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  • Animals  (104)
  • American Association for the Advancement of Science (AAAS)  (104)
  • American Geophysical Union
  • Blackwell Publishing Ltd
  • Springer
  • 2020-2024
  • 2020-2023
  • 1985-1989  (104)
  • 1980-1984
  • 1970-1974
  • 1987  (104)
Collection
Keywords
Publisher
  • American Association for the Advancement of Science (AAAS)  (104)
  • American Geophysical Union
  • Blackwell Publishing Ltd
  • Springer
Years
  • 2020-2024
  • 2020-2023
  • 1985-1989  (104)
  • 1980-1984
  • 1970-1974
Year
  • 1
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    A mammalian mitochondrial RNA processing activity contains nucleus-encoded RNA (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-03-06
    Description: Ribonuclease mitochondrial RNA processing, a site-specific endoribonuclease involved in primer RNA metabolism in mammalian mitochondria, requires an RNA component for its activity. On the basis of copurification and selective inactivation with complementary oligonucleotides, a 135-nucleotide RNA species, not encoded in the mitochondrial genome, is identified as the RNA moiety of the endoribonuclease. This finding implies transport of a nucleus-encoded RNA, essential for organelle DNA replication, to the mitochondrial matrix.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chang, D D -- Clayton, D A -- GM-33088-16/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1987 Mar 6;235(4793):1178-84.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2434997" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cell Nucleus/*physiology ; Chemical Phenomena ; Chemistry ; Drug Resistance ; Endonucleases/isolation & purification/metabolism ; Enzyme Activation/drug effects ; *Genetic Code ; Humans ; Mammals/*genetics/metabolism ; Micrococcal Nuclease/pharmacology ; Mitochondria/*metabolism ; Oligonucleotides/pharmacology ; Organoids/physiology ; RNA/*biosynthesis/genetics/isolation & purification/physiology ; Ribonucleases/metabolism ; Subcellular Fractions/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Conservation of brain amyloid proteins in aged mammals and humans with Alzheimer's disease (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-02-20
    Description: The formation of clusters of altered axons and dendrites surrounding extracellular deposits of amyloid filaments (neuritic plaques) is a major feature of the human brain in both aging and Alzheimer's disease. A panel of antibodies against amyloid filaments and their constituent proteins from humans with Alzheimer's disease cross-reacted with neuritic plaque and cerebrovascular amyloid deposits in five other species of aged mammals, including monkey, orangutan, polar bear, and dog. Antibodies to a 28-amino acid peptide representing the partial protein sequence of the human amyloid filaments recognized the cortical and microvascular amyloid of all of the aged mammals examined. Plaque amyloid, plaque neurites, and neuronal cell bodies in the aged animals showed no reaction with antibodies to human paired helical filaments. Thus, with age, the amyloid proteins associated with progressive cortical degeneration in Alzheimer's disease are also deposited in the brains of other mammals. Aged primates can provide biochemically relevant models for principal features of Alzheimer's disease: cerebrovascular amyloidosis and neuritic plaque formation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Selkoe, D J -- Bell, D S -- Podlisny, M B -- Price, D L -- Cork, L C -- AG05134/AG/NIA NIH HHS/ -- AG06173/AG/NIA NIH HHS/ -- NS23340/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1987 Feb 20;235(4791):873-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3544219" target="_blank"〉PubMed〈/a〉
    Keywords: *Aging ; Alzheimer Disease/pathology/*physiopathology ; Amyloid/immunology/*metabolism ; Amyloidosis/pathology/*physiopathology ; Animals ; Brain/pathology/*physiopathology ; Humans ; Immunoenzyme Techniques ; Macaca mulatta ; Pongo pygmaeus ; Saimiri ; Ursidae
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 3
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    Localization of amyloid beta protein messenger RNA in brains from patients with Alzheimer's disease (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-07-03
