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  • Humans  (192)
  • Molecular Sequence Data  (49)
  • ASTROPHYSICS
  • Life and Medical Sciences
  • American Association for the Advancement of Science (AAAS)  (221)
  • 1985-1989  (221)
  • 1989  (128)
  • 1987  (93)
Collection
Keywords
Publisher
  • American Association for the Advancement of Science (AAAS)  (221)
  • Wiley-Blackwell  (292)
Years
  • 1985-1989  (221)
Year
  • 1
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    Neurotoxicity of a fragment of the amyloid precursor associated with Alzheimer's disease (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-07-28
    Description: Amyloid deposition in senile plaques and the cerebral vasculature is a marker of Alzheimer's disease. Whether amyloid itself contributes to the neurodegenerative process or is simply a by-product of that process is unknown. Pheochromocytoma (PC12) and fibroblast (NIH 3T3) cell lines were transfected with portions of the gene for the human amyloid precursor protein. Stable PC12 cell transfectants expressing a specific amyloid-containing fragment of the precursor protein gradually degenerated when induced to differentiate into neuronal cells with nerve growth factor. Conditioned medium from these cells was toxic to neurons in primary hippocampal cultures, and the toxic agent could be removed by immunoabsorption with an antibody directed against the amyloid polypeptide. Thus, a peptide derived from the amyloid precursor may be neurotoxic.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yankner, B A -- Dawes, L R -- Fisher, S -- Villa-Komaroff, L -- Oster-Granite, M L -- Neve, R L -- HD 18655/HD/NICHD NIH HHS/ -- HD 18658/HD/NICHD NIH HHS/ -- NS 01240/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1989 Jul 28;245(4916):417-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, Harvard Medical School, Boston, MA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2474201" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/*etiology/pathology ; Amyloid/genetics/*physiology ; Blotting, Northern ; Cell Line ; Fibroblasts ; Gene Expression Regulation ; Humans ; Immunoblotting ; Neurons/pathology ; Nucleic Acid Hybridization ; Pheochromocytoma ; Protein Precursors/genetics/*physiology ; RNA/analysis/genetics ; Restriction Mapping ; Transfection ; Tumor Cells, Cultured
    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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    An assay for circulating antibodies to a major etiologic virus of human non-A, non-B hepatitis (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-04-21
    Description: A specific assay has been developed for a blood-borne non-A, non-B hepatitis (NANBH) virus in which a polypeptide synthesized in recombinant yeast clones of the hepatitis C virus (HCV) is used to capture circulating viral antibodies. HCV antibodies were detected in six of seven human sera that were shown previously to transmit NANBH to chimpanzees. Assays of ten blood transfusions in the United States that resulted in chronic NANBH revealed that there was at least one positive blood donor in nine of these cases and that all ten recipients seroconverted during their illnesses. About 80 percent of chronic, post-transfusion NANBH (PT-NANBH) patients from Italy and Japan had circulating HCV antibody; a much lower frequency (15 percent) was observed in acute, resolving infections. In addition, 58 percent of NANBH patients from the United States with no identifiable source of parenteral exposure to the virus were also positive for HCV antibody. These data indicate that HCV is a major cause of NANBH throughout the world.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kuo, G -- Choo, Q L -- Alter, H J -- Gitnick, G L -- Redeker, A G -- Purcell, R H -- Miyamura, T -- Dienstag, J L -- Alter, M J -- Stevens, C E -- New York, N.Y. -- Science. 1989 Apr 21;244(4902):362-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Chiron Corporation, Emeryville, CA 94608.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2496467" target="_blank"〉PubMed〈/a〉
    Keywords: Antibodies, Viral/*analysis ; Blood Donors ; Blood Transfusion ; Hepatitis C/*immunology/transmission ; Hepatitis Viruses/*immunology ; Hepatitis, Viral, Human/*immunology ; Humans ; Italy ; Japan ; United States
    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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  • 3
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    Purification and complementary DNA cloning of a receptor for basic fibroblast growth factor (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-07-07
