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  • Articles  (336)
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  • American Association for the Advancement of Science (AAAS)  (336)
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  • Articles  (336)
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  • American Association for the Advancement of Science (AAAS)  (336)
  • American Association for the Advancement of Science
  • American Chemical Society
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  • 101
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    Ablation of transplanted HTLV-I tax-transformed tumors in mice by antisense inhibition of NF-kappa B (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-03-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kitajima, I -- Shinohara, T -- Bilakovics, J -- Brown, D A -- Xu, X -- Nerenberg, M -- New York, N.Y. -- Science. 1993 Mar 12;259(5101):1523.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8456277" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cell Transformation, Neoplastic ; *Genes, pX ; Human T-lymphotropic virus 1/*genetics ; Humans ; Mice ; Molecular Sequence Data ; Oligodeoxyribonucleotides ; Oligonucleotides, Antisense
    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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    T cell receptor specificity and diabetes in nonobese diabetic mice (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-12-03
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mathis, D -- Benoist, C -- New York, N.Y. -- Science. 1993 Dec 3;262(5139):1583; author reply 1584.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8248810" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Diabetes Mellitus, Type 1/*immunology ; Mice ; Mice, Inbred NOD ; Mice, Transgenic ; Receptors, Antigen, T-Cell, alpha-beta/*genetics ; 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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  • 103
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    Linkage on chromosome 3 of autoimmune diabetes and defective Fc receptor for IgG in NOD mice (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-04-30
    Description: A congenic, non-obese diabetic (NOD) mouse strain that contains a segment of chromosome 3 from the diabetes-resistant mouse strain B6.PL-Thy-1a was less susceptible to diabetes than NOD mice. A fully penetrant immunological defect also mapped to this segment, which encodes the high-affinity Fc receptor for immunoglobulin G (IgG), Fc gamma RI. The NOD Fcgr1 allele, which results in a deletion of the cytoplasmic tail, caused a 73 percent reduction in the turnover of cell surface receptor-antibody complexes. The development of congenic strains and the characterization of Mendelian traits that are specific to the disease phenotype demonstrate the feasibility of dissecting the pathophysiology of complex, non-Mendelian diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Prins, J B -- Todd, J A -- Rodrigues, N R -- Ghosh, S -- Hogarth, P M -- Wicker, L S -- Gaffney, E -- Podolin, P L -- Fischer, P A -- Sirotina, A -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 1993 Apr 30;260(5108):695-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Nuffield Department of Surgery, University of Oxford, John Radcliffe Hospital, Headington, United Kingdom.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8480181" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autoimmune Diseases/*genetics ; Base Sequence ; Crosses, Genetic ; Diabetes Mellitus, Type 1/*genetics ; Endocytosis ; Female ; Gene Deletion ; *Genetic Linkage ; Genetic Markers ; Immunoglobulin G/metabolism ; Male ; Mice ; Mice, Inbred NOD ; Molecular Sequence Data ; Mutation ; Phenotype ; Receptors, IgG/*genetics/metabolism
    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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    Isolation of the cyclosporin-sensitive T cell transcription factor NFATp (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-10-29
    Description: Nuclear factor of activated T cells (NFAT) is a transcription factor that regulates expression of the cytokine interleukin-2 (IL-2) in activated T cells. The DNA-binding specificity of NFAT is conferred by NFATp, a phosphoprotein that is a target for the immunosuppressive compounds cyclosporin A and FK506. Here, the purification of NFATp from murine T cells and the isolation of a complementary DNA clone encoding NFATp are reported. A truncated form of NFATp, expressed as a recombinant protein in bacteria, binds specifically to the NFAT site of the murine IL-2 promoter and forms a transcriptionally active complex with recombinant protein fragment react with T cell NFATp. The molecular cloning of NFATp should allow detailed analysis of a T cell transcription factor that is central to initiation of the immune response.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McCaffrey, P G -- Luo, C -- Kerppola, T K -- Jain, J -- Badalian, T M -- Ho, A M -- Burgeon, E -- Lane, W S -- Lambert, J N -- Curran, T -- CA42471/CA/NCI NIH HHS/ -- GM46227/GM/NIGMS NIH HHS/ -- NS25078/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1993 Oct 29;262(5134):750-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Tumor Virology, Dana-Farber Cancer Institute, Boston, MA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8235597" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cell Line ; DNA, Complementary ; DNA-Binding Proteins/genetics/*isolation & purification/physiology ; Immunosuppressive Agents/pharmacology ; Interleukin-2/genetics ; Mice ; Molecular Sequence Data ; NFATC Transcription Factors ; *Nuclear Proteins ; Phosphoproteins/genetics/isolation & purification/physiology ; Promoter Regions, Genetic ; Proto-Oncogene Proteins c-fos/physiology ; Proto-Oncogene Proteins c-jun/physiology ; RNA, Messenger/analysis ; Recombinant Proteins ; T-Lymphocytes/*chemistry ; Transcription Factors/genetics/*isolation & purification/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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    Genetic 'master switch' for left-right symmetry found (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-04-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ewing, T -- New York, N.Y. -- Science. 1993 Apr 30;260(5108):624-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8480173" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Embryonic and Fetal Development/*genetics ; Female ; *Genes, Recessive ; Male ; Mice ; Mice, Transgenic ; Mutagenesis, Insertional ; Situs Inversus/*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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  • 106
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    Human Sos1: a guanine nucleotide exchange factor for Ras that binds to GRB2 (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-05-28
    Description: A human complementary DNA was isolated that encodes a widely expressed protein, hSos1, that is closely related to Sos, the product of the Drosophila son of sevenless gene. The hSos1 protein contains a region of significant sequence similarity to CDC25, a guanine nucleotide exchange factor for Ras from yeast. A fragment of hSos1 encoding the CDC25-related domain complemented loss of CDC25 function in yeast. This hSos1 domain specifically stimulated guanine nucleotide exchange on mammalian Ras proteins in vitro. Mammalian cells overexpressing full-length hSos1 had increased guanine nucleotide exchange activity. Thus hSos1 is a guanine nucleotide exchange factor for Ras. The hSos1 interacted with growth factor receptor-bound protein 2 (GRB2) in vivo and in vitro. This interaction was mediated by the carboxyl-terminal domain of hSos1 and the Src homology 3 (SH3) domains of GRB2. These results suggest that the coupling of receptor tyrosine kinases to Ras signaling is mediated by a molecular complex consisting of GRB2 and hSos1.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chardin, P -- Camonis, J H -- Gale, N W -- van Aelst, L -- Schlessinger, J -- Wigler, M H -- Bar-Sagi, D -- CA46370/CA/NCI NIH HHS/ -- CA55360/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1993 May 28;260(5112):1338-43.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut de Pharmacologie Moleculaire et Cellulaire, CNRS, Valbonne, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8493579" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptor Proteins, Signal Transducing ; Amino Acid Sequence ; Animals ; Base Sequence ; *Cell Cycle Proteins ; Cell Line ; Fungal Proteins/chemistry/*metabolism ; GRB2 Adaptor Protein ; Guanine Nucleotide Exchange Factors ; Guanosine Diphosphate/metabolism ; Guanosine Triphosphate/metabolism ; Humans ; Membrane Proteins/chemistry/genetics/*metabolism ; Mice ; Molecular Sequence Data ; Proteins/*metabolism ; Proto-Oncogene Proteins p21(ras)/*metabolism ; Recombinant Fusion Proteins/metabolism ; Sequence Alignment ; Son of Sevenless Proteins ; ras Guanine Nucleotide Exchange Factors ; *ras-GRF1
    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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  • 107
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    SH2-containing phosphotyrosine phosphatase as a target of protein-tyrosine kinases (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-03-12
    Description: A mouse phosphotyrosine phosphatase containing two Src homology 2 (SH2) domains, Syp, was identified. Syp bound to autophosphorylated epidermal growth factor (EGF) and platelet-derived growth factor (PDGF) receptors through its SH2 domains and was rapidly phosphorylated on tyrosine in PDGF- and EGF-stimulated cells. Furthermore, Syp was constitutively phosphorylated on tyrosine in cells transformed by v-src. This mammalian phosphatase is most closely related, especially in its SH2 domains, to the corkscrew (csw) gene product of Drosophila, which is required for signal transduction downstream of the Torso receptor tyrosine kinase. The Syp gene is widely expressed throughout embryonic mouse development and in adult tissues. Thus, Syp may function in mammalian embryonic development and as a common target of both receptor and nonreceptor tyrosine kinases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Feng, G S -- Hui, C C -- Pawson, T -- New York, N.Y. -- Science. 1993 Mar 12;259(5101):1607-11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Molecular and Developmental Biology, Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, Ontario, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8096088" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cell Line, Transformed ; Cell Transformation, Neoplastic ; Embryo, Mammalian ; Embryonic and Fetal Development ; Epidermal Growth Factor/pharmacology ; *Genes, src ; Humans ; Intracellular Signaling Peptides and Proteins ; Kinetics ; Mice ; Molecular Sequence Data ; Oligodeoxyribonucleotides ; Phosphorylation ; Platelet-Derived Growth Factor/pharmacology ; Poly A/isolation & purification/metabolism ; Polymerase Chain Reaction ; Protein Tyrosine Phosphatase, Non-Receptor Type 11 ; Protein Tyrosine Phosphatase, Non-Receptor Type 6 ; Protein Tyrosine Phosphatases/genetics/*metabolism ; Protein-Tyrosine Kinases/*metabolism ; RNA, Messenger/isolation & purification/metabolism ; Rats ; Receptor, Epidermal Growth Factor/metabolism ; Receptors, Platelet-Derived Growth Factor/genetics/metabolism ; Sequence Homology, Amino Acid ; Transfection
    Print ISSN: 0036-8075
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  • 108
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    Separable regulatory elements governing myogenin transcription in mouse embryogenesis (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-07-09
    Description: Expression of the myogenic helix-loop-helix (HLH) protein myogenin in muscle cell precursors within somites and limb buds is among the earliest events associated with myogenic lineage determination in vertebrates. Mutations in the myogenin promoter that abolish binding sites for myogenic HLH proteins or myocyte enhancer factor-2 (MEF-2) suppressed transcription of a linked lacZ transgene in subsets of myogenic precursors in mouse embryos. These results suggest that myogenic HLH proteins and MEF-2 participate in separable regulatory circuits leading to myogenin transcription and provide evidence for positional regulation of myogenic regulators in the embryo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cheng, T C -- Wallace, M C -- Merlie, J P -- Olson, E N -- New York, N.Y. -- Science. 1993 Jul 9;261(5118):215-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Biology, University of Texas M.D. Anderson Cancer Center, Houston 77030.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8392225" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites ; DNA-Binding Proteins/genetics/metabolism ; Embryo, Mammalian/*metabolism ; Extremities/embryology ; Female ; MEF2 Transcription Factors ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Inbred CBA ; Mice, Transgenic ; Muscle Proteins/*genetics ; Muscles/*embryology/metabolism ; Mutation ; Myogenic Regulatory Factors ; Myogenin ; Promoter Regions, Genetic ; Trans-Activators/*genetics ; Transcription Factors/genetics/metabolism ; *Transcription, Genetic
    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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    Researchers win decision on knockout mouse pricing (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-04-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Anderson, C -- New York, N.Y. -- Science. 1993 Apr 2;260(5104):23-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8465194" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Animals, Laboratory ; Breeding/economics ; *Cost Control ; Genes ; *Genetic Engineering ; Humans ; Mice ; *Mice, Mutant Strains ; National Institutes of Health (U.S.) ; Patents as Topic ; United States
    Print ISSN: 0036-8075
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  • 110
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    Molecular advances in cardiovascular biology (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-05-14
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chien, K R -- New York, N.Y. -- Science. 1993 May 14;260(5110):916-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of California, San Diego, School of Medicine, La Jolla 92093.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8493528" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cardiomyopathy, Hypertrophic/genetics/therapy ; Cardiovascular Diseases/*genetics/therapy ; Coronary Disease/genetics/therapy ; Genetic Therapy ; Heart Defects, Congenital/genetics/therapy ; Humans ; Hypertension/genetics/therapy ; Mice ; Mice, Transgenic
    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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  • 111
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    An unnatural biopolymer (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-09-03
    Description: A highly efficient method has been developed for the solid-phase synthesis of an "unnatural biopolymer" consisting of chiral aminocarbonate monomers linked via a carbamate backbone. Oligocarbamates were synthesized from N-protected p-nitrophenyl carbonate monomers, substituted with a variety of side chains, with greater than 99 percent overall coupling efficiencies per step. A spatially defined library of oligocarbamates was generated by using photochemical methods and screened for binding affinity to a monoclonal antibody. A number of high-affinity ligands were then synthesized and analyzed in solution with respect to their inhibition concentration values, water/octanol partitioning coefficients, and proteolytic stability. These and other unnatural polymers may provide new frameworks for drug development and for testing theories of protein and peptide folding and structure.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cho, C Y -- Moran, E J -- Cherry, S R -- Stephans, J C -- Fodor, S P -- Adams, C L -- Sundaram, A -- Jacobs, J W -- Schultz, P G -- 1 F32 GM14681/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1993 Sep 3;261(5126):1303-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry, University of California, Berkeley 94720.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7689747" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antibodies, Monoclonal/immunology ; *Biopolymers ; Carbonates/*chemical synthesis/chemistry/immunology ; Epitopes ; Mice ; Mice, Inbred BALB C ; Molecular Sequence Data ; Oligopeptides/chemistry
    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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    Predisposition to neoplastic transformation caused by gene replacement of H-ras1 (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-06-04
    Description: Homologous recombination was used to introduce a nominally transforming mutation into an endogenous H-ras1 gene in Rat1 fibroblasts. Although both the mutant and the remaining normal allele were expressed equally, the heterozygous cells were not neoplastically transformed. Instead, spontaneously transformed cells arose from the heterozygotes at a low frequency, and the majority of these cells had amplified the mutant allele. Thus, the activated H-ras1 allele was not by itself dominant over the normal allele but predisposed cells to transformation by independent events, such as amplification of the mutant allele.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Finney, R E -- Bishop, J M -- CA 44338/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1993 Jun 4;260(5113):1524-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉George Williams Hooper Foundation, University of California, San Francisco 94143.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8502998" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Base Sequence ; Cell Division/genetics ; Cell Line ; Cell Line, Transformed ; Cell Transformation, Neoplastic/*genetics ; Genes, ras/*genetics ; Mice ; Mice, Nude ; Molecular Sequence Data ; Neoplasm Transplantation ; Point Mutation ; Rats ; Recombination, Genetic
    Print ISSN: 0036-8075
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  • 113
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    Mutation of unique region of Bruton's tyrosine kinase in immunodeficient XID mice (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-07-16
    Description: The cytoplasmic tyrosine kinase, Bruton's tyrosine kinase (Btk, formerly bpk or atk), is crucial for B cell development. Loss of kinase activity results in the human immunodeficiency, X-linked agammaglobulinemia, characterized by a failure to produce B cells. In the murine X-linked immunodeficiency (XID), B cells are present but respond abnormally to activating signals. The Btk gene, btk, was mapped to the xid region of the mouse X chromosome by interspecific backcross analysis. A single conserved residue within the amino terminal unique region of Btk was mutated in XID mice. This change in xid probably interferes with normal B cell signaling mediated by Btk protein interactions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rawlings, D J -- Saffran, D C -- Tsukada, S -- Largaespada, D A -- Grimaldi, J C -- Cohen, L -- Mohr, R N -- Bazan, J F -- Howard, M -- Copeland, N G -- AR36834/AR/NIAMS NIH HHS/ -- N01-CO-74101/CO/NCI NIH HHS/ -- New York, N.Y. -- Science. 1993 Jul 16;261(5119):358-61.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Molecular Genetics, University of California, Los Angeles 90024.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8332901" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; B-Lymphocytes/*enzymology/immunology ; Base Sequence ; Cell Line ; Chromosome Mapping ; Crosses, Genetic ; Exons ; Female ; Genetic Linkage ; Immunologic Deficiency Syndromes/enzymology/*genetics/immunology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Inbred CBA ; Mice, Inbred DBA ; Mice, Mutant Strains ; Molecular Sequence Data ; Protein-Tyrosine Kinases/chemistry/*genetics/metabolism ; *X Chromosome
    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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  • 114