    Description: The distribution of cells containing messenger RNA that encodes amyloid beta protein was determined in hippocampi and in various cortical regions from cynomolgus monkeys, normal humans, and patients with Alzheimer's disease by in situ hybridization. Both 35S-labeled RNA antisense and sense probes to amyloid beta protein messenger RNA were used to ensure specific hybridization. Messenger RNA for amyloid beta protein was expressed in a subset of neurons in the prefrontal cortex from monkeys, normal humans, and patients with Alzheimer's disease. This messenger RNA was also present in the neurons of all the hippocampal fields from monkeys, normal humans and, although to a lesser extent in cornu ammonis 1, patients with Alzheimer's disease. The distribution of amyloid beta protein messenger RNA was similar to that of the neurofibrillary tangles of Alzheimer's disease in some regions, but the messenger RNA was also expressed in other neurons that are not usually involved in the pathology of Alzheimer's disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bahmanyar, S -- Higgins, G A -- Goldgaber, D -- Lewis, D A -- Morrison, J H -- Wilson, M C -- Shankar, S K -- Gajdusek, D C -- AG05131/AG/NIA NIH HHS/ -- MH00519/MH/NIMH NIH HHS/ -- NS23038/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1987 Jul 3;237(4810):77-80.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3299701" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/*genetics ; Amyloid/*genetics ; Amyloid beta-Peptides ; Animals ; Brain/*physiopathology ; Cerebral Cortex/physiology ; Gene Expression Regulation ; Hippocampus/physiology ; Humans ; Macaca fascicularis ; Nucleic Acid Hybridization ; RNA, Messenger/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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  • 4
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    Germline organization of the murine T cell receptor beta-chain genes (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-10-23
    Description: The complete germline organization of the beta-chain genes of the murine T cell receptor was elucidated in order to obtain the structural basis for understanding the mechanisms of somatic DNA rearrangements. Twenty of the 22 known variable (V beta) genes are clustered within 250 kilobases of DNA 5' to the constant region (C beta) genes. These V beta genes share the same transcriptional orientation as the diversity (D beta), joining (J beta), and C beta genes, which implies that chromosomal deletion is the mechanism for most V beta to D beta-J beta rearrangements. Within this V beta cluster, the distance between the most proximal V beta gene and the D beta-J beta-C beta cluster is 320 kilobases, as determined by field-inversion gel electrophoresis. The large distance between V beta and D beta, relative to that between D beta and J beta, may have significant implications for the ordered rearrangement of the T cell receptor beta-chain genes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chou, H S -- Nelson, C A -- Godambe, S A -- Chaplin, D D -- Loh, D Y -- GM07067/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1987 Oct 23;238(4826):545-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2821625" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromosome Deletion ; Chromosome Mapping ; DNA/genetics ; DNA Restriction Enzymes ; Electrophoresis ; Macromolecular Substances ; Mice ; Mice, Inbred BALB C ; Mice, Mutant Strains ; Nucleic Acid Hybridization ; Receptors, Antigen, T-Cell/*genetics ; Transcription, Genetic
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    Pancreatic neoplasia induced by SV40 T-antigen expression in acinar cells of transgenic mice (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-10-09
    Description: Three lines of transgenic mice were produced that develop pancreatic neoplasms as a consequence of expression of an elastase I-SV40 T-antigen fusion gene in the acinar cells. A developmental analysis suggests at least a two-stage process in the ontogeny of this disease. The first stage is a T antigen-induced, preneoplastic state characterized by a progression from hyperplasia to dysplasia of the exocrine pancreas, by an increased percentage of tetraploid cells, and by an arrest in acinar cell differentiation. The second stage is characterized by the formation of tumor nodules that appear to be monoclonal, because they have discrete aneuploid DNA contents. The cells within the nodules as compared to normal pancreatic tissue have less total RNA by a factor of 5, less pancreas-specific messenger RNA by a factor of about 50, and increased levels of T-antigen messenger RNA. A tumor cell line has been derived that retains both pancreatic and neoplastic properties.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ornitz, D M -- Hammer, R E -- Messing, A -- Palmiter, R D -- Brinster, R L -- GM-07266/GM/NIGMS NIH HHS/ -- HD-09172/HD/NICHD NIH HHS/ -- NS-00956/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1987 Oct 9;238(4824):188-93.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute Laboratory, University of Washington, Seattle 98195.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2821617" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Polyomavirus Transforming/*genetics ; *Cell Transformation, Neoplastic ; DNA Restriction Enzymes ; Genes ; Genes, Viral ; Mice ; Mice, Transgenic ; Pancreatic Elastase/genetics ; Pancreatic Neoplasms/genetics/*microbiology/pathology ; Protein Kinases/*genetics ; RNA, Messenger/genetics ; Simian virus 40/*genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
