P W -- Arnheiter, H -- Staudt, L M -- New York, N.Y. -- Science. 1991 Jul 12;253(5016):144-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Metabolism Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1853199" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; DNA Replication ; DNA-Binding Proteins/*physiology ; Embryo, Mammalian/*physiology ; Gene Expression Regulation ; Mice ; Octamer Transcription Factor-3 ; Stem Cells/physiology ; Teratoma/genetics/pathology ; Transcription Factors/*physiology
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  • 170
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    Hypotensive activity of fibroblast growth factor (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-11-22
    Description: Acidic and basic fibroblast growth factors (FGFs) are members of a family of proteins that are broad-spectrum mitogens, have diverse hormone-like activities, and function in tumorigenesis. FGF's ability to raise the concentration of intracellular calcium ion suggests that FGF could induce the synthesis of endothelium-derived relaxing factor (EDRF) and consequently vasodilation. Systemic administration of FGF decreased arterial blood pressure. This effect was mediated by EDRF and by adenosine triphosphate-sensitive potassium ion channels. The hypotensive effect of FGF was segregated from its mitogenic activity by protein engineering. These results extend the range of FGF autocrine activities and potential therapeutic applications, emphasize the role of endothelium as an arterial blood pressure--regulating organ, and provide insight on the structural basis of FGF functions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cuevas, P -- Carceller, F -- Ortega, S -- Zazo, M -- Nieto, I -- Gimenez-Gallego, G -- New York, N.Y. -- Science. 1991 Nov 22;254(5035):1208-10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Hospital Universitario Ramon y Cajal, Carretera de Colmenar, Madrid, Spain.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1957172" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Pressure/*drug effects ; Dose-Response Relationship, Drug ; Fibroblast Growth Factors/chemistry/*pharmacology ; Glyburide/pharmacology ; Nitric Oxide/physiology ; Potassium Channels/drug effects ; Rabbits ; Rats ; Structure-Activity Relationship ; Time Factors
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  • 171
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    MHC class I deficiency: susceptibility to natural killer (NK) cells and impaired NK activity (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-07-12
    Description: The role of major histocompatibility complex (MHC) class I expression in natural killer (NK) cell target recognition is controversial. Normal T cell blasts from MHC class I-deficient mutant mice were found to serve as target cells for NK cells in vitro, which suggests that MHC class I molecules are directly involved in NK cell recognition. Spleen cells from the mutant mice were deficient in their ability to lyse MHC class I-deficient target cells or NK-susceptible tumor targets, and mutant mice could not reject allogeneic bone marrow. Thus, class I molecules may participate in the positive selection or tolerance induction of NK cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liao, N S -- Bix, M -- Zijlstra, M -- Jaenisch, R -- Raulet, D -- R01 AI30171/AI/NIAID NIH HHS/ -- R35 CA44339/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1991 Jul 12;253(5016):199-202.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cell Biology, University of California, Berkeley 94720.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1853205" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cytotoxicity, Immunologic ; Histocompatibility Antigens Class I/*immunology ; *Immunity, Cellular ; *Immunity, Innate ; Killer Cells, Natural/*immunology ; Major Histocompatibility Complex ; Mice ; Mice, Inbred Strains ; T-Lymphocyte Subsets/immunology ; T-Lymphocytes, Cytotoxic/immunology ; beta 2-Microglobulin/physiology
    Print ISSN: 0036-8075
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  • 172
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    Inhibition of PDGF beta receptor signal transduction by coexpression of a truncated receptor (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-05-10
    Description: A mutated form of the platelet-derived growth factor (PDGF) beta receptor lacking most of its cytoplasmic domain was tested for its ability to block wild-type PDGF receptor function. PDGF induced the formation of complexes consisting of wild-type and truncated receptors. Such complexes were defective in autophosphorylation. When truncated receptors were expressed in excess compared to wild-type receptors, stimulation by PDGF of receptor autophosphorylation, association of phosphatidylinositol-3 kinase with the receptor, and calcium mobilization were blocked. Thus, a truncated receptor can inactivate wild-type receptor function by forming ligand-dependent receptor complexes (probably heterodimers) that are incapable of mediating the early steps of signal transduction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ueno, H -- Colbert, H -- Escobedo, J A -- Williams, L T -- P01 HL-43821/HL/NHLBI NIH HHS/ -- R01 HL-32898/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1991 May 10;252(5007):844-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of California, San Francisco 94143.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1851331" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Centrifugation, Density Gradient ; Cricetinae ; In Vitro Techniques ; Ligands ; Mice ; Mice, Inbred BALB C ; Phosphorylation ; Platelet-Derived Growth Factor ; Receptors, Cell Surface/*antagonists & inhibitors/physiology ; Receptors, Platelet-Derived Growth Factor ; Signal Transduction/*physiology
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    Enhanced motility in NIH 3T3 fibroblasts that overexpress gelsolin (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-03-08