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    Germ line transmission of a yeast artificial chromosome spanning the murine alpha 1(I) collagen locus (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-03-26
    Description: Molecular complementation of mutant phenotypes by transgenic technology is a potentially important tool for gene identification. A technology was developed that allows the transfer of a physically intact yeast artificial chromosome (YAC) into the germ line of the mouse. A purified 150-kilobase YAC encompassing the murine gene Col1a1 was efficiently introduced into embryonic stem (ES) cells via lipofection. Chimeric founder mice were derived from two transfected ES cell clones. These chimeras transmitted the full length transgene through the germ line, generating two transgenic mouse strains. Transgene expression was visualized as nascent transcripts in interphase nuclei and quantitated by ribonuclease protection analysis. Both assays indicated that the transgene was expressed at levels comparable to the endogenous collagen gene.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Strauss, W M -- Dausman, J -- Beard, C -- Johnson, C -- Lawrence, J B -- Jaenisch, R -- 5 F32 GM13756-02/GM/NIGMS NIH HHS/ -- 5 R35 CA44339-05/CA/NCI NIH HHS/ -- HG00198-01/HG/NHGRI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1993 Mar 26;259(5103):1904-7.〈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/8096090" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blastocyst/metabolism ; Blotting, Southern ; Chromosomes, Fungal ; Collagen/*genetics ; *Gene Expression ; Gene Library ; In Situ Hybridization ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Transgenic ; Mutagenesis, Insertional ; Polymerase Chain Reaction ; Polymorphism, Restriction Fragment Length ; Transfection
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    TH1 and TH2 cell antigen receptors in experimental leishmaniasis (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-03-05
    Description: The complexity and chronicity of parasitic infections have obscured the identification of biologically relevant antigens. Analysis of the T cell receptor repertoire used by mice infected with Leishmania major revealed the expansion of a restricted population of CD4+ cells. These cells expressed the V alpha 8-J alpha TA72, V beta 4 heterodimer in both progressive infection and protective immunity and across several major histocompatibility haplotypes. Thus, the same immunodominant parasite epitope drives the disparate outcomes of this infectious process, suggesting that candidate vaccine antigens selected by screening of immune individuals may be capable of exacerbating disease in genetically susceptible individuals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Reiner, S L -- Wang, Z E -- Hatam, F -- Scott, P -- Locksley, R M -- AI30663/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1993 Mar 5;259(5100):1457-60.〈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/8451641" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD4/analysis ; Base Sequence ; Cloning, Molecular ; *Leishmania tropica ; Leishmaniasis, Cutaneous/*immunology ; Mice ; Mice, Inbred BALB C ; Molecular Sequence Data ; Oligodeoxyribonucleotides ; Polymerase Chain Reaction/methods ; RNA, Messenger/genetics/isolation & purification ; Receptors, Antigen, T-Cell/analysis/genetics/*metabolism ; Receptors, Antigen, T-Cell, alpha-beta/analysis/genetics/*metabolism ; Reference Values ; T-Lymphocyte Subsets/immunology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Tethering ribozymes to a retroviral packaging signal for destruction of viral RNA (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-12-03
    Description: Cellular compartmentalization of RNAs is thought to influence their susceptibility to ribozyme cleavage. As a test of this idea, two retroviral vectors--one encoding a hammer-head ribozyme designed to cleave lacZ transcripts and another encoding the lacZ messenger RNA--were coexpressed inside retroviral packaging cells. Because of the retroviral packaging signal, the ribozyme would be expected to colocalize with the lacZ-containing viral genomic RNA but not with the lacZ messenger RNA. The ribozyme was found to reduce the titer of infectious virus containing lacZ by 90 percent, but had no effect on translation of lacZ messenger RNA. These results indicate that sorting gene inhibitors to appropriate intracellular sites may increase their effectiveness.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sullenger, B A -- Cech, T R -- New York, N.Y. -- Science. 1993 Dec 3;262(5139):1566-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry and Biochemistry, Howard Hughes Medical Institute, University of Colorado, Boulder 80309.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8248806" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Animals ; Base Sequence ; Biological Transport ; Cell Line ; Gene Transfer Techniques ; Genetic Vectors/genetics ; Mice ; Molecular Sequence Data ; Moloney murine leukemia virus/genetics ; RNA, Catalytic/administration & dosage/*genetics/metabolism ; RNA, Messenger/metabolism ; RNA, Viral/*metabolism ; beta-Galactosidase/genetics
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    The chlorine controversy (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-10-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Williams, G M -- New York, N.Y. -- Science. 1993 Oct 1;262(5130):15-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8211120" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chlorine/*adverse effects/toxicity ; Humans ; Mice ; Neoplasms/*chemically induced
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    Identification of a ten-amino acid proline-rich SH3 binding site (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-02-19
    Description: The Src homology 3 (SH3) region is a small protein domain present in a very large group of proteins, including cytoskeletal elements and signaling proteins. It is believed that SH3 domains serve as modules that mediate protein-protein associations and, along with Src homology 2 (SH2) domains, regulate cytoplasmic signaling. The SH3 binding sites of two SH3 binding proteins were localized to a nine- or ten-amino acid stretch very rich in proline residues. Similar SH3 binding motifs exist in the formins, proteins that function in pattern formation in embryonic limbs of the mouse, and one subtype of the muscarinic acetylcholine receptor. Identification of the SH3 binding site provides a basis for understanding the interaction between the SH3 domains and their targets.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ren, R -- Mayer, B J -- Cicchetti, P -- Baltimore, D -- CA 08875/CA/NCI NIH HHS/ -- CA 09673/CA/NCI NIH HHS/ -- CA 51462/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1993 Feb 19;259(5098):1157-61.〈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/8438166" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Binding Sites ; Cytoskeletal Proteins/genetics/*metabolism ; DNA/genetics/metabolism ; Genes, abl ; Glutathione Transferase/genetics/metabolism ; Kinetics ; Mice ; Molecular Sequence Data ; *Proline ; Proto-Oncogene Proteins c-abl/genetics/*metabolism ; Rats ; Receptors, Muscarinic/metabolism ; Recombinant Fusion Proteins/metabolism ; Sequence Homology, Amino Acid ; Signal Transduction
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Immune responses in interleukin-2-deficient mice (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-11-12
    Description: The role of costimulatory signals in T cell induction was evaluated in mice lacking the interleukin-2 (IL-2) gene. In vitro secondary antiviral T cell responses were absent unless IL-2 was added, confirming the crucial role of IL-2 in vitro. In vivo, primary and secondary cytotoxic T cell responses against vaccinia and lymphocytic choriomeningitis virus were within normal ranges. B cell reactivity to vesicular stomatitis virus was not impaired. T helper cell responses were delayed but biologically functional. Natural killer cell activity was markedly reduced but inducible. These normal in vivo immune responses in IL-2-deficient mice question the importance of IL-2 as defined by in vitro studies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kundig, T M -- Schorle, H -- Bachmann, M F -- Hengartner, H -- Zinkernagel, R M -- Horak, I -- New York, N.Y. -- Science. 1993 Nov 12;262(5136):1059-61.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Experimental Immunology, University of Zurich, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8235625" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Viral/*biosynthesis ; B-Lymphocytes/*immunology ; Cytotoxicity, Immunologic ; Immunoglobulin M/*biosynthesis ; Immunologic Memory ; Interleukin-2/deficiency/*immunology ; Killer Cells, Natural/immunology ; Lymphocytic Choriomeningitis/immunology ; Lymphocytic choriomeningitis virus/immunology ; Mice ; Mice, Inbred C57BL ; Neutralization Tests ; Rhabdoviridae Infections/immunology ; T-Lymphocytes/*immunology ; T-Lymphocytes, Cytotoxic/immunology ; Vaccinia/immunology ; Vaccinia virus/immunology ; Vesicular stomatitis Indiana virus/immunology ; Virus Diseases/*immunology
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    High spontaneous intrachromosomal recombination rates in ataxia-telangiectasia (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-05-28
    Description: Ataxia-telangiectasia (A-T) is an inherited human disease associated with neurologic degeneration, immune dysfunction, and high cancer risk. It has been proposed that the underlying abnormality in A-T is a defect in genetic recombination that interferes with immune gene rearrangements and the repair of DNA damage. Recombination was studied in A-T and control human fibroblast lines by means of two recombination vectors. Unexpectedly, spontaneous intrachromosomal recombination rates were 30 to 200 times higher in A-T fibroblast lines than in normal cells, whereas extrachromosomal recombination frequencies were near normal. Increased recombination is thus a component of genetic instability in A-T and may contribute to the cancer risk seen in A-T patients.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Meyn, M S -- GM38588/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1993 May 28;260(5112):1327-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, 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/8493577" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Ataxia Telangiectasia/*genetics ; Cell Line ; Cell Line, Transformed ; Chromosomes, Human/*physiology ; *Cinnamates ; Genetic Complementation Test ; Genetic Vectors ; Humans ; Hygromycin B/analogs & derivatives/pharmacology ; Mice ; Mitosis ; Neomycin/pharmacology ; Phenotype ; *Recombination, Genetic
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    Inhibition of human colon cancer growth by antibody-directed human LAK cells in SCID mice (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-03-05
    Description: Advanced human colon cancer does not respond to lymphokine-activated killer (LAK) cells. In order to direct cytotoxic cells to the tumor, human LAK cells linked with antibodies to a tumor cell surface antigen were tested with established hepatic metastases in severe combined immunodeficient (SCID) mice. These cells had increased uptake into the tumor and suppression of tumor growth as compared with LAK cells alone, thereby improving the survival of tumor-bearing mice. Thus, tumor growth can be inhibited by targeted LAK cells, and SCID mice can be used to test the antitumor properties of human effector cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Takahashi, H -- Nakada, T -- Puisieux, I -- CA-35711/CA/NCI NIH HHS/ -- CA-57584/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1993 Mar 5;259(5100):1460-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Hepatology Laboratory, Massachusetts General Hospital Cancer Center, Charlestown 02129.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8451642" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/immunology ; Antibodies, Neoplasm/*immunology ; Antigens, Neoplasm/*immunology ; Antigens, Surface/*immunology ; Cell Division ; Colonic Neoplasms/immunology/pathology/*therapy ; Humans ; Immunotherapy ; Killer Cells, Lymphokine-Activated/*immunology ; Liver Neoplasms/immunology/pathology/*secondary/therapy ; Mice ; Mice, SCID ; Neoplasm Transplantation ; Transplantation, Heterologous ; Tumor Cells, Cultured
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    Targeted insertion of a variable region gene into the immunoglobulin heavy chain locus (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-11-19
    Description: A mutant mouse strain has been generated in which a rearranged immunoglobulin heavy (H) chain variable (V) region gene is placed into the heavy chain locus in its natural position, replacing the JH elements. In homozygous mutant mice, essentially all B cells in the spleen express the transgenic VH region in their antibodies. The proper location of the transgene relative to the constant region genes allows it to participate in isotype switching and undergo somatic hypermutation. Immunoglobulin transgenic mice generated in this fashion by gene targeting should prove useful for the exploration of immunoregulatory mechanisms.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Taki, S -- Meiering, M -- Rajewsky, K -- New York, N.Y. -- Science. 1993 Nov 19;262(5137):1268-71.〈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/8235657" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; B-Lymphocytes/immunology ; Base Sequence ; Cells, Cultured ; *Genes, Immunoglobulin ; Homozygote ; *Immunoglobulin Class Switching ; Immunoglobulin Heavy Chains/*genetics ; Immunoglobulin Variable Region/*genetics ; Mice ; Mice, Transgenic ; Molecular Sequence Data ; Mutation
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    The influence of antigen organization on B cell responsiveness (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-11-26
    Description: The influence of antigen epitope density and order on B cell induction and antibody production was assessed with the glycoprotein of vesicular stomatitis virus serotype Indiana [VSV-G (IND)]. VSV-G (IND) can be found in a highly repetitive form the envelope of VSV-IND and in a poorly organized form on the surface of infected cells. In VSV-G (IND) transgenic mice, B cells were unresponsive to the poorly organized VSV-G (IND) present as self antigen but responded promptly to the same antigen presented in the highly organized form. Thus, antigen organization influences B cell tolerance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bachmann, M F -- Rohrer, U H -- Kundig, T M -- Burki, K -- Hengartner, H -- Zinkernagel, R M -- New York, N.Y. -- Science. 1993 Nov 26;262(5138):1448-51.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, University of Zurich, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8248784" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Viral/*biosynthesis/immunology ; Antibody Affinity ; B-Lymphocytes/*immunology ; *Immune Tolerance ; Immunization ; Immunoglobulin G/biosynthesis ; Immunoglobulin M/biosynthesis ; Lymphocyte Activation ; Macrophages, Peritoneal/microbiology ; *Membrane Glycoproteins ; Mice ; Mice, Transgenic ; Neutralization Tests ; T-Lymphocytes, Helper-Inducer/immunology ; Vesicular stomatitis Indiana virus/*immunology/physiology ; Viral Envelope Proteins/*immunology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Yin and yang of phosphorylation in cytokine signaling (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-10-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tan, Y H -- New York, N.Y. -- Science. 1993 Oct 15;262(5132):376-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Molecular and Cell Biology, National University of Singapore, Republic of Singapore.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7692598" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Cytokines/*metabolism/pharmacology ; Humans ; Interferons/metabolism/pharmacology ; Interleukins/metabolism/pharmacology ; Mice ; Models, Biological ; Phosphoprotein Phosphatases/*metabolism ; Phosphorylation ; Protein Kinases/*metabolism ; *Signal Transduction ; T-Lymphocytes/metabolism ; Tumor Necrosis Factor-alpha/metabolism/pharmacology
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    Deficiency in rhabdomyosarcomas of a factor required for MyoD activity and myogenesis (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-03-05
    Description: Rhabdomyosarcoma cells express the myogenic helix-loop-helix proteins of the MyoD family but do not differentiate into skeletal muscle cells. Gel shift and transient transfection assays revealed that MyoD in the rhabdomyosarcoma cells was capable of binding DNA but was relatively nonfunctional as a transcriptional activator. Heterokaryon formation with fibroblasts resulted in the restoration of transcriptional activation by MyoD and the differentiation of the rhabdomyosarcoma cells into skeletal muscle cells. These results suggest that rhabdomyosarcomas are deficient in a factor required for MyoD activity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tapscott, S J -- Thayer, M J -- Weintraub, H -- New York, N.Y. -- Science. 1993 Mar 5;259(5100):1450-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Fred Hutchinson Cancer Research Center, Seattle, WA 98104.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8383879" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites ; Cell Differentiation ; Cell Nucleus/metabolism/ultrastructure ; Chloramphenicol O-Acetyltransferase/genetics/metabolism ; Humans ; Mice ; Muscle Proteins/genetics/*metabolism ; Muscles/pathology ; MyoD Protein ; Promoter Regions, Genetic ; Recombinant Fusion Proteins/metabolism ; Rhabdomyosarcoma/genetics/*metabolism/pathology ; Transcription Factors/*metabolism ; Transcription, Genetic ; Transfection ; Tumor Cells, Cultured
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    Adipose expression of tumor necrosis factor-alpha: direct role in obesity-linked insulin resistance (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-01-01
    Description: Tumor necrosis factor-alpha (TNF-alpha) has been shown to have certain catabolic effects on fat cells and whole animals. An induction of TNF-alpha messenger RNA expression was observed in adipose tissue from four different rodent models of obesity and diabetes. TNF-alpha protein was also elevated locally and systemically. Neutralization of TNF-alpha in obese fa/fa rats caused a significant increase in the peripheral uptake of glucose in response to insulin. These results indicate a role for TNF-alpha in obesity and particularly in the insulin resistance and diabetes that often accompany obesity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hotamisligil, G S -- Shargill, N S -- Spiegelman, B M -- DK 42539/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1993 Jan 1;259(5091):87-91.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Dana-Farber Cancer Institute, Boston, MA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7678183" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Adipose Tissue/physiology/*physiopathology ; Animals ; Blood Glucose/metabolism ; Blotting, Northern ; Diabetes Mellitus, Experimental/physiopathology ; Glucose Clamp Technique ; Homeostasis ; Immunoglobulin G/genetics/pharmacology ; Insulin/pharmacology ; Insulin Infusion Systems ; Insulin Resistance/*genetics ; Male ; Mice ; Mice, Obese ; Obesity/chemically induced/*genetics/*physiopathology ; RNA/genetics/isolation & purification ; RNA, Messenger/*biosynthesis/isolation & purification ; Rats ; Rats, Zucker ; Receptors, Cell Surface/genetics/physiology ; Receptors, Tumor Necrosis Factor ; Recombinant Fusion Proteins/pharmacology ; Reference Values ; Sodium Glutamate ; Tumor Necrosis Factor-alpha/biosynthesis/*genetics
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    Formation and hydrolysis of cyclic ADP-ribose catalyzed by lymphocyte antigen CD38 (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-11-12
