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  • Mice  (30)
  • Cell Line  (12)
  • Molecular Weight
  • American Association for the Advancement of Science (AAAS)  (42)
  • American Chemical Society
  • International Union of Crystallography (IUCr)
  • 2020-2022
  • 1985-1989  (42)
  • 1980-1984
  • 1987  (42)
Collection
Keywords
Publisher
  • American Association for the Advancement of Science (AAAS)  (42)
  • American Chemical Society
  • International Union of Crystallography (IUCr)
Years
  • 2020-2022
  • 1985-1989  (42)
  • 1980-1984
Year
  • 1
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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
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Identification of an amplified, highly expressed gene in a human glioma (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-04-03
    Description: A gene, termed gli, was identified that is amplified more than 50-fold in a malignant glioma. The gene is expressed at high levels in the original tumor and its derived cell line and is located at chromosome 12 position (q13 to q14.3). The gli gene is a member of a select group of cellular genes that are genetically altered in primary human tumors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kinzler, K W -- Bigner, S H -- Bigner, D D -- Trent, J M -- Law, M L -- O'Brien, S J -- Wong, A J -- Vogelstein, B -- CA-09243/CA/NCI NIH HHS/ -- CA-43722/CA/NCI NIH HHS/ -- NS-20023/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1987 Apr 3;236(4797):70-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3563490" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; *Chromosomes, Human, Pair 12 ; Cloning, Molecular ; DNA, Neoplasm/*genetics ; *Gene Amplification ; Gene Expression Regulation ; Glioma/*genetics ; Humans ; RNA, Messenger/genetics ; RNA, Neoplasm/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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  • 3
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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
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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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
    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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    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
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    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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  • 7
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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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  • 8
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    Encystation and expression of cyst antigens by Giardia lamblia in vitro (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-02-27
    Description: The cyst form of Giardia lamblia is responsible for transmission of giardiasis, a common waterborne intestinal disease. In these studies, encystation of Giardia lamblia in vitro was demonstrated by morphologic, immunologic, and biochemical criteria. In the suckling mouse model, the jejunum was shown to be a major site of encystation of the parasite. Small intestinal factors were therefore tested as stimuli of encystation. An antiserum that reacted with cysts, but not with cultured trophozoites was raised in rabbits and used as a sensitive probe for differentiation in vitro. Cultured trophozoites that were exposed to bile salts showed a more than 20-fold increase in the number of oval, refractile cells that reacted strongly with anticyst antibodies, and in the expression of major cyst antigens. Exposure to primary bile salts resulted in higher levels of encystation than exposure to secondary bile salts. These studies will aid in understanding the differentiation of an important protozoan pathogen.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gillin, F D -- Reiner, D S -- Gault, M J -- Douglas, H -- Das, S -- Wunderlich, A -- Sauch, J F -- AI 19863/AI/NIAID NIH HHS/ -- AM 35108/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1987 Feb 27;235(4792):1040-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3547646" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Protozoan/*analysis ; Bile Acids and Salts/pharmacology ; Enzyme-Linked Immunosorbent Assay ; Fluorescent Antibody Technique ; Giardia/drug effects/immunology/*physiology ; Giardiasis/parasitology ; Intestines/parasitology ; Mice
    Print ISSN: 0036-8075
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  • 9
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    Genetic reconstitution of functional acetylcholine receptor channels in mouse fibroblasts (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-12-18
    Description: Foreign genes can be stably integrated into the genome of a cell by means of DNA-mediated gene transfer techniques, and large quantities of homogenous cells that continuously express these gene products can then be isolated. Such an expression system can be used to study the functional consequences of introducing specific mutations into genes and to study the expressed protein in the absence of cellular components with which it is normally in contact. All four Torpedo acetylcholine receptor (AChR) subunit complementary DNA's were introduced into the genome of a mouse fibroblast cell by DNA-mediated gene transfer. A clonal cell line that stably produced high concentrations of correctly assembled cell surface AChR's and formed proper ligand-gated ion channels was isolated. With this new expression system, recombinant DNA, biochemical, pharmacological, and electrophysiological techniques were combined to study Torpedo AChR's in a single intact system. The physiological and pharmacological profiles of Torpedo AChR's expressed in mouse fibroblast cells differ in some details from those described earlier, and may provide a more accurate reflection of the properties of this receptor in its natural environment.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Claudio, T -- Green, W N -- Hartman, D S -- Hayden, D -- Paulson, H L -- Sigworth, F J -- Sine, S M -- Swedlund, A -- NS 07102/NS/NINDS NIH HHS/ -- NS 21501/NS/NINDS NIH HHS/ -- NS 21714/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1987 Dec 18;238(4834):1688-94.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, CT 06510.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3686008" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cell Membrane/physiology ; Fibroblasts/metabolism ; *Genes ; Kinetics ; Mice ; Receptors, Cholinergic/*genetics/metabolism ; Torpedo ; *Transfection
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
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  • 10
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    Molecular cloning of complementary DNA encoding the avian receptor for vitamin D (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-03-06
    Description: Vitamin D3 receptors are intracellular proteins that mediate the nuclear action of the active metabolite 1,25-dihydroxyvitamin D3 [1,25(OH)2D3]. Two receptor-specific monoclonal antibodies were used to recover the complementary DNA (cDNA) of this regulatory protein from a chicken intestinal lambda gt11 cDNA expression library. The amino acid sequences that were deduced from this cDNA revealed a highly conserved cysteine-rich region that displayed homology with a domain characteristic of other steroid receptors and with the gag-erbA oncogene product of avian erythroblastosis virus. RNA selected via hybridization with this DNA sequence directed the cell-free synthesis of immunoprecipitable vitamin D3 receptor. Northern blot analysis of polyadenylated RNA with these cDNA probes revealed two vitamin D receptor messenger RNAs (mRNAs) of 2.6 and 3.2 kilobases in receptor-containing chicken tissues and a major cross-hybridizing receptor mRNA species of 4.2 kilobases in mouse 3T6 fibroblasts. The 4.2-kilobase species was substantially increased by prior exposure of 3T6 cells to 1,25(OH)2D3. This cDNA represents perhaps the rarest mRNA cloned to date in eukaryotes, as well as the first receptor sequence described for an authentic vitamin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McDonnell, D P -- Mangelsdorf, D J -- Pike, J W -- Haussler, M R -- O'Malley, B W -- New York, N.Y. -- Science. 1987 Mar 6;235(4793):1214-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3029866" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Calcitriol/metabolism ; Chickens/*metabolism ; Cholecalciferol/*metabolism ; Cloning, Molecular ; DNA/*genetics ; Genetic Code ; Mice ; Molecular Conformation ; RNA, Messenger/metabolism ; Receptors, Steroid/*genetics/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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