    Description: Increasing the content of the actin-binding protein gelsolin in cultured mouse fibroblasts by up to 125 percent by gene transfection proportionally enhanced the rate at which the cells migrated through porous filters toward a gradient of serum and closed a wound made on a confluent monolayer of cells in a tissue culture dish. These results provide direct evidence that gelsolin, which promotes both actin assembly and disassembly in vitro, is an important element in fibroblast locomotion and demonstrate that the manipulation of intracellular machinery can increase cell motility.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cunningham, C C -- Stossel, T P -- Kwiatkowski, D J -- AI28465/AI/NIAID NIH HHS/ -- HL07680/HL/NHLBI NIH HHS/ -- HL19429/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1991 Mar 8;251(4998):1233-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Hematology-Oncology Unit, Massachusetts General Hospital, Boston 02129.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1848726" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium-Binding Proteins/genetics/*physiology ; Cell Line ; *Chemotaxis ; Fibroblasts/physiology ; Gelsolin ; Gene Expression ; Humans ; Kinetics ; Mice ; Microfilament Proteins/genetics/*physiology ; RNA Splicing ; RNA, Messenger/genetics ; Transfection
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  • 174
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    Functional modulation of brain sodium channels by protein kinase C phosphorylation (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-10-04
    Description: Voltage-gated sodium channels, which are responsible for the generation of action potentials in the brain, are phosphorylated by protein kinase C (PKC) in purified form. Activation of PKC decreases peak sodium current up to 80 percent and slows its inactivation for sodium channels in rat brain neurons and for rat brain type IIA sodium channel alpha subunits heterologously expressed in Chinese hamster ovary cells. These effects are specific for PKC because they can be blocked by specific peptide inhibitors of PKC and can be reproduced by direct application of PKC to the cytoplasmic surface of sodium channels in excised inside-out membrane patches. Modulation of brain sodium channels by PKC is likely to have important effects on signal transduction and synaptic transmission in the central nervous system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Numann, R -- Catterall, W A -- Scheuer, T -- NS15751/NS/NINDS NIH HHS/ -- NS25704/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1991 Oct 4;254(5028):115-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of Washington, Seattle 98195.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1656525" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/physiology ; CHO Cells ; Cloning, Molecular ; Cricetinae ; Diglycerides/pharmacology ; In Vitro Techniques ; Neurons/physiology ; Phosphoproteins/physiology ; Phosphorylation ; Protein Kinase C/*physiology ; Protein Kinases/physiology ; Rats ; Sodium/*physiology ; Sodium Channels/*physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 175
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    Crystal structure of transforming growth factor-beta 2: an unusual fold for the superfamily (1992)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1992-07-17
    Description: The transforming growth factors-beta (TGF-beta 1 through -beta 5) are a family of homodimeric cytokines that regulate proliferation and function in many cell types. Family members have 66 to 80% sequence identity and nine strictly conserved cysteines. A crystal structure of a member of this family, TGF-beta 2, has been determined at 2.1 angstrom (A) resolution and refined to an R factor of 0.172. The monomer lacks a well-defined hydrophobic core and displays an unusual elongated nonglobular fold with dimensions of approximately 60 A by 20 A by 15 A. Eight cysteines form four intrachain disulfide bonds, which are clustered in a core region forming a network complementary to the network of hydrogen bonds. The dimer is stabilized by the ninth cysteine, which forms an interchain disulfide bond, and by two identical hydrophobic interfaces. Sequence profile analysis of other members of the TGF-beta superfamily, including the activins, inhibins, and several developmental factors, imply that they also adopt the TGF-beta fold.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Daopin, S -- Piez, K A -- Ogawa, Y -- Davies, D R -- New York, N.Y. -- Science. 1992 Jul 17;257(5068):369-73.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Biology, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1631557" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Crystallography ; Drosophila ; Humans ; Mice ; Models, Molecular ; Molecular Conformation ; Molecular Structure ; Transforming Growth Factor beta/*chemistry ; Xenopus laevis
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    Reversal of diabetes insipidus in Brattleboro rats: intrahypothalamic injection of vasopressin mRNA (1992)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1992-02-21
    Description: Messenger RNAs occur within the axons of magnocellular hypothalamic neurons known to secrete oxytocin and vasopressin. In Brattleboro rats, which have a genetic mutation that renders them incapable of vasopressin expression and secretion and thus causes diabetes insipidus, injection into the hypothalamus of purified mRNAs from normal rat hypothalami or of synthetic copies of the vasopressin mRNA leads to selective uptake, retrograde transport, and expression of vasopressin exclusively in the magnocellular neurons. Temporary reversal of their diabetes insipidus (for up to 5 days) can be observed within hours of the injection. Intra-axonal mRNAs may represent an additional category of chemical signals for neurons.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jirikowski, G F -- Sanna, P P -- Maciejewski-Lenoir, D -- Bloom, F E -- MH 47680/MH/NIMH NIH HHS/ -- NS 22347-03/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1992 Feb 21;255(5047):996-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuropharmacology, Scripps Research Institute, La Jolla, CA 92037.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1546298" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arginine Vasopressin/*genetics/metabolism ; Diabetes Insipidus/*therapy ; Hypothalamus ; RNA, Messenger/administration & dosage ; Rats ; Rats, Brattleboro ; Water-Electrolyte Balance