    Description: CD38 is a 42-kilodalton glycoprotein expressed extensively on B and T lymphocytes. CD38 exhibits a structural homology to Aplysia adenosine diphosphate (ADP)-ribosyl cyclase. This enzyme catalyzes the synthesis of cyclic ADP-ribose (cADPR), a metabolite of nicotinamide adenine dinucleotide (NAD+) with calcium-mobilizing activity. A complementary DNA encoding the extracellular domain of murine CD38 was constructed and expressed, and the resultant recombinant soluble CD38 was purified to homogeneity. Soluble CD38 catalyzed the formation and hydrolysis of cADPR when added to NAD+. Purified cADPR augmented the proliferative response of activated murine B cells, potentially implicating the enzymatic activity of CD38 in lymphocyte function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Howard, M -- Grimaldi, J C -- Bazan, J F -- Lund, F E -- Santos-Argumedo, L -- Parkhouse, R M -- Walseth, T F -- Lee, H C -- DA05695/DA/NIDA NIH HHS/ -- HD17484/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1993 Nov 12;262(5136):1056-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉DNAX Research Institute, Palo Alto, CA 94304.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8235624" target="_blank"〉PubMed〈/a〉
    Keywords: ADP-ribosyl Cyclase ; Adenosine Diphosphate Ribose/*analogs & derivatives/metabolism/pharmacology ; Amino Acid Sequence ; Animals ; *Antigens, CD ; Antigens, CD38 ; Antigens, Differentiation/isolation & purification/*metabolism ; B-Lymphocytes/drug effects/metabolism ; Calcium/metabolism ; Cyclic ADP-Ribose ; Lymphocyte Activation ; Membrane Glycoproteins ; Mice ; Molecular Sequence Data ; N-Glycosyl Hydrolases/metabolism ; NAD/metabolism ; Recombinant Proteins/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Antibody-catalyzed degradation of cocaine (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-03-26
    Description: Immunization with a phosphonate monoester transition-state analog of cocaine provided monoclonal antibodies capable of catalyzing the hydrolysis of the cocaine benzoyl ester group. An assay for the degradation of radiolabeled cocaine identified active enzymes. Benzoyl esterolysis yields ecgonine methyl ester and benzoic acid, fragments devoid of cocaine's stimulant activity. Passive immunization with such an artificial enzyme could provide a treatment for dependence by blunting reinforcement.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Landry, D W -- Zhao, K -- Yang, G X -- Glickman, M -- Georgiadis, T M -- T32 NS07258/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1993 Mar 26;259(5103):1899-901.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Columbia University College of Physicians and Surgeons, New York, NY 10032.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8456315" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Catalytic/*metabolism/therapeutic use ; Antibodies, Monoclonal/*metabolism/therapeutic use ; Antigens/immunology ; Benzoates/metabolism ; Benzoic Acid ; Cocaine/analogs & derivatives/immunology/*metabolism ; Esters/metabolism ; Humans ; Hybridomas/immunology ; Hydrolysis ; Immunization ; Immunization, Passive ; Mice ; Mice, Inbred BALB C ; Substance-Related Disorders/drug therapy
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    New protein steals the show as 'costimulator' of T cells (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-11-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, J -- New York, N.Y. -- Science. 1993 Nov 5;262(5135):844-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7694360" target="_blank"〉PubMed〈/a〉
    Keywords: Abatacept ; Animals ; Antigen-Presenting Cells/*immunology ; *Antigens, CD ; Antigens, CD28/immunology/metabolism ; Antigens, CD80/*immunology/metabolism ; Antigens, CD86 ; Antigens, Differentiation/immunology/metabolism ; B-Lymphocytes/immunology ; CTLA-4 Antigen ; *Immunoconjugates ; *Lymphocyte Activation ; *Membrane Glycoproteins ; Mice ; Mice, Knockout ; T-Lymphocytes/*immunology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    PAC-1: a mitogen-induced nuclear protein tyrosine phosphatase (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-03-19
    Description: Tyrosine phosphorylation of proteins is required for signal transduction in cells and for growth regulation. A mitogen-induced gene (PAC-1) has been cloned from human T cells and encodes a 32-kilodalton protein that contains a sequence that defines the enzymatic site of known protein phosphotyrosine phosphatases (PTPases). Other than this sequence, PAC-1 is different from several other known related PTPases exemplified by PTP-1b. PAC-1 is similar to a phosphatase induced by mitogens or heat shock in fibroblasts, a yeast gene, and a vaccinia virus-encoded serine-tyrosine phosphatase (VH1). PAC-1 was predominantly expressed in hematopoietic tissues and localized to the nucleus in transfected COS-7 cells and in mitogen-stimulated T cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rohan, P J -- Davis, P -- Moskaluk, C A -- Kearns, M -- Krutzsch, H -- Siebenlist, U -- Kelly, K -- New York, N.Y. -- Science. 1993 Mar 19;259(5102):1763-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Pathology, National Cancer Institute, NIH, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7681221" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Blotting, Northern ; Cell Line ; Cell Nucleus/enzymology ; Conserved Sequence ; Cytoplasm/enzymology ; Dual Specificity Phosphatase 2 ; Fluorescent Antibody Technique ; Humans ; Immunosorbent Techniques ; Mice ; Mitogens/*pharmacology ; Molecular Sequence Data ; Organ Specificity ; Protein Phosphatase 2 ; Protein Tyrosine Phosphatases/chemistry/*genetics ; RNA/analysis ; Sequence Homology, Amino Acid ; Signal Transduction/physiology ; T-Lymphocytes/enzymology ; Transfection
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    A divergence in the MAP kinase regulatory network defined by MEK kinase and Raf (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-04-16
    Description: Mitogen-activated protein kinases (MAPKs) are rapidly phosphorylated and activated in response to various extracellular stimuli in many different cell types. Such regulation of MAPK results from sequential activation of a series of protein kinases. The kinases that phosphorylate MAPKs, the MAP kinase kinases (MEKs) are also activated by phosphorylation. MEKs are related in sequence to the yeast protein kinases Byr1 (from Schizosaccharomyces pombe) and Ste7 (from Saccharomyces cerevisiae), which function in the pheromone-induced signaling pathway that results in mating. Byr1 and Ste7 are in turn regulated by the protein kinases Byr2 and Ste11. The amino acid sequence of the mouse homolog of Byr2 and Ste11, denoted MEKK (MEK kinase), was elucidated from a complementary DNA sequence encoding a protein of 672 amino acid residues (73 kilodaltons). MEKK was expressed in all mouse tissues tested, and it phosphorylated and activated MEK. Phosphorylation and activation of MEK by MEKK was independent of Raf, a growth factor-regulated protein kinase that also phosphorylates MEK. Thus, MEKK and Raf converge at MEK in the protein kinase network mediating the activation of MAPKs by hormones, growth factors, and neurotransmitters.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lange-Carter, C A -- Pleiman, C M -- Gardner, A M -- Blumer, K J -- Johnson, G L -- CA58187/CA/NCI NIH HHS/ -- DK 37871/DK/NIDDK NIH HHS/ -- GM 30324/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1993 Apr 16;260(5106):315-9.〈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/8385802" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Calcium-Calmodulin-Dependent Protein Kinases ; Cell Line, Transformed ; Cercopithecus aethiops ; Enzyme Activation ; *MAP Kinase Kinase Kinase 1 ; Mice ; Molecular Sequence Data ; Phosphorylation ; Protein Kinases/*metabolism ; Protein-Serine-Threonine Kinases/chemistry/genetics/*metabolism ; Protein-Tyrosine Kinases/chemistry/genetics/*metabolism ; Proto-Oncogene Proteins/*metabolism ; Proto-Oncogene Proteins c-raf ; Recombinant Proteins/metabolism ; Saccharomyces cerevisiae/enzymology/genetics ; Schizosaccharomyces/enzymology/genetics
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    T cell shift: key to AIDS therapy? (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-10-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, J -- New York, N.Y. -- Science. 1993 Oct 8;262(5131):175-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8211135" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/*immunology/therapy ; Animals ; Cytokines/biosynthesis ; Humans ; Interleukin-2/biosynthesis/physiology/therapeutic use ; Interleukin-4/biosynthesis/physiology ; Interleukins/*biosynthesis/physiology ; Mice ; Murine Acquired Immunodeficiency Syndrome/*immunology ; T-Lymphocytes, Helper-Inducer/classification/*immunology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    The cloning of PIG-A, a component in the early step of GPI-anchor biosynthesis (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-02-26
    Description: The glycosylphosphatidylinositol (GPI) anchor is a membrane attachment structure of many proteins and occurs in a wide variety of eukaryotes from yeasts to mammals. The structure of the core of the GPI anchor is conserved in protozoa and mammals and so is its biosynthetic pathway. A complementary DNA encoding a human protein termed PIG-A (phosphatidylinositol glycan-class A) was cloned. PIG-A was necessary for synthesis of N-acetylglucosaminyl-phosphatidylinositol, the very early intermediate in GPI-anchor biosynthesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miyata, T -- Takeda, J -- Iida, Y -- Yamada, N -- Inoue, N -- Takahashi, M -- Maeda, K -- Kitani, T -- Kinoshita, T -- New York, N.Y. -- Science. 1993 Feb 26;259(5099):1318-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunoregulation, Osaka University, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7680492" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antigens, CD/metabolism ; Antigens, CD55 ; Antigens, CD59 ; Antigens, Surface/metabolism ; Antigens, Thy-1 ; Cloning, Molecular ; DNA/genetics ; Genetic Complementation Test ; Glycosylphosphatidylinositols/*biosynthesis ; HeLa Cells ; Humans ; In Vitro Techniques ; Membrane Glycoproteins/metabolism ; Membrane Proteins/*genetics/metabolism ; Mice ; Molecular Sequence Data ; Solubility ; Species Specificity
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Inhibition of the EGF-activated MAP kinase signaling pathway by adenosine 3',5'-monophosphate (1993)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1993-11-12
    Description: Mitogen-activated protein (MAP) kinases p42mapk and p44mapk are activated in cells stimulated with epidermal growth factor (EGF) and other agents. A principal pathway for MAP kinase (MAPK) activation by EGF consists of sequential activations of the guanine nucleotide exchange factor Sos, the guanosine triphosphate binding protein Ras, and the protein kinases Raf-1, MAPK kinase (MKK), and MAPK. Because adenosine 3',5'-monophosphate (cAMP) does not activate MAPK and has some opposing physiologic effects, the effect of increasing intracellular concentrations of cAMP with forskolin and 3-isobutyl-1-methylxanthine on the EGF-stimulated MAPK pathway was studied. Increased concentrations of cAMP blocked activation of Raf-1, MKK, and MAPK in Rat1hER fibroblasts, accompanied by a threefold increase in Raf-1 phosphorylation on serine 43 in the regulatory domain. Phosphorylation of Raf-1 in vitro and in vivo reduces the apparent affinity with which it binds to Ras and may contribute to the blockade by cAMP.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wu, J -- Dent, P -- Jelinek, T -- Wolfman, A -- Weber, M J -- Sturgill, T W -- CA39076/CA/NCI NIH HHS/ -- DK41077/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1993 Nov 12;262(5136):1065-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Internal Medicine, University of Virginia, Health Sciences Center, Charlottesville 22908.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7694366" target="_blank"〉PubMed〈/a〉
    Keywords: 1-Methyl-3-isobutylxanthine/pharmacology ; 3T3 Cells ; Amino Acid Sequence ; Animals ; Cell Line ; Colforsin/pharmacology ; Cyclic AMP/*metabolism ; Cyclic AMP-Dependent Protein Kinases/metabolism ; Enzyme Activation/drug effects ; Epidermal Growth Factor/*pharmacology ; Mice ; Mitogen-Activated Protein Kinase 1 ; Mitogen-Activated Protein Kinase Kinases ; Molecular Sequence Data ; Phosphorylation ; Protein Kinases/metabolism ; Protein-Serine-Threonine Kinases/*metabolism ; Protein-Tyrosine Kinases/*metabolism ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins c-raf ; Proto-Oncogene Proteins p21(ras)/*metabolism ; Rats ; *Signal Transduction
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Development of TH1 CD4+ T cells through IL-12 produced by Listeria-induced macrophages (1993)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1993-04-23
    Description: Development of the appropriate CD4+ T helper (TH) subset during an immune response is important for disease resolution. With the use of naive, ovalbumin-specific alpha beta T cell receptor transgenic T cell, it was found that heat-killed Listeria monocytogenes induced TH1 development in vitro through macrophage production of interleukin-12 (IL-12). Moreover, inhibition of macrophage production of IL-12 may explain the ability of IL-10 to suppress TH1 development. Murine immune responses to L. monocytogenes in vivo are of the appropriate TH1 phenotype. Therefore, this regulatory pathway may have evolved to enable innate immune cells, through interactions with microbial pathogens, to direct development of specific immunity toward the appropriate TH phenotype.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hsieh, C S -- Macatonia, S E -- Tripp, C S -- Wolf, S F -- O'Garra, A -- Murphy, K M -- 1 PO1 A131238-01/PHS HHS/ -- 5 T32 GM07200-17/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1993 Apr 23;260(5107):547-9.〈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/8097338" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CD4-Positive T-Lymphocytes/cytology/*immunology ; Cell Differentiation ; Cells, Cultured ; Interferon-gamma/secretion ; Interleukin-10/pharmacology ; Interleukin-12 ; Interleukin-2/biosynthesis ; Interleukins/biosynthesis/*immunology/pharmacology ; Listeria monocytogenes/*immunology ; Macrophages/*immunology ; Mice ; Mice, Transgenic ; Phenotype ; Receptors, Antigen, T-Cell, alpha-beta/immunology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Immune response in mice that lack the interferon-gamma receptor (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-03-19
    Description: Interferon-gamma (IFN-gamma) exerts pleiotropic effects, including antiviral activity, stimulation of macrophages and natural killer cells, and increased expression of major histocompatibility complex antigens. Mice without the IFN-gamma receptor had no overt anomalies, and their immune system appeared to develop normally. However, mutant mice had a defective natural resistance, they had increased susceptibility to infection by Listeria monocytogenes and vaccinia virus despite normal cytotoxic and T helper cell responses. Immunoglobulin isotype analysis revealed that IFN-gamma is necessary for a normal antigen-specific immunoglobulin G2a response. These mutant mice offer the possibility for the further elucidation of IFN-gamma-mediated functions by transgenic cell- or tissue-specific reconstitution of a functional receptor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huang, S -- Hendriks, W -- Althage, A -- Hemmi, S -- Bluethmann, H -- Kamijo, R -- Vilcek, J -- Zinkernagel, R M -- Aguet, M -- CA 49731/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1993 Mar 19;259(5102):1742-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Molecular Biology I, University of Zurich, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8456301" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Viral/blood ; *Immunity ; Immunoglobulin G/blood ; Interferon-gamma/*physiology ; Listeriosis/immunology ; Lymphocyte Subsets ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Mutation ; Receptors, Interferon/genetics/*physiology ; T-Lymphocytes, Cytotoxic/immunology ; T-Lymphocytes, Helper-Inducer/immunology ; Vaccinia/immunology ; Virus Diseases/immunology ; Virus Replication
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Skepticism greets HIV coreceptor (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-11-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Balter, M -- New York, N.Y. -- Science. 1993 Nov 5;262(5135):843-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7901911" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD4/genetics/metabolism ; Antigens, Differentiation, T-Lymphocyte/genetics/*metabolism ; Dipeptidyl Peptidase 4 ; HIV/*metabolism/physiology ; Humans ; Mice ; Receptors, HIV/*metabolism ; Transfection ; Virus Replication
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 138
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    Mapping the main immunogenic region and toxin-binding site of the nicotinic acetylcholine receptor (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-01-02
    Description: The alpha-chain of the nicotinic acetylcholine receptor carries the binding sites both for cholinergic ligands and for most experimentally induced or naturally occurring antibodies to the native receptor. By means of expression cloning in Escherichia coli, fusion proteins were derived from specific fragments of a complementary DNA encoding the mouse alpha-chain, allowing the mapping of the toxin-binding site to residues 160-216 and the main immunogenic region to residues 6-85. This approach permits the independent study of different functional domains of a complex receptor molecule and should be generally applicable to other proteins for which complementary DNA clones are available.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barkas, T -- Mauron, A -- Roth, B -- Alliod, C -- Tzartos, S J -- Ballivet, M -- New York, N.Y. -- Science. 1987 Jan 2;235(4784):77-80.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2432658" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antibodies, Monoclonal/immunology ; Binding Sites ; Binding, Competitive ; Bungarotoxins/metabolism ; Cloning, Molecular ; Epitopes ; Humans ; Immunosorbent Techniques ; Ligands ; Mice ; Receptors, Nicotinic/genetics/*immunology ; Recombinant Fusion Proteins/immunology ; Species Specificity ; Structure-Activity Relationship
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 139
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    Differential expression of c-myb mRNA in murine B lymphomas by a block to transcription elongation (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-09-18
    Description: Expression of c-myb proto-oncogene messenger RNA (mRNA) and protein has been detected principally in tumors and in normal tissue of hematopoietic origin. In each hematopoietic lineage examined, expression of the c-myb gene is markedly downregulated during hematopoietic maturation. However, the mechanism by which differential expression of the c-myb gene is regulated is not known. In murine B-lymphoid tumor cell lines, the amount of steady-state c-myb mRNA is 10 to more than 100 times greater in pre-B cell lymphomas than in B cell lymphomas and plasmacytomas. The downregulation of c-myb mRNA correlates with events at the pre-B cell-B cell junction. Differential expression of c-myb mRNA levels detected between a pre-B cell lymphoma and a mature B cell lymphoma is now shown to be mediated by a block to transcription elongation in the first intron of the c-myb locus. In addition, this developmentally regulated difference in transcriptional activity is correlated with alterations in higher order chromatin structure as reflected by changes in the patterns of hypersensitivity to deoxyribonuclease I at the 5' end of the c-myb transcription unit. Regulation of transcription elongation may provide a more sensitive mechanism for rapidly increasing and decreasing mRNA levels in response to external stimuli than regulation of the initiation of transcription.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bender, T P -- Thompson, C B -- Kuehl, W M -- New York, N.Y. -- Science. 1987 Sep 18;237(4821):1473-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3498214" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes ; Chromosome Mapping ; *Gene Expression Regulation ; Introns ; Lymphoma/*genetics ; Mice ; Nucleic Acid Hybridization ; *Peptide Chain Elongation, Translational ; *Proto-Oncogenes ; RNA, Messenger/*metabolism ; *Transcription, Genetic