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  • 6
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    Primary structure and biochemical properties of an M2 muscarinic receptor (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-05-01
    Description: A partial amino acid sequence obtained for porcine atrial muscarinic acetylcholine receptor was used to isolate complementary DNA clones containing the complete receptor coding region. The deduced 466-amino acid polypeptide exhibits extensive structural and sequence homology with other receptors coupled to guanine nucleotide binding (G) proteins (for example, the beta-adrenergic receptor and rhodopsins); this similarity predicts a structure of seven membrane-spanning regions distinguished by the disposition of a large cytoplasmic domain. Stable transfection of the Chinese hamster ovary cell line with the atrial receptor complementary DNA leads to the binding of muscarinic antagonists in these cells with affinities characteristic of the M2 receptor subtype. The atrial muscarinic receptor is encoded by a unique gene consisting of a single coding exon and multiple, alternatively spliced 5' noncoding regions. The atrial receptor is distinct from the cerebral muscarinic receptor gene product, sharing only 38% overall amino acid homology and possessing a completely nonhomologous large cytoplasmic domain, suggesting a role for the latter region in differential effector coupling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Peralta, E G -- Winslow, J W -- Peterson, G L -- Smith, D H -- Ashkenazi, A -- Ramachandran, J -- Schimerlik, M I -- Capon, D J -- CA16417/CA/NCI NIH HHS/ -- HL23632/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1987 May 1;236(4801):600-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3107123" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cell Line ; DNA/genetics ; Exons ; GTP-Binding Proteins/metabolism ; Heart Atria/analysis ; Immunosorbent Techniques ; Membrane Proteins ; Molecular Weight ; Nucleic Acid Hybridization ; Peptide Fragments/metabolism ; Quinuclidinyl Benzilate/metabolism ; Receptors, Muscarinic/*genetics/metabolism ; Sequence Homology, Nucleic Acid ; Swine ; Transfection
    Print ISSN: 0036-8075
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  • 7
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    Myocardial failure in cats associated with low plasma taurine: a reversible cardiomyopathy (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-08-14
    Description: Thousands of pet cats die each year with dilated cardiomyopathy, the cause of which is unknown. Although taurine is present in millimolar concentrations in the myocardium of all mammals, taurine depletion has not previously been associated with a decrease in myocardial function in any species. In this study, low plasma taurine concentrations associated with echocardiographic evidence of myocardial failure were observed in 21 cats fed commercial cat foods and in 2 of 11 cats fed a purified diet containing marginally low concentrations of taurine for 4 years. Oral supplementation of taurine resulted in increased plasma taurine concentrations and was associated with normalization of left ventricular function in both groups of cats. Since myocardial concentrations of taurine are directly related to plasma concentrations and low plasma concentrations were found to be associated with myocardial failure in cats, a direct link between decreased taurine concentration in the myocardium and decreased myocardial mechanical function is proposed.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pion, P D -- Kittleson, M D -- Rogers, Q R -- Morris, J G -- New York, N.Y. -- Science. 1987 Aug 14;237(4816):764-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3616607" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cardiomyopathy, Dilated/diagnosis/etiology/*veterinary ; *Cat Diseases ; Cats ; Dogs ; Echocardiography ; Humans ; Myocardium/metabolism ; Retinal Degeneration/etiology/veterinary ; Taurine/blood/*deficiency/metabolism
    Print ISSN: 0036-8075
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  • 8
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    Three recessive loci required for insulin-dependent diabetes in nonobese diabetic mice (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-07-17