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    Regulatory elements that control the lineage-specific expression of myoD (1992)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1992-05-04
    Description: The molecular basis of skeletal muscle lineage determination was investigated by analyzing DNA control elements that regulate the myogenic determination gene myoD. A distal enhancer was identified that positively regulates expression of the human myoD gene. The myoD enhancer and promoter were active in myogenic and several nonmyogenic cell lines. In transgenic mouse embryos, however, the myoD enhancer and promoter together directed expression of a lacZ transgene specifically to the skeletal muscle lineage. These data suggest that during development myoD is regulated by mechanisms that restrict accessibility of myoD control elements to positive trans-acting factors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Goldhamer, D J -- Faerman, A -- Shani, M -- Emerson, C P Jr -- CA-06927/CA/NCI NIH HHS/ -- HD-07796/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1992 Apr 24;256(5056):538-42.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Cancer Research, Fox Chase Cancer Center, Philadelphia, PA 19111.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1315077" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cell Line ; Chloramphenicol O-Acetyltransferase/genetics ; Cloning, Molecular ; Enhancer Elements, Genetic ; *Gene Expression Regulation ; Humans ; Mice ; Mice, Transgenic ; Muscle Proteins/*genetics ; Muscles/embryology/metabolism ; MyoD Protein ; Promoter Regions, Genetic ; Transcription, Genetic ; Transfection ; Tumor Cells, Cultured ; beta-Galactosidase/genetics
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    GenPharm's knockout mice (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-08-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉MacQuitty, J J -- Kay, R M -- New York, N.Y. -- Science. 1992 Aug 28;257(5074):1188.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1519048" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Mice ; *Mice, Transgenic ; Patents as Topic
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Awakenings ... UV light and HIV gene activation (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-08-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wallace, B M -- Lasker, J S -- New York, N.Y. -- Science. 1992 Aug 28;257(5074):1211-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1519057" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cloning, Molecular ; DNA/radiation effects ; DNA Damage ; Gene Expression/*radiation effects ; Genes, Viral/*radiation effects ; HIV/*genetics ; HIV Long Terminal Repeat ; Humans ; Mice ; PUVA Therapy/adverse effects ; Sunlight/adverse effects ; Ultraviolet Rays/*adverse effects
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 180
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    Age-associated inclusions in normal and transgenic mouse brain (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-03-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jucker, M -- Walker, L C -- Martin, L J -- Kitt, C A -- Kleinman, H K -- Ingram, D K -- Price, D L -- New York, N.Y. -- Science. 1992 Mar 13;255(5050):1443-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1542796" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/*metabolism ; Amyloid beta-Peptides/*metabolism ; Animals ; Brain/*metabolism ; Female ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic/*metabolism
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Genome analysis and the human X chromosome (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-10-02
    Description: A unified genetic, physical, and functional map of the human X chromosome is being built through a concerted, international effort. About 40 percent of the 160 million base pairs of the X chromosome DNA have been cloned in overlapping, ordered contigs derived from yeast artificial chromosomes. This rapid progress toward a physical map is accelerating the identification of inherited disease genes, 26 of which are already cloned and more than 50 others regionally localized by linkage analysis. This article summarizes the mapping strategies now used and the impact of genome research on the understanding of X chromosome inactivation and X-linked diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mandel, J L -- Monaco, A P -- Nelson, D L -- Schlessinger, D -- Willard, H -- New York, N.Y. -- Science. 1992 Oct 2;258(5079):103-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratoire de Genetique Moleculaire des Eucaryotes du CNRS, INSERM, Strasbourg, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1439756" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Chromosome Mapping ; Dosage Compensation, Genetic ; Female ; *Genome, Human ; Humans ; Macropodidae ; Male ; Mice ; Mutation ; Sex Chromosome Aberrations ; *X Chromosome
    Print ISSN: 0036-8075
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  • 182
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    Regulation of the differentiation of teratocarcinoma cells into primitive endoderm by G alpha i2 (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-11-20