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    Oncogenes in radioresistant, noncancerous skin fibroblasts from a cancer-prone family (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-08-28
    Description: Li-Fraumeni syndrome is manifested in a variety of neoplasms that are transmitted in a dominantly inherited pattern. The noncancerous skin fibroblasts of family members exhibit a unique characteristic of being resistant to the killing effect of ionizing radiation. A three- to eightfold elevation in expression of c-myc and an apparent activation of c-raf-1 gene have been observed in these noncancerous skin fibroblasts. These results may provide insight into the heritable defect underlying the familial predisposition to a variety of cancers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chang, E H -- Pirollo, K F -- Zou, Z Q -- Cheung, H Y -- Lawler, E L -- Garner, R -- White, E -- Bernstein, W B -- Fraumeni, J W Jr -- Blattner, W A -- CA45158/CA/NCI NIH HHS/ -- CO7488/CO/NCI NIH HHS/ -- New York, N.Y. -- Science. 1987 Aug 28;237(4818):1036-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3616624" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Transformation, Neoplastic/radiation effects ; Cells, Cultured ; Fibroblasts/*radiation effects ; Humans ; Mice ; Mice, Nude ; Neoplastic Syndromes, Hereditary/*genetics ; Oncogenes/*radiation effects ; Pedigree ; *Radiation Tolerance ; Skin/cytology/*radiation effects ; Syndrome
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    erbB-2 is a potent oncogene when overexpressed in NIH/3T3 cells (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-07-10
    Description: A wide variety of human tumors contain an amplified or overexpressed erbB-2 gene, which encodes a growth factor receptor-like protein. When erbB-2 complementary DNA was expressed in NIH/3T3 cells under the control of the SV40 promoter, the gene lacked transforming activity despite expression of detectable levels of the erbB-2 protein. A further five- to tenfold increase in its expression under influence of the long terminal repeat of Moloney murine leukemia virus was associated with activation of erbB-2 as a potent oncogene. The high levels of the erbB-2 product associated with malignant transformation of NIH/3T3 cells were observed in human mammary tumor cells that overexpressed this gene. These findings demonstrate a new mechanism for acquisition of oncogenic properties by genes encoding growth factor receptor-like proteins and provide a functional basis for the role of their overexpression in the development of human malignancies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Di Fiore, P P -- Pierce, J H -- Kraus, M H -- Segatto, O -- King, C R -- Aaronson, S A -- New York, N.Y. -- Science. 1987 Jul 10;237(4811):178-82.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2885917" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Breast Neoplasms/genetics ; Cell Line ; *Cell Transformation, Neoplastic/genetics ; DNA/genetics ; Fibroblasts/*metabolism ; Gene Expression Regulation ; Genes, Viral ; Humans ; Mice ; Moloney murine leukemia virus/genetics ; Promoter Regions, Genetic ; Proto-Oncogene Proteins/biosynthesis/genetics/*physiology ; Rats ; Receptor, Epidermal Growth Factor ; Receptor, ErbB-2 ; Receptors, Cell Surface/genetics ; Recombinant Fusion Proteins/biosynthesis/genetics/physiology ; Simian virus 40/genetics ; Tumor Stem Cell Assay
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    Virus-induced increases in plasma corticosterone (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-12-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dunn, A J -- Powell, M L -- Gaskin, J M -- MH25486/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1987 Dec 4;238(4832):1423-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, College of Medicine, University of Florida, Gainesville 32610.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3685987" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Corticosterone/*blood ; Female ; Hypophysectomy ; Lymphocytes/physiology ; Male ; Mice ; Mice, Inbred Strains ; Models, Biological ; Newcastle Disease/*blood ; Pituitary-Adrenal System/*physiopathology ; Postoperative Complications/blood ; Stress, Physiological/blood
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  • 143
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    Transformation by oncogenes encoding protein kinases induces the metastatic phenotype (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-10-09
    Description: Oncogenes encoding serine/threonine or tyrosine kinases were introduced into the established rodent fibroblast cell line NIH 3T3 and tested for tumorigenic and metastatic behavior in T cell-deficient nude mice. Transforming oncogenes of the ras family were capable of converting fibroblast cell lines to fully metastatic tumors. Cell lines transformed by the kinase oncogenes mos, raf, src, fes, and fms formed experimental metastases and (in some cases) these genes were more efficient at metastatic conversion than a mutant ras gene. In contrast, cells transformed by either of two nuclear oncogenes, myc or p53, were tumorigenic when injected subcutaneously but were virtually nonmetastatic after intravenous injection. These data demonstrate that, in addition to ras, a structurally divergent group of kinase oncogenes can induce the metastatic phenotype.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Egan, S E -- Wright, J A -- Jarolim, L -- Yanagihara, K -- Bassin, R H -- Greenberg, A H -- New York, N.Y. -- Science. 1987 Oct 9;238(4824):202-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Manitoba Institute of Cell Biology, University of Manitoba, Winnipeg, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3659911" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Transformation, Neoplastic ; Cells, Cultured ; *Genes ; Mice ; *Neoplasm Metastasis ; *Oncogenes ; Phenotype ; Protein Kinases/*genetics
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  • 144
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    A defined medium for a fastidious Spiroplasma (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-07-31
    Description: A defined medium (H-1) was developed for cultivation of the suckling mouse cataract agent, Spiroplasma mirum, a fastidious member of the class Mollicutes that causes cataracts and chronic brain infection in inoculated neonate mice. The H-1 medium was used to show the importance of sphingomyelin as a growth factor for the culture of the spiroplasma in vitro. The growth of Spiroplasma mirum and the pathology it induces in sphingomyelin-rich tissues in vivo may be related to this dependency.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hackett, K J -- Ginsberg, A S -- Rottem, S -- Henegar, R B -- Whitcomb, R F -- New York, N.Y. -- Science. 1987 Jul 31;237(4814):525-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3603039" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cataract/microbiology ; *Culture Media ; Mice ; Spiroplasma/classification/*growth & development
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  • 145
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    Rheumatoid factor secretion from human Leu-1+ B cells (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-04-03
    Description: A human B cell subpopulation identifiable by the expression of the cell surface antigen Leu-1 (CD5) is responsible for most of the immunoglobulin M rheumatoid factor secreted in vitro after the cells are stimulated with Staphylococcus aureus. The ability of B cells bearing the Leu-1 marker (Leu-1+) to secrete rheumatoid factor is present early in development and extends to adulthood, since Leu-1+ B cells from cord blood and from peripheral blood lymphocytes of both normal adults and patients with certain autoimmune conditions secrete rheumatoid factor in comparable amounts. The neonatal enrichment of Leu-1+ B cells, the presence of Leu-1+ B cells in increased frequencies in patients with autoimmune disease, and the involvement of Leu-1+ B cells in autoantibody secretion suggest both developmental and functional homologies between this human B cell subpopulation and the murine Ly-1 B cell subpopulation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hardy, R R -- Hayakawa, K -- Shimizu, M -- Yamasaki, K -- Kishimoto, T -- New York, N.Y. -- Science. 1987 Apr 3;236(4797):81-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3105057" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Differentiation, B-Lymphocyte ; Antigens, Differentiation, T-Lymphocyte ; Antigens, Surface/*immunology ; Autoimmune Diseases/*immunology ; B-Lymphocytes/*classification/immunology ; Cell Separation ; Fetal Blood/cytology ; Flow Cytometry ; Humans ; Immunoglobulin M/secretion ; Leukocyte Count ; Mice ; Rheumatoid Factor/*secretion
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  • 146
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    A Mab to a unique cerebellar neuron generated by immunosuppression and rapid immunization (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-07-03
    Description: The cerebellar cortex is perhaps the best characterized structure in the mammalian central nervous system. Although the major cerebellar cell classes are well known, a new class of cerebellar cortical neuron has now been identified with a monoclonal antibody (Mab) generated by a procedure for rapid immunization and selective immunosuppression of antibody responses. This procedure generates a high frequency of immunoglobulin G-class antibodies of desired specificity, and has allowed the generation of two antibodies that recognize subsets of cerebellar cortical neurons. One of these antibodies defines a previously unrecognized class of cerebellar neuron. The distribution and antigenic characteristics of this neuron suggest that it has a distinct role in cerebellar circuitry.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hockfield, S -- R01 EY06511/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 1987 Jul 3;237(4810):67-70.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3603010" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn/immunology ; Antibodies, Monoclonal/*immunology ; Cerebellar Cortex/cytology/*immunology ; Immune Tolerance ; Mice ; Mice, Inbred BALB C/immunology ; Rats
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  • 147
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    Conservation of the Duchenne muscular dystrophy gene in mice and humans (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-10-16
    Description: A portion of the Duchenne muscular dystrophy (DMD) gene transcript from human fetal skeletal muscle and mouse adult heart was sequenced, representing approximately 25 percent of the total, 14-kb DMD transcript. The nucleic acid and predicted amino acid sequences from the two species are nearly 90 percent homologous. The amino acid sequence that is predicted from this portion of the DMD gene indicates that the protein product might serve a structural role in muscle, but the abundance and tissue distribution of the messenger RNA suggests that the DMD protein is not nebulin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hoffman, E P -- Monaco, A P -- Feener, C C -- Kunkel, L M -- 2T 32 GM07753-07/GM/NIGMS NIH HHS/ -- HD18658/HD/NICHD NIH HHS/ -- R01 NS23740/NS/NINDS NIH HHS/ -- T32 GM007753/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1987 Oct 16;238(4825):347-50.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Genetics, Children's Hospital, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3659917" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; DNA/*genetics ; DNA, Recombinant ; Exons ; Humans ; Male ; Mice ; Molecular Sequence Data ; Muscle Proteins/genetics ; Muscles/analysis/embryology ; Muscular Dystrophies/*genetics ; Muscular Dystrophy, Animal/*genetics ; Myocardium/analysis ; Nucleic Acid Hybridization ; RNA, Messenger/genetics ; X Chromosome
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  • 148
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    The raf oncogene is associated with a radiation-resistant human laryngeal cancer (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-08-28
    Description: In order to identify the genetic factors associated with the radiation-resistant human laryngeal carcinoma cell line (SQ-20B), tumor cell DNA was transfected into NIH/3T3 cells. A high incidence (six out of six) of raf sequences was found in transfected NIH/3T3 clones and the tumorigenic potential of SQ-20B DNA could be linked to genomic fragments that represent most of the kinase domain of human c-raf-1. An apparently unaltered 3.5-kilobase pair (kb) human c-raf transcript was identified in SQ-20B cells but was not observed in the transfected NIH/3T3 cell clones. Two new transcripts (4.2 kb and 2.6 kb) were found in tumorigenic clones; the large transcript was missing in a very poorly tumorigenic clone. Cytogenetic analysis indicated that the normal autosomes of chromosome 3 were absent in SQ-20B karyotypes and had formed apparently stable marker chromosomes. Unlike the recipient NIH/3T3 cell line, 30 percent of the transformed clone-1 metaphases had minute and double-minute chromosomes representative of amplified DNA sequences. The frequency of the c-raf-1 identification by NIH/3T3 transfection of SQ-20B DNA suggests the presence of some genetic abnormality within this locus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kasid, U -- Pfeifer, A -- Weichselbaum, R R -- Dritschilo, A -- Mark, G E -- CA425969/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1987 Aug 28;237(4818):1039-41.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3616625" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; DNA, Neoplasm/genetics ; Humans ; Karyotyping ; Laryngeal Neoplasms/*genetics/radiotherapy ; Mice ; Mice, Nude ; Nucleic Acid Hybridization ; Oncogenes/*radiation effects ; Proto-Oncogenes/radiation effects ; *Radiation Tolerance
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  • 149
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    Ouabain resistance conferred by expression of the cDNA for a murine Na+, K+-ATPase alpha subunit (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-08-21
    Description: The molecular basis for the marked difference between primate and rodent cells in sensitivity to the cardiac glycoside ouabain has been established by genetic techniques. A complementary DNA encoding the entire alpha 1 subunit of the mouse Na+- and K+-dependent adenosine triphosphatase (ATPase) was inserted into the expression vector pSV2. This engineered DNA molecule confers resistance against 10(-4) M ouabain to monkey CV-1 cells. Deletion of sequences encoding the carboxyl terminus of the alpha 1 subunit abolish the activity of the complementary DNA. The ability to assay the biological activity of this ATPase in a transfection protocol permits the application of molecular genetic techniques to the analysis of structure-function relationships for the enzyme that establishes the internal Na+/K+ environment of most animal cells. The full-length alpha 1 subunit complementary DNA will also be useful as a dominant selectable marker for somatic cell genetic studies utilizing ouabain-sensitive cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kent, R B -- Emanuel, J R -- Ben Neriah, Y -- Levenson, R -- Housman, D E -- CA-07919/CA/NCI NIH HHS/ -- CA-26712/CA/NCI NIH HHS/ -- CA-38992/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1987 Aug 21;237(4817):901-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3039660" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Cercopithecus aethiops ; DNA/genetics ; Drug Resistance ; Gene Expression Regulation ; Macromolecular Substances ; Mice ; Ouabain/*pharmacology ; Sodium-Potassium-Exchanging ATPase/antagonists & inhibitors/*genetics ; Species Specificity ; Structure-Activity Relationship ; Transfection
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    Chemical identification of a tumor-derived angiogenic factor (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-05-15
    Description: Neoplasms produce substances that induce blood vessel formation (angiogenesis). Fractions from ethanol extracts of the Walker 256 carcinoma were isolated by silica column chromatography and C18 reversed-phase high-performance liquid chromatography. Two of the isolated fractions induced neovascularization when tested in the rabbit corneal micropocket assay. One of the fractions was identified as nicotinamide by desorption-electron impact mass spectrometry, nuclear magnetic resonance spectroscopy, and gas chromatography-mass spectrometry. The second active fraction contained nicotinamide as part of a more complex, as yet unidentified, molecular arrangement. Microgram quantities of commercial nicotinamide induced neovascularization in the corneal micropocket assay and in the chick chorioallantoic membrane assay.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kull, F C Jr -- Brent, D A -- Parikh, I -- Cuatrecasas, P -- New York, N.Y. -- Science. 1987 May 15;236(4803):843-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2437656" target="_blank"〉PubMed〈/a〉
    Keywords: Angiogenesis Inducing Agents/*isolation & purification/pharmacology ; Animals ; Carcinoma 256, Walker/*physiopathology ; Cells, Cultured ; Chick Embryo ; Cornea/blood supply ; Endothelium/cytology/drug effects ; Gas Chromatography-Mass Spectrometry ; Growth Substances/*isolation & purification ; Magnetic Resonance Spectroscopy ; Mass Spectrometry ; Mice ; Neovascularization, Pathologic ; Niacinamide/isolation & purification/pharmacology
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    Neuronal pp60c-src contains a six-amino acid insertion relative to its non-neuronal counterpart (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-07-24
    Description: Neuronal cells express a pp60c-src variant that displays an altered electrophoretic mobility and a different V8 peptide pattern relative to pp60c-src expressed in tissues of non-neuronal origin. To determine whether the neuronal form of pp60c-src is encoded by a brain-specific messenger RNA, a mouse brain complementary DNA (cDNA) library was screened with a chicken c-src probe and a 3.8-kilobase c-src cDNA clone was isolated. This clone encodes a 60-kilodalton protein that differs from chicken or human pp60c-src primarily in having six extra amino acids (Arg-Lys-Val-Asp-Val-Arg) within the NH2-terminal 16 kilodaltons of the molecule. S1 nuclease protection analysis confirmed that brain c-src RNA contains an 18-nucleotide insertion at the position of the extra six amino acids. This insertion occurs at a position that corresponds to a splice junction in the chicken and human c-src genes. The isolated c-src cDNA clone encodes a protein that displays an identical V8 peptide pattern to that observed in pp60c-src isolated from tissues of neuronal origin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Martinez, R -- Mathey-Prevot, B -- Bernards, A -- Baltimore, D -- P0I CA38497/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1987 Jul 24;237(4813):411-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2440106" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Brain/enzymology ; Chickens ; Cloning, Molecular ; DNA/metabolism ; DNA Restriction Enzymes ; DNA Transposable Elements ; Humans ; Isoenzymes/*genetics ; Mice ; Neurons/*enzymology ; Protein Kinases/*genetics ; Proto-Oncogene Proteins/*genetics ; Proto-Oncogene Proteins pp60(c-src) ; Sequence Homology, Nucleic Acid ; Species Specificity
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    Cloned gene of Rickettsia rickettsii surface antigen: candidate vaccine for Rocky Mountain spotted fever (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-01-02