    Description: Basic fibroblast growth factor (bFGF) participates in many processes including early developmental events, angiogenesis, wound healing, and maintenance of neuronal cell viability. A 130-kilodalton protein was isolated on the basis of its ability to specifically bind to bFGF. A complementary DNA clone was isolated with an oligonucleotide probe corresponding to determined amino acid sequences of tryptic peptide fragments of the purified protein. The putative bFGF receptor encoded by this complementary DNA is a transmembrane protein that contains three extracellular immunoglobulin-like domains, an unusual acidic region, and an intracellular tyrosine kinase domain. These domains are arranged in a pattern that is different from that of any growth factor receptor described.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, P L -- Johnson, D E -- Cousens, L S -- Fried, V A -- Williams, L T -- CA 21765/CA/NCI NIH HHS/ -- R01 HL32898/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1989 Jul 7;245(4913):57-60.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, 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/2544996" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cells, Cultured ; Chick Embryo ; *Cloning, Molecular ; DNA/*genetics ; Fibroblast Growth Factors/*genetics ; Kinetics ; Mice ; Molecular Sequence Data ; Peptide Fragments/analysis ; Receptors, Cell Surface/*genetics/metabolism ; Receptors, Fibroblast Growth Factor ; Recombinant Proteins/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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  • 4
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    Purification, cloning, and expression of ciliary neurotrophic factor (CNTF) (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-11-24
    Description: Ciliary neurotrophic factor (CNTF) is one of a small number of proteins with neurotrophic activities distinct from nerve growth factor (NGF). CNTF has now been purified and cloned and the primary structure of CNTF from rabbit sciatic nerve has been determined. Biologically active CNTF has been transiently expressed from a rabbit complementary DNA clone. CNTF is a neural effector without significant sequence homologies to any previously reported protein.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lin, L F -- Mismer, D -- Lile, J D -- Armes, L G -- Butler, E T 3rd -- Vannice, J L -- Collins, F -- New York, N.Y. -- Science. 1989 Nov 24;246(4933):1023-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Protein Chemistry Group, Synergen, Inc., Boulder, CO 80301.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2587985" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cell Line ; Ciliary Neurotrophic Factor ; Cloning, Molecular ; DNA/genetics ; Molecular Sequence Data ; Nerve Growth Factors/*genetics ; Nerve Tissue Proteins/biosynthesis/*genetics/isolation & purification ; Rabbits ; Recombinant Proteins/biosynthesis ; Sciatic Nerve/metabolism ; Transfection
    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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    Absence of duplication of chromosome 21 genes in familial and sporadic Alzheimer's disease (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-10-30
    Description: The possibility that Alzheimer's disease (AD) is caused by overexpression or duplication of one or more genes on chromosome 21 has been raised by the observation of AD-like neuropathologic changes in individuals with Down syndrome and by the mapping of both the defect for familial AD and the amyloid beta protein gene to this autosome. Possible duplication on chromosome 21 was investigated in both familial and sporadic AD by means of restriction fragment length polymorphisms for the amyloid and SODI loci, as well as for DNA markers in the vicinity of the familial AD defect and in the critical Down syndrome region of chromosome 21. No evidence of increased DNA dosage was observed in either brain or leukocytes of patients with inherited or sporadic forms of AD. Duplication of these regions is therefore not a frequent event in either form of AD. Furthermore, no significant allelic association was detected between AD and any of the loci, including the amyloid and SODI genes, providing no support for the hypothesis that defects in these specific genes are the primary cause of AD.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉St George-Hyslop, P H -- Tanzi, R E -- Polinsky, R J -- Neve, R L -- Pollen, D -- Drachman, D -- Growdon, J -- Cupples, L A -- Nee, L -- Myers, R H -- ADRC P50 AGO5134-02/AD/ADAMHA HHS/ -- NS20012/NS/NINDS NIH HHS/ -- R01 AGO6865-1/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 1987 Oct 30;238(4827):664-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neurogenetics Laboratory, Massachusetts General Hospital, Boston.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2890206" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Alzheimer Disease/*genetics ; Amyloid/genetics ; *Chromosomes, Human, Pair 21 ; Genes ; Genetic Linkage ; Humans ; Polymorphism, Restriction Fragment Length