    Description: The amount of the heterotrimeric G protein subunit G alpha i2 decreases after the induction of F9 teratocarcinoma cells to become primitive endoderm in the presence of retinoic acid (RA). The reduction of the G alpha i2 protein in F9 cells by antisense RNA expression was associated with (i) loss of receptor-mediated inhibition of adenylyl cyclase; (ii) decreased cell doubling time; (iii) induction of a primitive, endoderm-like phenotype in the absence of RA; and (iv) production of the differentiation marker tissue-type plasminogen activator. Expression of a constitutively active, mutant G alpha i2 blocked RA-induced differentiation. These data suggest the involvement of G alpha i2 in the control of stem cell differentiation and provide insight into the involvement of G proteins in growth regulation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Watkins, D C -- Johnson, G L -- Malbon, C C -- New York, N.Y. -- Science. 1992 Nov 20;258(5086):1373-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Diabetes and Metabolic Diseases Research Program, State University of New York, Stony Brook 11794.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1455234" target="_blank"〉PubMed〈/a〉
    Keywords: Adenylyl Cyclases/metabolism ; Animals ; Base Sequence ; *Cell Differentiation/drug effects ; GTP-Binding Proteins/genetics/*physiology ; Gene Expression ; Mice ; Molecular Sequence Data ; RNA, Antisense ; Teratoma/*pathology ; Thrombin/pharmacology ; Tretinoin/pharmacology ; Tumor Cells, Cultured
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  • 183
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    Impaired long-term potentiation, spatial learning, and hippocampal development in fyn mutant mice (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-12-18
    Description: Mice with mutations in four nonreceptor tyrosine kinase genes, fyn, src, yes, and abl, were used to study the role of these kinases in long-term potentiation (LTP) and in the relation of LTP to spatial learning and memory. All four kinases were expressed in the hippocampus. Mutations in src, yes, and abl did not interfere with either the induction or the maintenance of LTP. However, in fyn mutants, LTP was blunted even though synaptic transmission and two short-term forms of synaptic plasticity, paired-pulse facilitation and post-tetanic potentiation, were normal. In parallel with the blunting of LTP, fyn mutants showed impaired spatial learning, consistent with a functional link between LTP and learning. Although fyn is expressed at mature synapses, its lack of expression during development resulted in an increased number of granule cells in the dentate gyrus and of pyramidal cells in the CA3 region. Thus, a common tyrosine kinase pathway may regulate the growth of neurons in the developing hippocampus and the strength of synaptic plasticity in the mature hippocampus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grant, S G -- O'Dell, T J -- Karl, K A -- Stein, P L -- Soriano, P -- Kandel, E R -- AG08702/AG/NIA NIH HHS/ -- HD24875/HD/NICHD NIH HHS/ -- MH45923/MH/NIMH NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1992 Dec 18;258(5090):1903-10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Neurobiology and Behavior, Howard Hughes Medical Institute, 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/1361685" target="_blank"〉PubMed〈/a〉
    Keywords: 2-Amino-5-phosphonovalerate/pharmacology ; Acetylcholinesterase/analysis ; Animals ; Brain/cytology/*physiology ; Cerebral Cortex/cytology/physiology ; Electric Stimulation ; Genes, abl ; Genes, src ; Hippocampus/drug effects/growth & development/*physiology ; In Vitro Techniques ; *Learning ; Mice ; Mice, Neurologic Mutants ; Neurons/drug effects/*physiology ; Protein-Tyrosine Kinases/*genetics/metabolism ; Proto-Oncogene Proteins/*genetics/metabolism ; Proto-Oncogene Proteins c-fyn ; Proto-Oncogene Proteins c-yes ; Pyramidal Tracts/physiology ; Receptors, N-Methyl-D-Aspartate/physiology ; Space Perception ; Synapses/physiology ; *src-Family Kinases
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 184
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    Nitric oxide and arginine-evoked insulin secretion (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-11-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vincent, S R -- New York, N.Y. -- Science. 1992 Nov 20;258(5086):1376-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1455235" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arginine/*pharmacology ; Insulin/*secretion ; Islets of Langerhans/secretion ; Nitric Oxide/*metabolism ; Rats ; Secretory Rate/drug effects
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  • 185
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    NF-kappa B subunit regulation in nontransformed CD4+ T lymphocytes (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-06-05
    Description: Regulation of interleukin-2 (IL-2) gene expression by the p50 and p65 subunits of the DNA binding protein NF-kappa B was studied in nontransformed CD4+ T lymphocyte clones. A homodimeric complex of the NF-kappa B p50 subunit was found in resting T cells. The amount of p50-p50 complex decreased after full antigenic stimulation, whereas the amount of the NF-kappa B p50-p65 heterodimer was increased. Increased expression of the IL-2 gene and activity of the IL-2 kappa B DNA binding site correlated with a decrease in the p50-p50 complex. Overexpression of p50 repressed IL-2 promoter expression. The switch from p50-p50 to p50-p65 complexes depended on a protein that caused sequestration of the p50-p50 complex in the nucleus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kang, S M -- Tran, A C -- Grilli, M -- Lenardo, M J -- New York, N.Y. -- Science. 1992 Jun 5;256(5062):1452-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Immunology, National Institute for Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1604322" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD4/*immunology ; Base Sequence ; Binding Sites ; Cell Line ; Cell Nucleus/physiology ; Chloramphenicol O-Acetyltransferase/genetics/metabolism ; Clone Cells ; Columbidae ; DNA/genetics ; *Gene Expression Regulation ; Interleukin-2/*genetics ; Macromolecular Substances ; Mice ; Molecular Sequence Data ; NF-kappa B/*metabolism ; Oligonucleotide Probes ; Promoter Regions, Genetic ; RNA, Messenger/metabolism ; Recombinant Fusion Proteins/metabolism ; T-Lymphocyte Subsets/*immunology ; Transfection ; Tumor Necrosis Factor-alpha/pharmacology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 186