    Description: Two major protective antigens of Rickettsia rickettsii have been previously described. In this study, we cloned the gene encoding one of these antigens into Escherichia coli and tested the effectiveness of the recombinant-made product as a vaccine for Rocky Mountain spotted fever. A clone bank of R strain R. rickettsii DNA was made in E. coli K-12 by using the plasmid vector pBR322. Transformants were screened for their ability to make rickettsial antigens by reactivity with rabbit antibodies to R. rickettsii. One of the transformants, EM24(pGAM21), made a product reactive with two monoclonal antibodies that recognize a 155-kilodalton protein of R. rickettsii. One of the monoclonal antibodies was a member of a class of antibodies that react to heat-sensitive epitopes and protect mice injected with a potentially lethal dose of viable R. rickettsii. The cloned product contained this protective heat-sensitive epitope. In order to obtain enhanced expression, the gene was subcloned downstream of the lactose promoter on the plasmid vector pUC8. A sonic lysate of E. coli harboring the pUC8 subclone was used successfully as a vaccine to protect mice injected with a lethal dose of the viable R. rickettsii.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McDonald, G A -- Anacker, R L -- Garjian, K -- New York, N.Y. -- Science. 1987 Jan 2;235(4784):83-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3099387" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens/*genetics ; Antigens, Bacterial/*genetics ; Bacterial Proteins/genetics/immunology ; Bacterial Vaccines/*genetics ; Cloning, Molecular ; Genes, Bacterial ; Mice ; Rickettsia rickettsii/*genetics/immunology ; Rocky Mountain Spotted Fever/*prevention & control ; Vaccines, Synthetic/*genetics/immunology
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  • 153
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    Mapping patterns of c-fos expression in the central nervous system after seizure (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-07-10
    Description: A dramatic and specific induction of c-fos was observed in identifiable neuronal populations in vivo after administration of the convulsant Metrazole. This effect was time- and dose-dependent and was abolished by prior treatment with the anticonvulsant drugs diazepam or pentobarbital. About 60 minutes after administration of Metrazole, c-fos messenger RNA reached a maximum and declined to basal levels after 180 minutes. A further decrease below that in normal brain was observed before a return to basal levels after 16 hours. While Metrazole still elicited seizures during this period, reinduction of c-fos was largely refractory. At 90 minutes, c-fos protein was observed in the nuclei of neurons in the dentate gyrus, and in the pyriform and cingulate cortices. Subsequently, c-fos protein appeared throughout the cortex, hippocampus, and limbic system. Thus, seizure activity results in increased c-fos gene expression in particular subsets of neurons.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Morgan, J I -- Cohen, D R -- Hempstead, J L -- Curran, T -- New York, N.Y. -- Science. 1987 Jul 10;237(4811):192-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3037702" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Brain Chemistry/drug effects ; DNA-Binding Proteins/biosynthesis/genetics ; Diazepam/pharmacology ; Fluorescent Antibody Technique ; Gene Expression Regulation ; Mice ; Mice, Inbred BALB C ; Neurons/metabolism ; Pentobarbital/pharmacology ; Pentylenetetrazole/antagonists & inhibitors/toxicity ; Proto-Oncogene Proteins/*biosynthesis/genetics ; Proto-Oncogene Proteins c-fos ; Receptors, GABA-A/drug effects ; Seizures/chemically induced/*metabolism
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  • 154
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    Selective inactivation of influenza C esterase: a probe for detecting 9-O-acetylated sialic acids (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-06-05
    Description: The influenza C virus (INF-C) hemagglutinin recognizes 9-O-acetyl-N-acetylneuraminic acid. The same protein contains the receptor-destroying enzyme (RDE), which is a 9-O-acetyl-esterase. The RDE was inactivated by the serine esterase inhibitor di-isopropyl fluorophosphate (DFP). [3H]DFP-labeling localized the active site to the heavy chain of the glycoprotein. DFP did not alter the hemagglutination or fusion properties of the protein, but markedly decreased infectivity of the virus, demonstrating that the RDE is important for primary infection. Finally, DFP-treated INF-C bound specifically and irreversibly to cells expressing 9-O-acetylated sialic acids. This provides a probe for a molecule that was hitherto very difficult to study.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Muchmore, E A -- Varki, A -- 1-K12-AM01408/AM/NIADDK NIH HHS/ -- R01 GM32373/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1987 Jun 5;236(4806):1293-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3589663" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Animals ; Binding Sites ; Biological Assay ; Hemagglutination Tests ; Influenzavirus C/drug effects/*enzymology ; Isoflurophate/metabolism/*pharmacology ; Mice ; Orthomyxoviridae/*enzymology ; Protein Binding ; Sialic Acids/*analysis ; Viral Proteins/metabolism
    Print ISSN: 0036-8075
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  • 155
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    Allelic exclusion in transgenic mice that express the membrane form of immunoglobulin mu (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-05-15
    Description: Antibody-producing cells display a special form of regulation whereby each cell produces immunoglobulin from only one of its two sets of antibody genes. This phenomenon, called allelic exclusion, is thought to be mediated by the product of one heavy chain allele restricting the expression of the other. Heavy chains are synthesized in two molecular forms, secreted and membrane bound. In order to determine whether it is specifically the membrane-bound form of the immunoglobulin M (IgM) heavy chain (mu) that mediates this regulation, transgenic mice were created that carry a human mu chain gene altered so that it can only direct the synthesis of the membrane-bound protein. The membrane-bound form of the human mu chain was made by most of the B cells in these animals as measured by assays of messenger RNA and surface immunoglobulins. Further, the many B cells that express the human gene do not express endogenous mouse IgM, and the few B cells that express endogenous mouse mu do not express the transgene. Thus, the membrane-bound form of the mu chain is sufficient to mediate allelic exclusion. In addition, the molecular structures recognized for this purpose are conserved between human and mouse systems.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nussenzweig, M C -- Shaw, A C -- Sinn, E -- Danner, D B -- Holmes, K L -- Morse, H C 3rd -- Leder, P -- New York, N.Y. -- Science. 1987 May 15;236(4803):816-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3107126" target="_blank"〉PubMed〈/a〉
    Keywords: *Alleles ; Animals ; Antibody-Producing Cells/*immunology ; Gene Expression Regulation ; *Genes ; Humans ; Immunoglobulin M/genetics ; Immunoglobulin mu-Chains/*genetics ; Mice ; Mice, Inbred Strains ; RNA, Messenger/genetics ; Transcription, Genetic
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  • 156
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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)
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    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
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  • 157
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    Zinc selectively blocks the action of N-methyl-D-aspartate on cortical neurons (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-05-01
    Description: Large amounts of zinc are present in synaptic vesicles of mammalian central excitatory boutons and may be released during synaptic activity, but the functional significance of the metal for excitatory neurotransmission is currently unknown. Zinc (10 to 1000 micromolar) was found to have little intrinsic membrane effect on cortical neurons, but invariably produced a zinc concentration-dependent, rapid-onset, reversible, and selective attenuation of the membrane responses to N-methyl-D-aspartate, homocysteate, or quinolinate. In contrast, zinc generally potentiated the membrane responses to quisqualate or alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate and often did not affect the response to kainate. Zinc also attenuated N-methyl-D-aspartate receptor-mediated neurotoxicity but not quisqualate or kainate neurotoxicity. The ability of zinc to specifically modulate postsynaptic neuronal responses to excitatory amino acid transmitters, reducing N-methyl-to-aspartate receptor-mediated excitation while often increasing quisqualate receptor-mediated excitation, is proposed to underlie its normal function at central excitatory synapses and furthermore could be relevant to neuronal cell loss in certain disease states.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Peters, S -- Koh, J -- Choi, D W -- NS07280/NS/NINDS NIH HHS/ -- NS21628/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1987 May 1;236(4801):589-93.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2883728" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aspartic Acid/*analogs & derivatives/pharmacology ; Cell Membrane/physiology ; Cerebral Cortex/*cytology ; Drug Interactions ; Electrophysiology ; Homocysteine/analogs & derivatives/pharmacology ; Ibotenic Acid/analogs & derivatives/pharmacology ; Kainic Acid/pharmacology ; Magnesium/pharmacology ; Membrane Potentials/drug effects ; Mice ; N-Methylaspartate ; Neurons/drug effects/*physiology ; Oxadiazoles/pharmacology ; Quinolinic Acid ; Quinolinic Acids/pharmacology ; Quisqualic Acid ; Receptors, N-Methyl-D-Aspartate ; Receptors, Neurotransmitter/drug effects/physiology ; Zinc/*pharmacology ; alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid
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  • 158
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    Avian v-myc replaces chromosomal translocation in murine plasmacytomagenesis (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-02-13
    Description: Deregulation of c-myc expression in association with chromosomal translocations occurs in over 95% of murine plasmacytomas, rat immunocytomas, and human Burkitt lymphomas. Infection with a murine retrovirus (J-3) containing an avian v-myc rapidly induced plasmacytomas in pristane-primed BALB/cAn mice. Only 17% of the induced plasmacytomas that were karyotyped showed the characteristic chromosomal translocations involving the c-myc locus. Instead, all of the translocation-negative tumors demonstrated characteristic J-3 virus integration sites that were actively transcribed. Thus, the high levels of v-myc expression have replaced the requirement for chromosomal translocation in plasmacytomagenesis and accelerated the process of transformation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Potter, M -- Mushinski, J F -- Mushinski, E B -- Brust, S -- Wax, J S -- Wiener, F -- Babonits, M -- Rapp, U R -- Morse, H C 3rd -- New York, N.Y. -- Science. 1987 Feb 13;235(4790):787-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3810165" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Birds ; *Cell Transformation, Neoplastic ; *Genes, Viral ; Mice ; Mice, Inbred BALB C ; Mice, Inbred Strains ; Moloney murine leukemia virus/*genetics ; Nucleic Acid Hybridization ; *Oncogenes ; Plasmacytoma/genetics/*microbiology ; Retroviridae/*genetics ; Transcription, Genetic ; *Translocation, Genetic
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  • 159
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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)
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    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
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  • 160
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    Evolutionary and somatic selection of the antibody repertoire in the mouse (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-11-20
    Description: The repertoire of antibody variable (V) regions has been subject to evolutionary selection, affecting both the diversity of V region genes in the germline and their expression in the B lymphocyte population and its subsets. In ontogeny, contact with an antigen leads to the expansion of B cells expressing antibodies complementary to it. In a defined phase of B cell differentiation, new sets of V regions are generated from the existing repertoire through somatic hypermutation. Cells carrying advantageous antibody mutants are selected into the memory compartment and produce a stable secondary response upon reexposure to the antigen.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rajewsky, K -- Forster, I -- Cumano, A -- New York, N.Y. -- Science. 1987 Nov 20;238(4830):1088-94.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Genetics, University of Cologne, Koln, FRG.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3317826" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies/*genetics ; *Antibody Diversity ; B-Lymphocytes/*physiology ; *Biological Evolution ; *Genes, Immunoglobulin ; Genes, Switch ; Immunity ; Immunoglobulin Isotypes/genetics ; Immunoglobulin Variable Region/genetics ; Mice ; Mutation ; Selection, Genetic
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    Nerve terminal remodeling visualized in living mice by repeated examination of the same neuron (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-11-20
    Description: The distribution of presynaptic endings on the surfaces of autonomic ganglion cells was mapped in living mice after intravenous administration of a styryl pyridinium dye. The staining and imaging techniques did not appear to damage the ganglion cells, or the synapses on them; these procedures could therefore be repeated after an arbitrary period. Observations of the same neurons at intervals of up to 3 weeks indicate that the pattern of preganglionic terminals on many of these nerve cells gradually changes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Purves, D -- Voyvodic, J T -- Magrassi, L -- Yawo, H -- New York, N.Y. -- Science. 1987 Nov 20;238(4830):1122-6.〈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/3685967" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Coloring Agents ; Fluorescent Dyes ; Ganglia, Parasympathetic/*cytology/physiology ; Membrane Potentials ; Mice ; Nerve Endings/ultrastructure ; Neuronal Plasticity ; Pyridinium Compounds ; Time Factors ; Video Recording
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  • 162
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    Activated oncogenes in B6C3F1 mouse liver tumors: implications for risk assessment (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-09-11
    Description: The validity of mouse liver tumor end points in assessing the potential hazards of chemical exposure to humans is a controversial but important issue, since liver neoplasia in mice is the most frequent tumor target tissue end point in 2-year carcinogenicity studies. The ability to distinguish between promotion of background tumors versus a genotoxic mechanism of tumor initiation by chemical treatment would aid in the interpretation of rodent carcinogenesis data. Activated oncogenes in chemically induced and spontaneously occurring mouse liver tumors were examined and compared as one approach to determine the mechanism by which chemical treatment caused an increased incidence of mouse liver tumors. Data suggest that furan and furfural caused an increased incidence in mouse liver tumors at least in part by induction of novel weakly activating point mutations in ras genes even though both chemicals did not induce mutations in Salmonella assays. In addition to ras oncogenes, two activated raf genes and four non-ras transforming genes were detected. The B6C3F1 mouse liver may thus provide a sensitive assay system to detect various classes of proto-oncogenes that are susceptible to activation by carcinogenic insult. As illustrated with mouse liver tumors, analysis of activated oncogenes in spontaneously occurring and chemically induced rodent tumors will provide information at a molecular level to aid in the use of rodent carcinogenesis data for risk assessment.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Reynolds, S H -- Stowers, S J -- Patterson, R M -- Maronpot, R R -- Aaronson, S A -- Anderson, M W -- New York, N.Y. -- Science. 1987 Sep 11;237(4820):1309-16.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3629242" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; *Cell Transformation, Neoplastic ; Cells, Cultured ; Liver Neoplasms/*genetics ; Mice ; Mutation ; Nucleic Acid Hybridization ; *Oncogenes ; *Proto-Oncogenes ; Risk
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    Thrombospondin promotes cell-substratum adhesion (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-06-19
    Description: The physiological role of the platelet-secreted protein thrombospondin (TSP) is poorly understood, although it has been postulated to be involved in platelet aggregation and cellular adhesion. In this report, TSP isolated from human platelets was found to promote, in vitro, the cell-substratum adhesion of a variety of cells, including platelets, melanoma cells, muscle cells, endothelial cells, fibroblasts, and epithelial cells. The adhesion-promoting activity of TSP was species independent, specific, and not due to contamination by fibronectin, vitronectin, laminin, or platelet factor 4. The cell surface receptor for TSP is protein in nature and appears distinct from that for fibronectin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tuszynski, G P -- Rothman, V -- Murphy, A -- Siegler, K -- Smith, L -- Smith, S -- Karczewski, J -- Knudsen, K A -- New York, N.Y. -- Science. 1987 Jun 19;236(4808):1570-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2438772" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD36 ; Cattle ; Cell Adhesion/*drug effects ; Fibroblasts/drug effects ; Fibronectins/pharmacology ; Glycoproteins/*pharmacology ; Humans ; Melanoma/metabolism ; Mice ; Platelet Aggregation/drug effects ; Rabbits ; Rats ; Receptors, Mitogen/metabolism ; Swine ; Thrombospondins
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  • 164
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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)
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    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
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  • 165
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    The molecular basis of the sparse fur mouse mutation (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-07-24
    Description: The ornithine transcarbamylase-deficient sparse fur mouse is an excellent model to study the most common human urea cycle disorder. The mutation has been well characterized by both biochemical and enzymological methods, but its exact nature has not been revealed. A single base substitution in the complementary DNA for ornithine transcarbamylase from the sparse fur mouse has been identified by means of a combination of two recently described techniques for rapid mutational analysis. This strategy is simpler than conventional complementary DNA library construction, screening, and sequencing, which has often been used to find a new mutation. The ornithine transcarbamylase gene in the sparse fur mouse contains a C to A transversion that alters a histidine residue to an asparagine residue at amino acid 117.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Veres, G -- Gibbs, R A -- Scherer, S E -- Caskey, C T -- HD21452/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1987 Jul 24;237(4813):415-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3603027" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; DNA/analysis ; Disease Models, Animal ; *Genes ; Mice ; Mice, Mutant Strains ; *Mutation ; Ornithine Decarboxylase/deficiency/*genetics ; RNA, Messenger/genetics
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  • 166
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    Retroviruses and mouse embryos: a rapid model for neurovirulence and transplacental antiviral therapy (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-06-26