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  • 6
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    Tissue distribution and developmental expression of the messenger RNA encoding angiogenin (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-07-17
    Description: New blood vessel growth occurs during normal fetal development and in diseases such as cancer and diabetes. The polypeptide angiogenin induces new blood vessel growth in two biological assays and may play a role in the vascular development of the fetus and in the neovascularization that accompanies diseases and wound healing. A complementary DNA probe for human angiogenin was used to examine the tissue distribution of angiogenin messenger RNA (mRNA) in the developing rat and in selected transformed cell lines. Angiogenin mRNA was detected predominantly in adult liver but was also detectable at low levels in other tissues. The expression of the angiogenin gene in rat liver was found to be developmentally regulated; mRNA levels were low in the developing fetus, increased in the neonate, and maximal in the adult. The amount of angiogenin mRNA in human HT-29 colon carcinoma and SK-HEP hepatoma cells was not greater than that in normal rat liver. These results demonstrate that angiogenin is predominantly expressed in adult liver, that the pattern of angiogenin gene expression is not temporally related to vascular development in the rat, and that the transformed cells studied do not contain more angiogenin mRNA than does normal liver. If angiogenin activity is controlled at the transcriptional level, the results of this study suggest that the primary function of angiogenin in vivo may be in processes other than the regulation of vascular growth.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weiner, H L -- Weiner, L H -- Swain, J L -- HL26831/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1987 Jul 17;237(4812):280-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2440105" target="_blank"〉PubMed〈/a〉
    Keywords: Age Factors ; Animals ; Cell Line ; Gene Expression Regulation ; Humans ; Liver/physiology ; Neoplasm Proteins/*genetics ; Neovascularization, Pathologic ; RNA, Messenger/genetics ; Rats ; *Ribonuclease, Pancreatic ; Tissue Distribution
    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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  • 7
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    Overexpression of transforming growth factor alpha in psoriatic epidermis (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-02-10
    Description: Transforming growth factor alpha (TGF-alpha) is produced by and required for the growth of epithelial cells and is angiogenic in vivo. Since epidermal hyperplasia and angiogenesis are hallmarks of psoriasis, TGF-alpha gene expression was analyzed in epidermal biopsies of normal and psoriatic skin. TGF-alpha messenger RNA and protein are much more abundant in lesional psoriatic epidermis than in normal-appearing skin of psoriatic patients or in normal epidermis. In contrast, messenger RNA levels of transforming growth factor beta 1 (TGF-beta 1), which inhibits epithelial cell growth, are not significantly different in normal, uninvolved, and lesional psoriatic epidermis. Thus, psoriatic epidermal hyperplasia may involve increased expression of a keratinocyte mitogen (TGF-alpha) rather than deficient expression of a growth inhibitor (TGF-beta 1).〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Elder, J T -- Fisher, G J -- Lindquist, P B -- Bennett, G L -- Pittelkow, M R -- Coffey, R J Jr -- Ellingsworth, L -- Derynck, R -- Voorhees, J J -- 5-T32-AM07197-10/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1989 Feb 10;243(4892):811-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Dermatology, University of Michigan, Ann Arbor 48109.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2916128" target="_blank"〉PubMed〈/a〉
    Keywords: Blotting, Northern ; Epidermis/physiopathology ; Gene Expression Regulation/drug effects ; Humans ; Immunoassay ; Psoriasis/*genetics ; Transforming Growth Factors/*genetics/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
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    Cl- channels in CF: lack of activation by protein kinase C and cAMP-dependent protein kinase (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-06-16