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    MacroH2A, a core histone containing a large nonhistone region (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-09-04
    Description: A histone, macroH2A, nearly three times the size of conventional H2A histone, was found in rat liver nucleosomes. Its N-terminal third is 64 percent identical to a full-length mouse H2A. However, it also contains a large nonhistone region. This region has a segment that resembles a leucine zipper, a structure known to be involved in dimerization of some transcription factors. Nucleosomes containing macroH2A may have novel functions, possibly involving interactions with other nuclear proteins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pehrson, J R -- Fried, V A -- CA 06927/CA/NCI NIH HHS/ -- GM 24019/GM/NIGMS NIH HHS/ -- RR 05539/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1992 Sep 4;257(5075):1398-400.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Fox Chase Cancer Center, Institute for Cancer Research, Philadelphia, PA 19111.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1529340" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; DNA/chemistry ; Histones/*chemistry/genetics ; Leucine Zippers ; Liver/*ultrastructure ; Macromolecular Substances ; Mice ; Molecular Sequence Data ; Nucleosomes/*chemistry ; Polymerase Chain Reaction ; Rats ; Sequence Homology, Nucleic Acid
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  • 187
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    Selfish genes (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-04-03
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bull, J J -- Molineux, I J -- Werren, J H -- New York, N.Y. -- Science. 1992 Apr 3;256(5053):65.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Zoology, University of Texas, Austin 78712.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1566058" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Biological Evolution ; Crosses, Genetic ; Drosophila/*genetics ; Female ; *Genes ; Heterozygote ; Male ; Mice
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  • 188
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    Synaptotagmin: a calcium sensor on the synaptic vesicle surface (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-05-15
    Description: Neurons release neurotransmitters by calcium-dependent exocytosis of synaptic vesicles. However, the molecular steps transducing the calcium signal into membrane fusion are still an enigma. It is reported here that synaptotagmin, a highly conserved synaptic vesicle protein, binds calcium at physiological concentrations in a complex with negatively charged phospholipids. This binding is specific for calcium and involves the cytoplasmic domain of synaptotagmin. Calcium binding is dependent on the intact oligomeric structure of synaptotagmin (it is abolished by proteolytic cleavage at a single site). These results suggest that synaptotagmin acts as a cooperative calcium receptor in exocytosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brose, N -- Petrenko, A G -- Sudhof, T C -- Jahn, R -- New York, N.Y. -- Science. 1992 May 15;256(5059):1021-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurochemistry, Max-Planck-Institute for Psychiatry, Martinsried, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1589771" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Brain Chemistry ; Calcium/*metabolism/pharmacology ; *Calcium-Binding Proteins ; Cell Membrane/metabolism ; Cytoplasmic Granules/metabolism ; Dansyl Compounds/metabolism ; Energy Transfer ; Exocytosis ; Fluorescent Dyes ; Liposomes/metabolism ; Macromolecular Substances ; Membrane Glycoproteins/chemistry/isolation & purification/*metabolism ; Nerve Tissue Proteins/chemistry/isolation & purification/*metabolism ; Phosphatidylethanolamines/metabolism ; Rats ; Synaptic Vesicles/*metabolism ; Synaptotagmins
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  • 189
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    Calcium-dependent transmitter secretion reconstituted in Xenopus oocytes: requirement for synaptophysin (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-07-31
    Description: Calcium-dependent glutamate secretion was reconstituted in Xenopus oocytes by injecting the oocyte with total rat cerebellar messenger RNA (mRNA). Co-injection of total mRNA with antisense oligonucleotides to synaptophysin message decreased the expression of synaptophysin in the oocyte and reduced the calcium-dependent secretion. A similar effect on secretion was observed for oocytes injected with total mRNA together with an antibody to rat synaptophysin. These results indicate that synaptophysin is necessary for transmitter secretion and that the oocyte expression system may be useful for dissecting the molecular events associated with the secretory process.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Alder, J -- Lu, B -- Valtorta, F -- Greengard, P -- Poo, M M -- MH 39327/MH/NIMH NIH HHS/ -- NS 22764/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1992 Jul 31;257(5070):657-61.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, Columbia University, New York, NY 10027.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1353905" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Blotting, Western ; Calcimycin/pharmacology ; Calcium/*pharmacology ; Cerebellum/chemistry ; Fluorescent Antibody Technique ; Gene Expression ; Glutamates/*secretion ; Glutamic Acid ; Kinetics ; Liver/chemistry ; Microscopy, Immunoelectron ; Molecular Sequence Data ; Oligonucleotides, Antisense/pharmacology ; Oocytes/*physiology ; RNA, Messenger/genetics ; Rats ; Synaptophysin/genetics/*physiology ; Transfection ; Xenopus