    Description: A murine model in which neurotropic retroviral infection can be studied over short periods of time was developed. Microinjection of Cas-Br-E virus into midgestation mouse embryos caused paralysis and death within 25 days after birth, in contrast to virus-infected neonates which develop disease only after 4 months. To evaluate whether antiviral drugs could cross the placental barrier and influence the course of the disease, the drug 3'-azido-3'-deoxythymidine (AZT) was administered to infected embryos through the drinking water of pregnant females. AZT treatment markedly retarded the onset and course of virus-induced central nervous system disease, permitting animals to survive beyond 4 months of age. These results are evidence for effective antiviral treatment during gestation and in the perinatal period and are of potential significance for the management of maternal transmission of the acquired immune deficiency syndrome (AIDS) virus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sharpe, A H -- Jaenisch, R -- Ruprecht, R M -- CA38497/CA/NCI NIH HHS/ -- HD19015/HD/NICHD NIH HHS/ -- U01-AI24845-01/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1987 Jun 26;236(4809):1671-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3037694" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Antiviral Agents/*therapeutic use ; Central Nervous System Diseases/drug therapy/embryology/*microbiology ; Female ; Fetal Diseases/*drug therapy/microbiology ; Gestational Age ; Maternal-Fetal Exchange ; Mice ; Pregnancy ; *Prenatal Exposure Delayed Effects ; Retroviridae/pathogenicity ; Thymidine/*analogs & derivatives/therapeutic use ; Tumor Virus Infections/*drug therapy/embryology ; Virulence ; Zidovudine
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  • 167
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    Islet allograft survival after a single course of treatment of recipient with antibody to L3T4 (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-07-17
    Description: Allografts of pancreatic islets of Langerhans were induced to survive for an indefinite period in diabetic mice if, at the time of engraftment, the mice received a single course of treatment with a monoclonal antibody directed against the L3T4 determinant, a nonpolymorphic cell surface glycoprotein present on the cell surface of the murine T helper-inducer lymphocyte subset. This treatment allowed the survival of islets of Langerhans transplanted across a major histocompatibility barrier without additional immunosuppression. The results demonstrate that the lymphocyte subset defined by the expression of the L3T4 molecules is central to the induction of allograft rejection and provides a model for tolerance induction for organ allograft transplantation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shizuru, J A -- Gregory, A K -- Chao, C T -- Fathman, C G -- DK32075/DK/NIDDK NIH HHS/ -- DK37104/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1987 Jul 17;237(4812):278-80.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2955518" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/therapeutic use ; Antigens, Differentiation, T-Lymphocyte ; Antigens, Surface/*immunology ; Diabetes Mellitus, Experimental/*therapy ; *Graft Survival ; Immune Tolerance ; *Islets of Langerhans Transplantation ; Mice ; T-Lymphocytes, Helper-Inducer/*immunology
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  • 168
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    Reversible inhibition of mammary gland growth by transforming growth factor-beta (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-07-17
    Description: Transforming growth factor-beta (TGF-beta) can stimulate or inhibit growth of cells in vitro, as well as induce the transformed phenotype. Although widely distributed in animal tissue, the effects of TGF-beta in vivo are largely unknown, and a physiological role for the peptide hormone has not been demonstrated. The effect of TGF-beta on developing epithelial tissue in situ was studied by using slow-release plastic pellets containing TGF-beta to treat developing mouse mammary gland. Powerful inhibition of mammary growth and morphogenesis was observed. This growth-inhibited mammary tissue was histologically normal, and the inhibitory effect was fully reversible. Under the conditions of these experiments, TGF-beta displayed many of the characteristics expected of a physiologically active growth-regulatory molecule.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Silberstein, G B -- Daniel, C W -- 1050/PHS HHS/ -- New York, N.Y. -- Science. 1987 Jul 17;237(4812):291-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3474783" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; DNA/biosynthesis ; Drug Implants ; Epithelial Cells ; Extracellular Matrix/physiology ; Mammary Glands, Animal/*growth & development ; Mice ; Peptides/*pharmacology ; Transforming Growth Factors
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  • 169
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    Downregulation of L3T4+ cytotoxic T lymphocytes by interleukin-2 (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-10-16
    Description: Proliferation of activated cytotoxic T lymphocytes (CTLs) that recognize foreign histocompatibility antigens is induced by interleukin-2, a potent immunoregulatory molecule originally described as T cell growth factor. Interleukin-2 (IL-2) is widely used to isolate and induce clonal expansion of CTLs for functional studies in vitro and in vivo. However, in studies with CTLs specific for class I and class II histocompatibility antigens, IL-2 rapidly downregulated the lytic activity of some class II-specific CTLs in a time- and dose-dependent manner. Lytic activity of L3T4+ CTLs specific for the murine class II antigen I-Ek was repeatedly up- and downregulated in vitro by alternate exposure to specific (alloantigen) and nonspecific (recombinant IL-2) signals, respectively. These results demonstrate that some CTLs modulate their functional property (cytolysis) while undergoing IL-2-driven cell proliferation without loss of antigen specificity or ability to revert to a lytic phenotype.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shih, C C -- Truitt, R L -- AI-22312/AI/NIAID NIH HHS/ -- CA-39854/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1987 Oct 16;238(4825):344-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatrics, Medical College of Wisconsin, Children's Hospital of Wisconsin, Milwaukee 53233.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2443976" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antigens, Differentiation, T-Lymphocyte/genetics ; Cell Line ; Clone Cells/immunology ; Cytotoxicity, Immunologic ; Epitopes ; H-2 Antigens/immunology ; Interleukin-2/*physiology ; Isoantigens/immunology ; *Lymphocyte Activation ; Mice ; Phenotype ; T-Lymphocytes, Cytotoxic/*immunology
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  • 170
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    Interferon-gamma and B cell stimulatory factor-1 reciprocally regulate Ig isotype production (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-05-22
    Description: Gamma interferon (IFN-gamma) and B cell stimulatory factor-1 (BSF-1), also known as interleukin-4, are T cell-derived lymphokines that have potent effects on B cell proliferation and differentiation. They are often secreted by distinct T cell clones. It is now shown that IFN-gamma stimulates the expression of immunoglobulin (Ig) of the IgG2a isotype and inhibits the production of IgG3, IgG1, IgG2b, and IgE. By contrast, BSF-1 has powerful effects in promoting switching to the expression of IgG1 and IgE but markedly inhibits IgM, IgG3, IgG2a, and IgG2b. These results indicate that BSF-1 and IFN-gamma as well as the T cells that produce them may act as reciprocal regulatory agents in the determination of Ig isotype responses. The effects of IFN-gamma and BSF-1 on isotype expression are independent.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Snapper, C M -- Paul, W E -- New York, N.Y. -- Science. 1987 May 22;236(4804):944-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3107127" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal ; Antigen-Antibody Complex ; B-Lymphocytes/drug effects/*immunology ; Cricetinae ; Growth Substances/*pharmacology ; Immunoglobulin Isotypes/*biosynthesis ; Interferon-gamma/immunology/*pharmacology ; Interleukin-4 ; Kinetics ; Lymphocyte Activation ; Lymphokines/*pharmacology ; Mice ; Mice, Inbred DBA ; Recombinant Proteins/*pharmacology
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  • 171
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    Two pairs of recombination signals are sufficient to cause immunoglobulin V-(D)-J joining (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-11-20
    Description: The minimum sequence requirements for antigen receptor V-(D)-J joining were studied by constructing recombination-substrates containing synthetic recombination signals and introducing them into a recombination-competent pre-B cell line. Two sets of heptamer (CACTGTG) and nonamer (GGTTTTTGT) sequences were shown to be sufficient to cause the V-(D)-J joining, if the 12- and 23-base pair spacer rule is satisfied. A point mutation in the heptamer sequence, or a change in the combination of the two spacer lengths, drastically reduced the recombination.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Akira, S -- Okazaki, K -- Sakano, H -- AI-18790/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1987 Nov 20;238(4830):1134-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, University of California, Berkeley 94720.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3120312" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Chromosome Inversion ; *Genes, Immunoglobulin ; Genetic Vectors ; Humans ; Immunoglobulin Variable Region/*genetics ; Immunoglobulin kappa-Chains/genetics ; Mice ; Receptors, Antigen, T-Cell/genetics ; *Recombination, Genetic ; Retroviridae/genetics ; Sequence Homology, Nucleic Acid ; Structure-Activity Relationship
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  • 172
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    Three-dimensional structure of interleukin-2 (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-12-18
    Description: Interleukin-2 is an effector protein that participates in modulating the immune response; it has become a focal point for the study of lymphokine structure and function. The three-dimensional structure of the interleukin molecule has been solved to 3.0 angstrom resolution. Interleukin-2 has a novel alpha-helical tertiary structure that suggests one portion of the molecule forms a structural scaffold, which underlies the receptor binding facets of the molecule.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brandhuber, B J -- Boone, T -- Kenney, W C -- McKay, D B -- A1-00631/PHS HHS/ -- A1-19762/PHS HHS/ -- New York, N.Y. -- Science. 1987 Dec 18;238(4834):1707-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry and Biochemistry, University of Colorado, Boulder 80309.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3500515" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Interleukin-2/isolation & purification ; Mice ; Models, Molecular ; Protein Conformation ; Solvents ; X-Ray Diffraction
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  • 173
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    Genetic ablation: targeted expression of a toxin gene causes microphthalmia in transgenic mice (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-12-11
    Description: Lineage-specific regulatory elements can be used to direct expression of a variety of genes to specific tissues in transgenic mice. If the hybrid constructs contain a gene encoding a cytotoxic gene product, then genetic ablation of a specific cell lineage can be achieved. We have generated six transgenic mice by introducing into fertilized eggs the mouse gamma 2-crystallin promoter fused to the coding region of the diphtheria toxin A-chain gene. Three of these mice and all the transgenic offspring analyzed were microphthalmic. The lenses of these mice displayed considerable heterogeneity: some were almost normal morphologically but reduced in size, whereas others were grossly aberrant and deficient in nuclear fiber cells. These studies indicate that programmed ablation of specific cell types can be stably transmitted through the germ line.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Breitman, M L -- Clapoff, S -- Rossant, J -- Tsui, L C -- Glode, L M -- Maxwell, I H -- Bernstein, A -- CA 42354/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1987 Dec 11;238(4833):1563-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Mount Sinai Hospital Research Institute, Toronto, Ontario, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3685993" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Crystallins/*genetics ; Diphtheria Toxin/*genetics ; Eye/pathology ; *Genes ; Mice ; Mice, Transgenic ; Microphthalmos/*genetics/pathology ; Promoter Regions, Genetic
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  • 174
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    The relation between major histocompatibility complex (MHC) restriction and the capacity of Ia to bind immunogenic peptides (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-03-13
    Description: The capacity of purified I-Ad, I-Ed, I-Ak, and I-Ek to bind to protein derived peptides that have been previously reported to be T cell immunogens has been examined. For each of the 12 peptides studied strong binding to the relevant Ia restriction element was observed. All the peptides bound more than one Ia molecule; however, for 11 of 12 peptides, the dominant binding was to the restriction element, whereas in one instance the dominant binding was to a nonrestriction element. When the peptides were used to inhibit the presentation of antigen by prefixed accessory cells to T cells, an excellent correlation was found between the capacity of a peptide to inhibit the binding of an antigen to purified Ia and the capacity of the peptide to inhibit accessory cell presentation of the antigen. Thus, the binding of peptide to purified Ia is immunologically relevant, and Ia seems to be the only saturable molecule on the surface of the accessory cell involved in antigen presentation. Inhibition analysis also indicated that all peptides restricted to a particular Ia molecule competitively inhibited one another, suggesting that each Ia restriction element has a single binding site for antigen. Cross-linking of labeled peptides to Ia followed by electrophoretic analysis and autoradiography suggested that this single binding site is made up of portions of both alpha and beta chains of Ia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Buus, S -- Sette, A -- Colon, S M -- Miles, C -- Grey, H M -- AI 18634/AI/NIAID NIH HHS/ -- AI 22295/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1987 Mar 13;235(4794):1353-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2435001" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens/immunology ; Binding, Competitive ; Columbidae ; Cross-Linking Reagents ; Cytochrome c Group/immunology ; Epitopes/genetics/immunology ; Glutaral ; Histocompatibility Antigens Class II/*metabolism ; Hybridomas/immunology ; *Major Histocompatibility Complex ; Mice ; Moths ; Peptide Fragments/immunology ; Peptides/*immunology ; T-Lymphocytes/immunology
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  • 175
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    Efficacy of murine malaria sporozoite vaccines: implications for human vaccine development (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-04-24
    Description: As part of a study of potential vaccines against malaria, the protective efficacy of sporozoite subunit vaccines was determined by using the Plasmodium berghei murine malaria model. Mice were immunized with recombinant DNA-produced or synthetic peptide-carrier subunit vaccines derived from the repetitive epitopes of the Plasmodium berghei circumsporozoite gene, or with radiation-attenuated sporozoites. Immunization with subunit vaccines elicited humoral responses that were equivalent to or greater than those elicited by irradiated sporozoites, yet the protection against sporozoite challenge induced by either of the subunit vaccines was far less than that achieved by immunization with attenuated sporozoites. Passive and adoptive transfer studies demonstrated that subunit vaccines elicited predominantly antibody-mediated protection that was easily overcome whereas irradiated sporozoites induced potent cell-mediated immunity that protected against high challenge doses of sporozoites. These studies indicate that new strategies designed to induce cellular immunity will be required for efficacious sporozoite vaccines.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Egan, J E -- Weber, J L -- Ballou, W R -- Hollingdale, M R -- Majarian, W R -- Gordon, D M -- Maloy, W L -- Hoffman, S L -- Wirtz, R A -- Schneider, I -- New York, N.Y. -- Science. 1987 Apr 24;236(4800):453-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3551073" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antigens, Protozoan ; Antigens, Surface/*immunology ; Dose-Response Relationship, Immunologic ; Immunity, Cellular ; Immunization, Passive ; Malaria/*prevention & control ; Mice ; Oligopeptides/immunology ; Plasmodium berghei/*immunology ; *Protozoan Proteins ; Recombinant Fusion Proteins/immunology ; *Vaccines, Synthetic
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  • 176
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    Construction of synthetic immunogen: use of new T-helper epitope on malaria circumsporozoite protein (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-02-27
    Description: The circumsporozoite (CS) protein of Plasmodium falciparum is the focus of intense efforts to develop an antisporozoite malaria vaccine. Localization of sites for T-cell recognition on this molecule is critical for vaccine design. By using an algorithm designed to predict T-cell sites and a large panel of H-2 congenic mice, a major nonrepetitive T-cell site was located. When a synthetic peptide corresponding to this site was covalently linked to the major B-cell site on the molecule, an immunogen capable of eliciting a high-titer antibody response was formed. This peptide sequence could prime helper T cells for a secondary response to the intact CS protein. The new helper T-cell site is located outside the repetitive region of the CS protein and appears to be the immunodominant T site on the molecule. This approach should be useful in the rational design and construction of vaccines.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Good, M F -- Maloy, W L -- Lunde, M N -- Margalit, H -- Cornette, J L -- Smith, G L -- Moss, B -- Miller, L H -- Berzofsky, J A -- New York, N.Y. -- Science. 1987 Feb 27;235(4792):1059-62.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2434994" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antibody Formation ; Antigens, Protozoan/immunology ; Antigens, Surface/*immunology ; B-Lymphocytes/immunology ; Epitopes/*immunology ; Mice ; Peptide Fragments/chemical synthesis/*immunology ; Plasmodium falciparum/*immunology ; *Protozoan Proteins ; Receptors, Antigen, B-Cell/immunology ; Receptors, Antigen, T-Cell/immunology ; T-Lymphocytes/immunology ; T-Lymphocytes, Helper-Inducer/*immunology ; Vaccines/immunology
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    Clonal gene therapy: transplanted mouse fibroblast clones express human alpha 1-antitrypsin gene in vivo (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-08-14