    Description: A polygenic basis for susceptibility to insulin-dependent diabetes in nonobese diabetic (NOD) mice has been established by outcross to a related inbred strain, nonobese normal (NON). Analysis of first and second backcross progeny has shown that at least three recessive genes are required for development of overt diabetes. One, Idd-1s, is tightly linked to the H-2K locus on chromosome 17; another, Idd-2s, is localized proximal to the Thy-1/Alp-1 cluster on chromosome 9. Segregation of a third, Idd-3s, could be shown in a second backcross. Neither Idd-1s nor Idd-2s could individually be identified as the locus controlling insulitis; leukocytic infiltrates in pancreas were common in most asymptomatic BC1 mice. Both F1 and BC1 mice exhibited the unusually high percentage of splenic T lymphocytes characteristic of NOD, suggesting dominant inheritance of this trait. The polygenic control of diabetogenesis in NOD mice, in which a recessive gene linked to the major histocompatibility complex is but one of several controlling loci, suggests that similar polygenic interactions underlie this type of diabetes in humans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Prochazka, M -- Leiter, E H -- Serreze, D V -- Coleman, D L -- AM 14461/AM/NIADDK NIH HHS/ -- AM 27722/AM/NIADDK NIH HHS/ -- AM 36175/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1987 Jul 17;237(4812):286-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2885918" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromosome Mapping ; Diabetes Mellitus, Type 1/*genetics/immunology ; *Genes, Recessive ; Islets of Langerhans/immunology ; Mice ; Mice, Inbred Strains ; Mice, Mutant Strains ; Polymorphism, Genetic ; Polymorphism, Restriction Fragment Length ; T-Lymphocytes/physiology
    Print ISSN: 0036-8075
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  • 9
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    A cell-cycle constraint on the regulation of gene expression by platelet-derived growth factor (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-11-27
    Description: In density-arrested monolayer cultures of Balb/c 3T3 cells, platelet-derived growth factor (PDGF) stimulates expression of the c-myc and c-fos proto-oncogenes, as well as the functionally uncharacterized genes, JE, KC, and JB. These genes are not coordinately regulated. Under ordinary conditions, c-fos, JE, KC, and JB respond to PDGF only when the cells are in a state of G0 growth arrest at the time of PDGF addition. The c-myc gene is regulated in opposition to the other genes, responding best to PDGF in cycling cultures.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rollins, B J -- Morrison, E D -- Stiles, C D -- CA 20042-09/CA/NCI NIH HHS/ -- GM 31489-04/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1987 Nov 27;238(4831):1269-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Medicine, Dana-Farber Cancer Institute, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3685976" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Cycle/drug effects ; Cell Division/drug effects ; Cells, Cultured ; Gene Expression Regulation/*drug effects ; Interphase ; Mice ; Mice, Inbred BALB C ; Platelet-Derived Growth Factor/*pharmacology ; Proto-Oncogenes/*drug effects ; Transcription, Genetic/*drug effects
    Print ISSN: 0036-8075
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  • 10
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    Blocking of HIV-1 infectivity by a soluble, secreted form of the CD4 antigen (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-12-18
    Description: The initial event in the infection of human T lymphocytes, macrophages, and other cells by human immunodeficiency virus (HIV-1) is the attachment of the HIV-1 envelope glycoprotein gp120 to its cellular receptor, CD4. As a step toward designing antagonists of this binding event, soluble, secreted forms of CD4 were produced by transfection of mammalian cells with vectors encoding versions of CD4 lacking its transmembrane and cytoplasmic domains. The soluble CD4 so produced binds gp120 with an affinity and specificity comparable to intact CD4 and is capable of neutralizing the infectivity of HIV-1. These studies reveal that the high-affinity CD4-gp120 interaction does not require other cell or viral components and may establish a novel basis for therapeutic intervention in the acquired immune deficiency syndrome (AIDS).〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Smith, D H -- Byrn, R A -- Marsters, S A -- Gregory, T -- Groopman, J E -- Capon, D J -- New York, N.Y. -- Science. 1987 Dec 18;238(4834):1704-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Genentech, Inc., South San Francisco, CA 94080.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3500514" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/immunology ; Animals ; Antigens, Differentiation, T-Lymphocyte/*immunology ; Cell Line ; HIV/immunology/*pathogenicity/physiology ; Humans ; Receptors, Virus/immunology/*physiology ; Recombinant Proteins/immunology ; T-Lymphocytes/*immunology ; Viral Envelope Proteins/immunology/*physiology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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