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  • 190
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    Gz-mediated hormonal inhibition of cyclic AMP accumulation (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-01-17
    Description: Hormones inhibit synthesis of adenosine 3',5'-monophosphate (cAMP) in most cells via receptors coupled to pertussis toxin (PTX)-sensitive guanine nucleotide-binding (G) proteins. Mutationally activated alpha subunits of Gi2 (alpha i2) constitutively inhibit cAMP accumulation when transfected into cells. Cells have now been transfected with mutant alpha subunits of four other G proteins--Gz, a PTX-insensitive G protein of unknown function, and Gi1, Gi3, and G(o), which are PTX-sensitive. Mutant alpha z, alpha i1, and alpha i3 inhibited cAMP accumulation but alpha o did not. Moreover, expression of wild-type alpha z produced cells in which PTX did not block hormonal inhibition of cAMP accumulation. Thus, Gz can trigger an effector pathway in response to hormone receptors that ordinarily interact with PTX-sensitive Gi proteins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wong, Y H -- Conklin, B R -- Bourne, H R -- New York, N.Y. -- Science. 1992 Jan 17;255(5042):339-42.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of California, San Francisco 94143.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1347957" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenergic alpha-Agonists/pharmacology ; Animals ; Brimonidine Tartrate ; Chorionic Gonadotropin/pharmacology ; Colforsin/pharmacology ; Cyclic AMP/*biosynthesis ; Dinoprostone/pharmacology ; Dopamine/pharmacology ; GTP-Binding Proteins/*physiology ; Gene Expression Regulation/*physiology ; Hormones/*physiology ; In Vitro Techniques ; Lysophospholipids/pharmacology ; Pertussis Toxin ; Quinoxalines/pharmacology ; Rats ; Signal Transduction/physiology ; Transfection ; Virulence Factors, Bordetella/pharmacology
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  • 191
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    Lymphoid development in mice congenitally lacking T cell receptor alpha beta-expressing cells (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-06-05
    Description: Vertebrate T cells express either an alpha beta or gamma delta T cell receptor (TCR). The developmental relatedness of the two cell types is unresolved. alpha beta + T cells respond to specific pathogens by collaborating with immunoglobulin-producing B cells in distinct lymphoid organs such as the spleen and Peyer's patches. The precise influence of alpha beta + T cells on B cell development is poorly understood. To investigate the developmental effects of alpha beta + T cells on B cells and gamma delta + T cells, mice homozygous for a disrupted TCR alpha gene were generated. The homozygotes showed elimination of alpha beta + T cells and the loss of thymic medullae. Despite this, gamma delta + T cells developed in normal numbers, and there was an increase in splenic B cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Philpott, K L -- Viney, J L -- Kay, G -- Rastan, S -- Gardiner, E M -- Chae, S -- Hayday, A C -- Owen, M J -- GM37759/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1992 Jun 5;256(5062):1448-52.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Imperial Cancer Research Fund, London, United Kingdom.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1604321" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/*immunology ; Blastocyst ; Blotting, Southern ; Chimera ; Clone Cells ; DNA/genetics/isolation & purification ; Female ; Lymphoid Tissue/growth & development/*immunology ; Macromolecular Substances ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Mutant Strains ; Peyer's Patches/immunology ; Polymerase Chain Reaction ; Receptors, Antigen, T-Cell/*genetics ; Spleen/immunology ; T-Lymphocytes/*immunology ; Thymus Gland/immunology
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  • 192
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    New genes may shed light on cell growth control (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-07-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J -- New York, N.Y. -- Science. 1992 Jul 24;257(5069):484-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1636083" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Cycle Proteins ; Cell Division/*genetics ; Fungal Proteins/genetics/metabolism ; GTPase-Activating Proteins ; Guanosine Triphosphate/metabolism ; Homeostasis ; Mice ; Proteins/genetics/*metabolism ; Proto-Oncogene Proteins p21(ras)/*genetics/metabolism ; Saccharomyces cerevisiae/genetics ; Saccharomyces cerevisiae Proteins ; ras GTPase-Activating Proteins ; *ras-GRF1
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 193
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    An amino acid mutation in a potassium channel that prevents inhibition by protein kinase C (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-03-27
    Description: A slowly activating, voltage-dependent potassium channel protein cloned from rat kidney was expressed in Xenopus oocytes. Two activators of protein kinase C, 1-oleoyl-2-acetyl-rac-glycerol and phorbol 12,13-didecanoate, inhibited the current. This inhibition was blocked by the kinase inhibitor staurosporine. Inhibition of the current was not seen in channels in which Ser103 was replaced by Ala, although other properties of the current were unchanged. These results indicate that inhibition of the potassium current results from direct phosphorylation of the channel subunit protein at Ser103.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Busch, A E -- Varnum, M D -- North, R A -- Adelman, J P -- DA03160/DA/NIDA NIH HHS/ -- NS28504/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1992 Mar 27;255(5052):1705-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Vollum Institute, Oregon Health Sciences University, Portland 97201.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1553557" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; DNA/genetics ; Diglycerides/pharmacology ; Ion Channel Gating ; Membrane Potentials ; Molecular Sequence Data ; Mutagenesis, Site-Directed ; Phorbol Esters/pharmacology ; Phosphorylation ; Potassium Channels/*physiology ; Protein Kinase C/*metabolism ; Rats ; Structure-Activity Relationship