    Description: A retroviral vector was used to insert human alpha 1-antitrypsin (alpha 1AT) complementary DNA into the genome of mouse fibroblasts to create a clonal population of mouse fibroblasts secreting human alpha 1AT. After demonstrating that this clone of fibroblasts produced alpha 1AT after more than 100 population doublings in the absence of selection pressure, the clone was transplanted into the peritoneal cavities of nude mice. When the animals were evaluated 4 weeks later, human alpha 1AT was detected in both sera and the epithelial surface of the lungs. The transplanted clone of fibroblasts could be recovered from the peritoneal cavities of those mice and demonstrated to still be producing human alpha 1AT. Thus, even after removal of selective pressure, a single clone of retroviral vector-infected cells that expressed an exogenous gene in vitro, continued to do so in vivo, and when recovered, continued to produce the product of the exogenous gene.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Garver, R I Jr -- Chytil, A -- Courtney, M -- Crystal, R G -- New York, N.Y. -- Science. 1987 Aug 14;237(4816):762-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3497452" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Clone Cells/metabolism ; DNA/*genetics ; DNA, Recombinant ; Fibroblasts/metabolism/*transplantation ; Humans ; Lung/metabolism ; Mice ; Mice, Nude ; Peritoneal Cavity ; Retroviridae/genetics ; *Transformation, Genetic ; alpha 1-Antitrypsin/biosynthesis/*genetics
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  • 178
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    Beta 1-6 branching of Asn-linked oligosaccharides is directly associated with metastasis (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-05-01
    Description: Neoplastic transformation has been associated with a variety of structural changes in cell surface carbohydrates, most notably increased sialylation and beta 1-6-linked branching of complex-type asparagine (Asn)-linked oligosaccharides (that is, -GlcNAc beta 1-6Man alpha 1-6Man beta 1-). However, little is known about the relevant glycoproteins or how these transformation-related changes in oligosaccharide biosynthesis may affect the malignant phenotype. Here it is reported that a cell surface glycoprotein, gp 130, is a major target of increased beta 1-6-linked branching and that the expression of these oligosaccharide structures is directly related to the metastatic potential of the cells. Glycosylation mutants of a metastatic tumor cell line were selected that are deficient in both beta 1-6 GlcNAc transferase V activity and metastatic potential in situ. Moreover, induction of increased beta 1-6 branching in clones of a nonmetastatic murine mammary carcinoma correlated strongly with acquisition of metastatic potential. The results indicate that increased beta 1-6-linked branching of complex-type oligosaccharides on gp 130 may be an important feature of tumor progression related to increased metastatic potential.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dennis, J W -- Laferte, S -- Waghorne, C -- Breitman, M L -- Kerbel, R S -- R0I-CA41233/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1987 May 1;236(4801):582-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2953071" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Asparagine ; Carbohydrate Conformation ; Cell Line ; Cell Transformation, Neoplastic ; Glucosyltransferases/metabolism ; Glycosylation ; Lysosome-Associated Membrane Glycoproteins ; *Membrane Glycoproteins ; Membrane Proteins/metabolism ; Mice ; Mutation ; *N-Acetylglucosaminyltransferases ; *Neoplasm Metastasis ; Neoplasms, Experimental/genetics/metabolism ; *Oligosaccharides/biosynthesis ; Structure-Activity Relationship
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  • 179
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    Severely impaired adipsin expression in genetic and acquired obesity (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-07-24
    Description: Adipsin, a serine protease homolog, is synthesized and secreted by adipose cells and is found in the bloodstream. The expression of adipsin messenger RNA (mRNA) and protein was analyzed in rodents during metabolic perturbations and in several experimental models of obesity. Adipsin mRNA abundance is increased in adipose tissue during fasting in normal rats and in diabetes due to streptozotocin-induced insulin deficiency. Adipsin mRNA abundance decreased during the continuous infusion of glucose, which induces a hyperglycemic, hyperinsulinemic state that is accompanied by an increased adipose mass; it is suppressed (greater than 100-fold) in two strains of genetically obese mice (db/db and ob/ob), compared to their congenic counterparts, and is also reduced when obesity is induced chemically by injection of monosodium glutamate into newborn mice. Circulating adipsin protein is decreased in these animal models of obesity, as determined by immunoblotting with antisera to adipsin. Little change in adipsin expression is observed in a model of obesity obtained by pure overfeeding of normal rats (cafeteria model). These data suggest a possible role for adipsin in the above-mentioned disordered metabolic states, and raise the possibility that adipsin expression may be used to distinguish obesities that arise from certain genetic or metabolic defects from those that result from pure overfeeding.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Flier, J S -- Cook, K S -- Usher, P -- Spiegelman, B M -- AM28082/AM/NIADDK NIH HHS/ -- AM31405/AM/NIADDK NIH HHS/ -- DK34605/DK/NIDDK NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1987 Jul 24;237(4813):405-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3299706" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue/enzymology ; Animals ; Antigen-Antibody Complex ; Complement Factor D ; Endopeptidases/*genetics/metabolism ; Immune Sera ; Mice ; Mice, Obese ; Obesity/*enzymology/genetics ; RNA, Messenger/genetics ; Reference Values ; *Serine Endopeptidases ; *Transcription, Genetic
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  • 180
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    Modulation of memory processing by cholecystokinin: dependence on the vagus nerve (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-05-15
    Description: Allowing mice access to food immediately after an aversive training session enhances memory retention. Cholecystokinin-octapeptide (CCK-8), which is a gastrointestinal hormone released during feeding, also enhances memory retention when administered intraperitoneally. This memory-enhancing effect of CCK-8 is blocked when the vagus nerve is cut, indicating that CCK-8 may produce its effect on memory retention by activating ascending fibers in the vagus nerve. Thus, CCK-8, a peripherally acting peptide, may mediate the memory-enhancing effects of feeding.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Flood, J F -- Smith, G E -- Morley, J E -- New York, N.Y. -- Science. 1987 May 15;236(4803):832-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3576201" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Avoidance Learning/drug effects ; Electroshock ; Male ; Memory/*drug effects ; Mice ; Mice, Inbred Strains ; Sincalide/*pharmacology ; Vagotomy ; Vagus Nerve/drug effects/*physiology
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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
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  • 182
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    Tumor necrosis factor (cachectin) as an essential mediator in murine cerebral malaria (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-09-04
    Description: Tumor necrosis factor, or cachectin (TNF-alpha), a protein with a wide range of biological activities, is produced mainly by macrophages and may be important in inflammatory processes. The role of TNF-alpha in the pathogenesis of cerebral malaria was investigated in a murine model. Most CBA mice infected with Plasmodium berghei anka die between days 6 and 14 with acute neurological manifestations unrelated to the level of parasitemia, whereas mice of some other strains have malaria of the same severity that ends in death after 3 to 4 weeks without neurological manifestations. The activity of serum TNF-alpha was considerably increased in CBA/Ca mice with cerebral malaria but not in Plasmodium berghei-infected mice that did not develop this complication. One injection of rabbit antibody to TNF-alpha on day 4 or 7 fully protected infected mice from cerebral malaria without modifying the parasitemia, whereas immunoglobulins from normal rabbit had no effect. In mice with cerebral malaria, the cerebral vessels showed focal accumulations of packed macrophages often containing infected erythrocytes; this lesion was not seen in mice treated with antibody to TNF-alpha or in untreated mice without cerebral malaria. These findings indicate that TNF-alpha has an important role in the pathogenesis of cerebral malaria in this murine model and suggest that local accumulation and activation of macrophages may lead to the predominance of lesions in the central nervous system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grau, G E -- Fajardo, L F -- Piguet, P F -- Allet, B -- Lambert, P H -- Vassalli, P -- New York, N.Y. -- Science. 1987 Sep 4;237(4819):1210-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3306918" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain Diseases/etiology/pathology/*physiopathology ; Cerebral Cortex/pathology ; Glycoproteins/*physiology ; *Macrophage Activation ; Macrophages/cytology ; Malaria/complications/pathology/*physiopathology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred CBA ; Plasmodium berghei ; Tumor Necrosis Factor-alpha
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  • 183
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    Immunological self, nonself discrimination (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-02-20
    Description: The ability of immunodominant peptides derived from several antigen systems to compete with each other for T cell activation was studied. Only peptides restricted by a given transplantation antigen are mutually competitive. There is a correlation between haplotype restriction, ability to bind to the appropriate transplantation antigen, and ability to inhibit activation of other T cells restricted by the same transplantation antigen. An exception was noted in that a peptide derived from an antigen, bacteriophage lambda cI repressor, binds to the I-Ed molecule in a specific way, yet is not I-Ed-restricted. Comparison of the sequence of the repressor peptide with that of other peptides able to bind to (and be restricted by) I-Ed and a polymorphic region of the I-Ed molecule itself revealed a significant degree of homology. Thus, peptides restricted by a given class II molecule appear to be homologous to a portion of the class II molecule itself. The repressor-derived peptide is identical at several polymorphic residues at this site, and this may account for the failure of I-Ed to act as a restriction element. Comparison of antigenic peptide sequences with transplantation antigen sequences suggests a model that provides a basis for explaining self, nonself discrimination as well as alloreactivity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Guillet, J G -- Lai, M Z -- Briner, T J -- Buus, S -- Sette, A -- Grey, H M -- Smith, J A -- Gefter, M L -- AI13357/AI/NIAID NIH HHS/ -- AI18634/AI/NIAID NIH HHS/ -- CA28900/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1987 Feb 20;235(4791):865-70.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2433769" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens/*immunology ; Autoantigens/immunology ; *DNA-Binding Proteins ; Epitopes ; Histocompatibility Antigens Class II/*immunology ; Hybridomas ; Isoantigens/immunology ; Lymphocyte Activation ; Mice ; Micrococcal Nuclease/immunology ; Ovalbumin/immunology ; Protein Binding ; Receptors, Immunologic/*immunology ; Repressor Proteins/immunology ; T-Lymphocytes/*immunology ; T-Lymphocytes, Helper-Inducer/immunology ; Viral Proteins ; Viral Regulatory and Accessory Proteins
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  • 184
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    Recombinant interferon enhances monoclonal antibody-targeting of carcinoma lesions in vivo (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-02-20
    Description: Heterogeneity in the expression of tumor-associated antigens, as defined by the binding of monoclonal antibodies, is a characteristic common to most, if not all, human carcinoma cell populations. Antigen-negative cells within the population can escape detection and therapy by their failure to bind the appropriate antibody. Therefore, the extent of antigenic heterogeneity is an important consideration when designing protocols for the management of cancer by administration of monoclonal antibodies. One approach to counteracting the effect of antigenic heterogeneity is the use of clone A of recombinant human leukocyte interferon (Hu-IFN-alpha A). Administration of Hu-IFN-alpha A in vivo effectively increased the amount of tumor antigen expressed by a human colon xenograft in situ and augmented the localization of a radiolabeled monoclonal antibody to the tumor site. Concomitant administration of Hu-IFN-alpha A and monoclonal antibody may thus be effective in overcoming the antigenic heterogeneity of carcinoma cell populations and in enhancing the efficacy of monoclonal antibodies in the detection and treatment of carcinoma lesions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Greiner, J W -- Guadagni, F -- Noguchi, P -- Pestka, S -- Colcher, D -- Fisher, P B -- Schlom, J -- New York, N.Y. -- Science. 1987 Feb 20;235(4791):895-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3580039" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/*administration & dosage ; Antigens, Neoplasm/*immunology ; Antigens, Surface/immunology ; Carcinoma/*immunology ; Colonic Neoplasms/*immunology ; HLA Antigens/immunology ; Humans ; Interferon Type I/*administration & dosage ; Mice ; Mice, Nude ; Neoplasm Transplantation
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  • 185
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    Forskolin and phorbol esters reduce the same potassium conductance of mouse neurons in culture (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-01-16
    Description: Second messenger systems may modulate neuronal activity through protein phosphorylation. However, interactions between two major second messenger pathways, the cyclic AMP and phosphatidylinositol systems, are not well understood. The effects of activators of cyclic AMP-dependent protein kinase and protein kinase C on resting membrane properties, action potentials, and currents recorded from mouse dorsal root ganglion neurons and cerebral hemisphere neurons grown in primary dissociated cell culture were investigated. Neither forskolin (FOR) nor phorbol 12,13-dibutyrate (PDBu) altered resting membrane properties but both increased the duration of calcium-dependent action potentials in both central and peripheral neurons. By means of the single-electrode voltage clamp technique, FOR and PDBu were shown to decrease the same voltage-dependent potassium conductance. This suggests that two independent second messenger systems may affect the same potassium conductance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grega, D S -- Werz, M A -- Macdonald, R L -- NS 07231/NS/NINDS NIH HHS/ -- NS 19613/NS/NINDS NIH HHS/ -- NS 19692/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1987 Jan 16;235(4786):345-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2432663" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials/*drug effects ; Animals ; Brain/cytology ; Calcium/physiology ; Cells, Cultured ; Colforsin/*pharmacology ; Electric Conductivity ; Ganglia, Spinal/cytology ; Ion Channels/physiology ; Membrane Potentials ; Mice ; Neurons/drug effects/*physiology ; Phorbol Esters/*pharmacology ; Potassium/*physiology
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  • 186
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    Diversity of alpha-fetoprotein gene expression in mice is generated by a combination of separate enhancer elements (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-01-02
    Description: The 5' flanking region of the mouse alpha-fetoprotein (AFP) gene contains a tissue-specific promoter and three upstream regulatory elements that behave as classical enhancers. At least one of these enhancers is now shown to be required for the tissue-specific expression of the AFP gene when it is introduced into the mouse genome by microinjection of cloned DNA fragments into fertilized eggs. Each enhancer can direct expression in the appropriate tissues, the visceral endoderm of the yolk sac, the fetal liver, and the gastrointestinal tract, but each exerts different influence in these three tissues. These differences may explain the tissue-specific diversity in the levels of expression characteristic of the AFP gene. The postnatal repression of transcription of the AFP gene in both liver and gut, as well as the reinitiation of its transcription during liver regeneration, is mimicked by the introduced gene when it is linked to the enhancer domains together or singly. Thus, the DNA sequence elements responsible for directing the activation of AFP transcription, its repression, and reinduction are contained in a limited segment of DNA within or 5' to the gene (or both) and are operative in the absence of the closely linked albumin gene.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hammer, R E -- Krumlauf, R -- Camper, S A -- Brinster, R L -- Tilghman, S M -- CA06927/CA/NCI NIH HHS/ -- CA28050/CA/NCI NIH HHS/ -- HD17321/HD/NICHD NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1987 Jan 2;235(4784):53-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2432657" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cloning, Molecular ; *Enhancer Elements, Genetic ; Gene Expression Regulation ; Genes ; *Genes, Regulator ; Intestines/physiology ; Liver/physiology ; Mice ; Promoter Regions, Genetic ; RNA, Messenger/genetics ; Tissue Distribution ; Transcription, Genetic ; Transfection ; Yolk Sac/physiology ; alpha-Fetoproteins/*genetics
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  • 187
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    A transgenic mouse model for human neurofibromatosis (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-09-11
    Description: Human T-lymphotropic virus type 1 (HTLV-1) has been associated with the neurologic disorder tropical spastic paraparesis and possibly with multiple sclerosis. The tat gene of HTLV-1 under control of its own long terminal repeat is capable of inducing tumors in transgenic mice. The morphologic and biologic properties of these tumors indicate their close resemblance to human neurofibromatosis (von Recklinghausen's disease), the most common single gene disorder to affect the nervous system. The high spontaneous incidence of this disease, together with the diverse clinical and pathologic features associated with it, suggests that environmental factors may account for some of the observed cases. Multiple tumors developed simultaneously in the transgenic tat mice at approximately 3 months of age, and the phenotype was successfully passed through three generations. The tumors arise from the nerve sheaths of peripheral nerves and are composed of perineural cells and fibroblasts. Tumor cells from these mice adapt easily to propagation in culture and continue to express the tat protein in significant amounts. When transplanted into nude mice, these cultured cells efficiently induce tumors. Evidence of HTLV-1 infection in patients with neural and other soft tissue tumors is needed in order to establish a link between infection by this human retrovirus and von Recklinghausen's disease and other nonlymphoid tumors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hinrichs, S H -- Nerenberg, M -- Reynolds, R K -- Khoury, G -- Jay, G -- New York, N.Y. -- Science. 1987 Sep 11;237(4820):1340-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2888191" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Deltaretrovirus Infections/*genetics/pathology ; Disease Models, Animal ; Fluorescent Antibody Technique ; Genetic Engineering ; Humans ; Mice ; Mice, Nude ; Neurofibromatosis 1/*genetics/microbiology/pathology ; Viral Fusion Proteins/analysis