    Description: Secretory chloride channels can be activated by adenosine 3',5'-monophosphate (cAMP)-dependent protein kinase in normal airway epithelial cells but not in cells from individuals with cystic fibrosis (CF). In excised, inside-out patches of apical membrane of normal human airway cells and airway cells from three patients with CF, the chloride channels exhibited a characteristic outwardly rectifying current-voltage relation and depolarization-induced activation. Channels from normal tissues were activated by both cAMP-dependent protein kinase and protein kinase C. However, chloride channels from CF patients could not be activated by either kinase. Thus, gating of normal epithelial chloride channels is regulated by both cAMP-dependent protein kinase and protein kinase C, and regulation by both kinases is defective in CF.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hwang, T C -- Lu, L -- Zeitlin, P L -- Gruenert, D C -- Huganir, R -- Guggino, W B -- 1-K08-HL02188/HL/NHLBI NIH HHS/ -- R01-DK 39619/DK/NIDDK NIH HHS/ -- R01-HL 40178/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1989 Jun 16;244(4910):1351-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, Johns Hopkins University, Baltimore, MD 21205.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2472005" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Chloride Channels ; Chlorides/*physiology ; Cystic Fibrosis/*physiopathology ; Electrophysiology ; Fetus ; Humans ; In Vitro Techniques ; Ion Channels/*physiology ; Membrane Proteins/*physiology ; Protein Kinase C/*physiology ; Protein Kinases/*physiology ; Respiratory System/cytology/physiopathology
    Print ISSN: 0036-8075
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  • 9
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    Membrane anchoring of a human IgG Fc receptor (CD16) determined by a single amino acid (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-12-22
    Description: CD16 is a low-affinity immunoglobulin G (IgG) Fc receptor that is expressed on natural killer (NK) cells, granulocytes, activated macrophages, and some T lymphocytes. Two similar genes, CD16-I and CD16-II, encode membrane glycoproteins that are anchored by phosphatidylinositol (PI)-glycan and transmembrane polypeptides, respectively. The primary structural requirements for PI-linkage were examined by constructing a series of hybrid cDNA molecules. Although both cDNA's have an identical COOH-terminal hydrophobic segment, CD16-I has Ser203 whereas CD16-II has Phe203. Conversion of Phe to Ser in CD16-II permits expression of a PI-glycan-anchored glycoprotein, whereas conversion of Ser to Phe in CD16-I prevents PI-glycan linkage.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lanier, L L -- Cwirla, S -- Yu, G -- Testi, R -- Phillips, J H -- New York, N.Y. -- Science. 1989 Dec 22;246(4937):1611-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Becton Dickinson Monoclonal Center, Inc., Mountain View, CA 94043.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2531919" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD/*genetics ; Antigens, Differentiation/*genetics/metabolism ; Base Sequence ; Cell Line ; Cell Membrane/immunology ; Codon/genetics ; *Genes, Immunoglobulin ; Granulocytes/immunology ; Humans ; Membrane Glycoproteins/*genetics ; Molecular Sequence Data ; *Phenylalanine ; Receptors, Fc/*genetics/metabolism ; Receptors, IgG ; *Serine ; Transfection
    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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  • 10
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    Polymerase chain reaction with single-sided specificity: analysis of T cell receptor delta chain (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-01-13
    Description: In the polymerase chain reaction (PCR), two specific oligonucleotide primers are used to amplify the sequences between them. However, this technique is not suitable for amplifying genes that encode molecules where the 5' portion of the sequences of interest is not known, such as the T cell receptor (TCR) or immunoglobulins. Because of this limitation, a novel technique, anchored polymerase chain reaction (A-PCR), was devised that requires sequence specificity only on the 3' end of the target fragment. It was used to analyze TCR delta chain mRNA's from human peripheral blood gamma delta T cells. Most of these cells had a V delta gene segment not previously described (V delta 3), and the delta chain junctional sequences formed a discrete subpopulation compared with those previously reported.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Loh, E Y -- Elliott, J F -- Cwirla, S -- Lanier, L L -- Davis, M M -- New York, N.Y. -- Science. 1989 Jan 13;243(4888):217-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departments of Medicine and Microbiology and Immunology, Stanford University School of Medicine, CA 94305-5402.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2463672" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; Cell Line ; Gene Amplification ; *Genes ; Humans ; Macromolecular Substances ; Molecular Sequence Data ; Oligonucleotide Probes ; RNA, Messenger/genetics ; RNA-Directed DNA Polymerase ; Receptors, Antigen, T-Cell/*genetics ; T-Lymphocytes/immunology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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