    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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  • 194
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    Do antidepressants promote tumors? (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-07-03
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J -- New York, N.Y. -- Science. 1992 Jul 3;257(5066):22-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1621088" target="_blank"〉PubMed〈/a〉
    Keywords: Amitriptyline/*toxicity ; Animals ; Breast Neoplasms/drug therapy/prevention & control ; Carcinogens/*toxicity ; Female ; Fluoxetine/*toxicity ; Humans ; Mice ; Neoplasms, Experimental/chemically induced ; Rats ; Tamoxifen/therapeutic use ; United States ; United States Food and Drug Administration
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 195
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    Participation of non-zinc finger residues in DNA binding by two nuclear orphan receptors (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-04-03
    Description: Steroid-thyroid hormone receptors typically bind as dimers to DNA sequences that contain repeated elements termed half-sites. NGFI-B, an early response protein and orphan member of this receptor superfamily, binds to a DNA sequence that contains only one half-site (5'-AAAGGTCA-3'). A domain separate from the NGFI-B zinc fingers, termed the A box, was identified and is required for recognition of the two adenine-thymidine (A-T) base pairs at the 5' end of the NGFI-B DNA binding element. In addition, a domain downstream of the zinc fingers of the orphan receptor H-2 region II binding protein, termed the T box, determined binding to tandem repeats of the estrogen receptor half-site (5'-AGGTCA-3').〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wilson, T E -- Paulsen, R E -- Padgett, K A -- Milbrandt, J -- NS01018/NS/NINDS NIH HHS/ -- P01 CA49712/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1992 Apr 3;256(5053):107-10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, 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/1314418" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Binding Sites ; CHO Cells ; Cell Nucleus/*physiology ; Cricetinae ; DNA/*metabolism ; DNA-Binding Proteins/genetics/*metabolism ; Kinetics ; Mice ; Molecular Sequence Data ; Nuclear Receptor Subfamily 4, Group A, Member 1 ; Oligodeoxyribonucleotides/metabolism ; Polymerase Chain Reaction ; Receptors, Cell Surface/*metabolism ; Receptors, Cytoplasmic and Nuclear ; Receptors, Steroid ; Recombinant Fusion Proteins/metabolism ; Sequence Homology, Nucleic Acid ; Substrate Specificity ; Transcription Factors/genetics/*metabolism ; Transfection ; Zinc Fingers/genetics
    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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  • 196
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    An animal model for cystic fibrosis made by gene targeting (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-08-21
    Description: Cystic fibrosis results from defects in the gene encoding a cyclic adenosine monophosphate-dependent chloride ion channel known as the cystic fibrosis transmembrane conductance regulator (CFTR). To create an animal model for cystic fibrosis, mice were generated from embryonic stem cells in which the CFTR gene was disrupted by gene targeting. Mice homozygous for the disrupted gene display many features common to young human cystic fibrosis patients, including failure to thrive, meconium ileus, alteration of mucous and serous glands, and obstruction of glandlike structures with inspissated eosinophilic material. Death resulting from intestinal obstruction usually occurs before 40 days of age.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Snouwaert, J N -- Brigman, K K -- Latour, A M -- Malouf, N N -- Boucher, R C -- Smithies, O -- Koller, B H -- GM20069/GM/NIGMS NIH HHS/ -- HL 42384/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1992 Aug 21;257(5073):1083-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of North Carolina, Chapel Hill 27599-7020.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1380723" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cystic Fibrosis/*genetics/pathology/physiopathology ; Cystic Fibrosis Transmembrane Conductance Regulator ; Digestive System/metabolism/pathology ; *Disease Models, Animal ; Exocrine Glands/pathology ; Gallbladder/pathology ; Genitalia, Male/pathology ; Genotype ; Growth ; Intestinal Obstruction/etiology/pathology ; Liver/pathology ; Male ; Meconium/metabolism ; Membrane Proteins/*genetics ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mucus/metabolism ; Mutagenesis ; Pancreas/pathology ; RNA, Messenger/metabolism ; Salivary Glands/pathology
    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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  • 197
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    Immunodominant T cell epitope from signal sequence (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-08-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Buchmeier, M J -- Zinkernagel, R M -- New York, N.Y. -- Science. 1992 Aug 21;257(5073):1142.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1380726" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Epitopes/*immunology ; Glycoproteins/immunology ; Mice ; Protein Sorting Signals/*immunology ; T-Lymphocytes/*immunology
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    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 198
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    A surface protease and the invasive character of plague (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-11-06