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    Antibody research garners Nobel Prize (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-10-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J L -- New York, N.Y. -- Science. 1987 Oct 23;238(4826):484-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3310235" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies/genetics ; *Antibody Diversity ; History, 20th Century ; Humans ; Japan/ethnology ; Mice ; *Nobel Prize ; United States
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  • 189
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    The molecular control of blood cell development (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-12-04
    Description: The establishment of a cell culture system for the clonal development of blood cells has made it possible to identify the proteins that regulate the growth and differentiation of different blood cell lineages and to discover the molecular basis of normal and abnormal cell development in blood forming tissues. A model system with myeloid blood cells has shown that (i) normal blood cells require different proteins to induce cell multiplication (growth inducers) and cell differentiation (differentiation inducers), (ii) there is a hierarchy of growth inducers as cells become more restricted in their developmental program, and (iii) a cascade of interactions between proteins determines the correct balance between immature and mature cells in normal blood cell development. Gene cloning has shown that there is a family of different genes for these proteins. Normal protein regulators of blood cell development can control the abnormal growth of certain types of leukemic cells and suppress malignancy by inducing differentiation to mature nondividing cells. Chromosome abnormalities that give rise to malignancy in these leukemic cells can be bypassed and their effects nullified by inducing differentiation, which stops cells from multiplying. These blood cell regulatory proteins are active in culture and in the body, and they can be used clinically to correct defects in blood cell development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sachs, L -- New York, N.Y. -- Science. 1987 Dec 4;238(4832):1374-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Weizmann Institute of Science, Rehovot, Israel.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3317831" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bone Marrow Cells ; Cell Differentiation/drug effects ; Cells, Cultured ; Clone Cells/cytology ; Colony-Stimulating Factors/physiology/therapeutic use ; *Hematopoiesis/drug effects ; Hematopoietic Stem Cells/cytology ; Humans ; Interleukin-3/physiology/therapeutic use ; Leukemia, Myeloid/drug therapy/physiopathology ; Mice ; Neoplastic Stem Cells/drug effects/pathology
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  • 190
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    The biology and chemistry of fertilization (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-01-30
    Description: Fertilization of eggs by sperm, the means by which sexual reproduction takes place in nearly all multicellular organisms, is fundamental to the maintenance of life. In both mammals and nonmammals, the pathway that leads to fusion of an egg with a single sperm consists of many steps that occur in a compulsory order. These steps include species-specific cellular recognition, intracellular and intercellular membrane fusions, and enzyme-catalyzed modifications of cellular investments. In several instances, the molecular mechanisms that underlie these events during mammalian fertilization are beginning to be revealed.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wassarman, P M -- New York, N.Y. -- Science. 1987 Jan 30;235(4788):553-60.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3027891" target="_blank"〉PubMed〈/a〉
    Keywords: Acrosome/physiology ; Animals ; *Fertilization ; Glycoproteins/physiology ; Humans ; Male ; Membrane Fusion ; Mice ; Ovum/*physiology ; Receptors, Cell Surface/physiology ; Sea Urchins ; Spermatozoa/*physiology
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  • 191
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    Early restriction of the human antibody repertoire (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-11-06
    Description: Diversification of the antibody repertoire in mammals results from a series of apparently random somatically propagated gene rearrangement and mutational events. Nevertheless, it is well known that the adult repertoire of antibody specificities is acquired in a developmentally programmed fashion. As previously shown, rearrangement of the gene segments encoding the heavy-chain variable regions (VH) of mouse antibodies is also developmentally ordered: the number of VH gene segments rearranged in B lymphocytes of fetal mice is small but increased progressively after birth. In this report, human fetal B-lineage cells were also shown to rearrange a highly restricted set of VH gene segments. In a sample of heavy-chain transcripts from a 130-day human fetus the most frequently expressed human VH element proved to be closely related to the VH element most frequently expressed in murine fetal B-lineage cells. These observations are important in understanding the development of immunocompetence.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schroeder, H W Jr -- Hillson, J L -- Perlmutter, R M -- AI07470/AI/NIAID NIH HHS/ -- GM07454/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1987 Nov 6;238(4828):791-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, University of Washington, Seattle 98195.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3118465" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Amino Acid Sequence ; Animals ; B-Lymphocytes/immunology ; Base Sequence ; Fetus ; *Genes, Immunoglobulin ; Humans ; Immunoglobulin Heavy Chains/genetics ; Immunoglobulin Variable Region/genetics ; Mice ; Molecular Sequence Data ; Mutation ; Sequence Homology, Nucleic Acid
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  • 192
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    Implantation of genetically engineered fibroblasts into mice: implications for gene therapy (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-05-08
    Description: In a variety of human genetic diseases, replacement of the absent or defective protein provides significant therapeutic benefits. As a model for a somatic cell gene therapy system, cultured murine fibroblasts were transfected with a human growth hormone (hGH) fusion gene and cells from one of the resulting clonal lines were subsequently implanted into various locations in mice. Such implants synthesized and secreted hGH, which was detectable in the serum. The function of the implants depended on their location and size, and on the histocompatibility of the donor cells with their recipients. The expression of hGH could be modified by addition of regulatory effectors, and, with appropriate immunosuppression, the implants survived for more than 3 months. This approach to gene therapy, here termed "transkaryotic implantation," is potentially applicable to many genetic diseases in that the transfected cell line can be extensively characterized prior to implantation, several anatomical sites are suitable for implantation, and regulated expression of the gene of therapeutic interest can be obtained.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Selden, R F -- Skoskiewicz, M J -- Howie, K B -- Russell, P S -- Goodman, H M -- AM-07055/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1987 May 8;236(4802):714-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3472348" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; DNA, Recombinant ; Fibroblasts/immunology/*transplantation ; *Genetic Engineering ; Graft Survival ; Growth Hormone/biosynthesis/*genetics ; Humans ; Immunosuppression ; Kidney ; Kinetics ; Mice ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Plasmids ; Therapeutics ; Transfection
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  • 193
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    The glucocorticoid receptor protein binds to transfer RNA (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-01-23
    Description: The glucocorticoid receptor from mouse AtT-20 cells exists in three forms: the untransformed receptor (9.1S; Mr of 319,000), a large oligomeric molecule that does not bind to DNA; the transformed receptor (4S; Mr of 96,000), which is formed by dissociation of untransformed receptor after steroid binding and which binds to DNA to modulate gene expression; and an intermediate size receptor (6S; Mr of 132,000), which also binds to DNA and contains a bound small RNA molecule. This RNA species has now been purified and identified as transfer RNA (tRNA). The three tRNA's for the basic amino acids accounted for about 78% of the total amino acid-accepting activity [arginine (52%), lysine (17%), and histidine (9%)], while the remaining 22% was represented by six other tRNA species. This tRNA-binding activity of the glucocorticoid receptor may reflect post-transcriptional mechanisms of regulating gene expression, such as alterations in the translational efficiency of or the modulation of the stability of hormone-induced proteins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ali, M -- Vedeckis, W V -- AM-36086/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1987 Jan 23;235(4787):467-70.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3798121" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; DNA-Binding Proteins/metabolism ; Gene Expression Regulation ; Mice ; Molecular Weight ; RNA, Transfer/classification/*metabolism ; Receptors, Glucocorticoid/*metabolism
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  • 194
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    Adrenal medulla grafts enhance recovery of striatal dopaminergic fibers (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-08-21
    Description: The drug, 1-methyl-4-phenyl-1,2,5,6-tetrahydropyridine (MPTP), depletes striatal dopamine levels in primates and certain rodents, including mice, and produces parkinsonian-like symptoms in humans and nonhuman primates. To investigate the consequences of grafting adrenal medullary tissue into the brain of a rodent model of Parkinson's disease, a piece of adult mouse adrenal medulla was grafted unilaterally into mouse striatum 1 week after MPTP treatment. This MPTP treatment resulted in the virtual disappearance of tyrosine hydroxylase-immunoreactive fibers and severely depleted striatal dopamine levels. At 2, 4, and 6 weeks after grafting, dense tyrosine hydroxylase-immunoreactive fibers were observed in the grafted striatum, while only sparse fibers were seen in the contralateral striatum. In all cases, tyrosine hydroxylase-immunoreactive fibers appeared to be from the host rather than from the grafts, which survived poorly. These observations suggest that, in mice, adrenal medullary grafts exert a neurotrophic action in the host brain to enhance recovery of dopaminergic neurons. This effect may be relevant to the symptomatic recovery in Parkinson's disease patients who have received adrenal medullary grafts.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bohn, M C -- Cupit, L -- Marciano, F -- Gash, D M -- NS00910/NS/NINDS NIH HHS/ -- NS15109/NS/NINDS NIH HHS/ -- NS20832/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1987 Aug 21;237(4817):913-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2887034" target="_blank"〉PubMed〈/a〉
    Keywords: 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine ; Adrenal Medulla/*transplantation ; Animals ; Corpus Striatum/*physiology ; Dopamine/*physiology ; Fluorescent Antibody Technique ; Mice ; Neurons/drug effects ; Phenylethanolamine N-Methyltransferase/metabolism ; Pyridines/pharmacology ; Substantia Nigra/physiology ; Tyrosine 3-Monooxygenase/metabolism
    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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  • 195
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    Solo actions of AIDS virus coat (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-08-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barnes, D M -- New York, N.Y. -- Science. 1987 Aug 28;237(4818):971-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3039663" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/microbiology ; Animals ; Chick Embryo ; HIV/*physiology ; HIV Envelope Protein gp120 ; Humans ; Mice ; Neurons/microbiology ; Retroviridae Proteins/physiology ; Viral Envelope Proteins/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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  • 196
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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
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 197
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    Glucocorticoid receptor-like antigen in lymphoma cell membranes: correlation to cell lysis (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-04-24
    Description: S-49 mouse lymphoma cells undergo lysis when treated with glucocorticoids; the mechanism of this effect is not understood. A protein was detected in the plasma membrane of these cells by means of direct immunofluorescent labeling with a monoclonal antibody to the soluble glucocorticoid receptor. Cellular heterogeneity in the content of this glucocorticoid receptor-like molecule was evident. By immunoadsorption to antibody-coated tissue culture plates, the cells were separated into populations positive (100%) and depleted (38%) for this membrane antigen. Gel electrophoresis, specific immunoblot, and autoradiographic (binding of [3H]dexamethasone mesylate) analysis of the membrane proteins from the membrane antigen-positive group revealed multiple protein bands ranging in size from 85 to 145 kilodaltons. Furthermore, comparison of the glucocorticoid sensitivity of these groups of cells showed complete lysis of the membrane antigen-positive cells and only partial lysis of the antigen-deficient group, which suggests that the lysis response of cells to glucocorticoids is mediated by a glucocorticoid receptor-like molecule located in the plasma membrane.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gametchu, B -- CA17701/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1987 Apr 24;236(4800):456-61.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3563523" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Neoplasm/*analysis ; Antigens, Surface/*analysis ; Cell Line ; Cell Membrane/immunology/metabolism ; Cell Nucleus/metabolism ; Cell Survival/drug effects ; Cytoplasm/metabolism ; Dexamethasone/metabolism/pharmacology ; Lymphoma/*immunology ; Mice ; Molecular Weight ; Receptors, Glucocorticoid/*immunology/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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  • 198
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    A chicken transferrin gene in transgenic mice escapes X-chromosome inactivation (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-05-01
    Description: Mammalian X-chromosome inactivation involves a coordinate shutting down of physically linked genes. Several proposed models require the presence of specific sequences near genes to permit the spread of inactivation into these regions. If such models are correct, one might predict that heterologous genes transferred onto the X chromosome might lack the appropriate signal sequences and therefore escape inactivation. To determine whether a foreign gene inserted into the X chromosome is subject to inactivation, transgenic mice harboring 11 copies of the complete, 17-kilobase chicken transferrin gene on the X chromosome were used. Male mice hemizygous for this insert were bred with females bearing Searle's translocation, an X-chromosome rearrangement that is always active in heterozygous females (the unrearranged X chromosome is inactive). Female offspring bearing the Searle's translocation and the chicken transferrin gene had the same amount of chicken transferrin messenger RNA in liver as did transgenic male mice or transgenic female mice lacking the Searle's chromosome. This result shows that the inserted gene is not subject to X-chromosome inactivation and suggests that the inactivation process cannot spread over 187 kilobases of DNA in the absence of specific signal sequences required for inactivation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Goldman, M A -- Stokes, K R -- Idzerda, R L -- McKnight, G S -- Hammer, R E -- Brinster, R L -- Gartler, S M -- HD14412/HD/NICHD NIH HHS/ -- HD16659/HD/NICHD NIH HHS/ -- HD17321/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1987 May 1;236(4801):593-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2437652" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chickens ; DNA/metabolism ; *Dosage Compensation, Genetic ; Female ; Male ; Methylation ; Mice ; Transferrin/*genetics ; *Transformation, Genetic ; Translocation, Genetic ; X Chromosome ; Y Chromosome ; alpha-Fetoproteins/genetics
    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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    In situ detection of beta-galactosidase in lenses of transgenic mice with a gamma-crystallin/lacZ gene (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-01-23
    Description: Transgenic mice carrying the gamma 2-crystallin promoter fused to the coding region of the bacterial lacZ gene were generated. The offspring of three founder mice expressed high levels of the enzyme solely in the central nuclear fiber cells of the lens as measured by an in situ assay for the detection of beta-galactosidase activity. These results suggest that gamma 2-crystallin sequences between -759 to +45 contain essential information required for appropriate tissue-specific and temporal regulation of the mouse gamma 2-crystallin gene. In a broader context, this study also demonstrates the utility of beta-galactosidase hybrid gene constructs for monitoring the activity of gene regulatory elements in transgenic mice.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Goring, D R -- Rossant, J -- Clapoff, S -- Breitman, M L -- Tsui, L C -- New York, N.Y. -- Science. 1987 Jan 23;235(4787):456-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3099390" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cataract/enzymology ; Crystallins/*genetics ; Galactosidases/*genetics ; Gene Expression Regulation ; *Lac Operon ; Lens, Crystalline/*physiology ; Mice ; Promoter Regions, Genetic ; Recombinant Fusion Proteins/*genetics ; Recombinant Proteins/*genetics ; Tissue Distribution ; Transfection ; beta-Galactosidase/*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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  • 200
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    YIGSR, a synthetic laminin pentapeptide, inhibits experimental metastasis formation (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-11-20
    Description: The invasion of tumor cells through basement membranes is a critical step in the formation of metastases. The binding of the malignant cells to laminin in the basement membranes allows their attachment and activates their invasiveness. Recently a synthetic nonapeptide from the B1 chain sequence of laminin was identified as a major site for cell binding. A pentapeptide within the nonapeptide sequence was found to reduce the formation of lung colonies in mice injected with melanoma cells and also to inhibit the invasiveness of the cells in vitro.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Iwamoto, Y -- Robey, F A -- Graf, J -- Sasaki, M -- Kleinman, H K -- Yamada, Y -- Martin, G R -- New York, N.Y. -- Science. 1987 Nov 20;238(4830):1132-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Developmental Biology and Anomalies, National Institute of Drug Research, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2961059" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Basement Membrane/physiopathology ; Binding Sites ; Cell Adhesion/*drug effects ; *Laminin ; Lung Neoplasms/secondary ; Melanoma, Experimental/pathology/physiopathology ; Mice ; Neoplasm Metastasis/*prevention & control ; Oligopeptides/*chemical synthesis/pharmacology ; Receptors, Immunologic/*drug effects ; Receptors, Laminin ; Structure-Activity Relationship
    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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