    Description: A 9.5-kilobase plasmid of Yersinia pestis, the causative agent of plague, is required for high virulence when mice are inoculated with the bacterium by subcutaneous injection. Inactivation of the plasmid gene pla, which encodes a surface protease, increased the median lethal dose of the bacteria for mice by a millionfold. Moreover, cloned pla was sufficient to restore segregants lacking the entire pla-bearing plasmid to full virulence. Both pla+ strains injected subcutaneously and pla- mutants injected intravenously reached high titers in liver and spleen of infected mice, whereas pla- mutants injected subcutaneously failed to do so even though they establish a sustained local infection at the injection site. More inflammatory cells accumulated in lesions caused by the pla- mutants than in lesions produced by the pla+ parent. The Pla protease was shown to be a plasminogen activator with unusual kinetic properties. It can also cleave complement C3 at a specific site.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sodeinde, O A -- Subrahmanyam, Y V -- Stark, K -- Quan, T -- Bao, Y -- Goguen, J D -- AI22176/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1992 Nov 6;258(5084):1004-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics and Microbiology, University of Massachusetts Medical School, Worcester 01655.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1439793" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; *Bacterial Proteins ; Colony Count, Microbial ; Escherichia coli/enzymology ; Fibrinolysin/chemistry/metabolism ; Injections, Intravenous ; Kinetics ; Liver/microbiology ; Mice ; Molecular Sequence Data ; Mutation ; Plague/microbiology ; Plasmids ; Plasminogen Activators/genetics/*physiology ; Recombinant Proteins/metabolism ; Spleen/microbiology ; Tissue Plasminogen Activator/metabolism ; Urokinase-Type Plasminogen Activator/metabolism ; Yersinia pestis/*enzymology/isolation & purification/*pathogenicity
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 199
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    Trypsin-sensitive, rapid inactivation of a calcium-activated potassium channel (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-09-18
    Description: Most calcium-activated potassium channels couple changes in intracellular calcium to membrane excitability by conducting a current with a probability that depends directly on submembrane calcium concentration. In rat adrenal chromaffin cells, however, a large conductance, voltage- and calcium-activated potassium channel (BK) undergoes rapid inactivation, suggesting that this channel has a physiological role different than that of other BK channels. The inactivation of the BK channel, like that of the voltage-gated Shaker B potassium channel, is removed by trypsin digestion and channels are blocked by the Shaker B amino-terminal inactivating domain. Thus, this BK channel shares functional and possibly structural homologies with other inactivating voltage-gated potassium channels.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Solaro, C R -- Lingle, C J -- New York, N.Y. -- Science. 1992 Sep 18;257(5077):1694-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anesthesiology, 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/1529355" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenal Glands/physiology ; Animals ; Calcium/*pharmacology ; Cattle ; Cell Line ; Cell Membrane/physiology ; Chromaffin System/physiology ; Electric Conductivity ; Ion Channel Gating/drug effects/physiology ; Male ; Membrane Potentials/physiology ; Potassium Channels/*physiology ; Rats ; Rats, Inbred Strains ; Trypsin/*pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 200
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    Mutation of the POU-specific domain of Pit-1 and hypopituitarism without pituitary hypoplasia (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-08-21
    Description: A point mutation in the POU-specific portion of the human gene that encodes the tissue-specific POU-domain transcription factor, Pit-1, results in hypopituitarism, with deficiencies of growth hormone, prolactin, and thyroid-stimulating hormone. In two unrelated Dutch families, a mutation in Pit-1 that altered an alanine in the first putative alpha helix of the POU-specific domain to proline was observed. This mutation generated a protein capable of binding to DNA response elements but unable to effectively activate its known target genes, growth hormone and prolactin. The phenotype of the affected individuals suggests that the mutant Pit-1 protein is competent to initiate other programs of gene activation required for normal proliferation of somatotrope, lactotrope, and thyrotrope cell types. Thus, a mutation in the POU-specific domain of Pit-1 has a selective effect on a subset of Pit-1 target genes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pfaffle, R W -- DiMattia, G E -- Parks, J S -- Brown, M R -- Wit, J M -- Jansen, M -- Van der Nat, H -- Van den Brande, J L -- Rosenfeld, M G -- Ingraham, H A -- HD24960/HD/NICHD NIH HHS/ -- HD2697/HD/NICHD NIH HHS/ -- NIDDK 18477/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1992 Aug 21;257(5073):1118-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatrics, Emory University School of Medicine, Atlanta, GA 30322.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1509263" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Blotting, Northern ; DNA/chemistry/metabolism ; DNA-Binding Proteins/*genetics/metabolism ; Growth Hormone/deficiency ; Humans ; Hypopituitarism/*genetics/pathology ; Mice ; Molecular Sequence Data ; *Mutation ; Nucleic Acid Hybridization ; Pituitary Gland, Anterior/*pathology ; Pituitary Hormones/*deficiency ; Polymerase Chain Reaction ; Prolactin/deficiency ; Rats ; Sequence Homology, Nucleic Acid ; Thyrotropin/deficiency ; Transcription Factor Pit-1 ; Transcription Factors/*genetics/metabolism ; Transfection
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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