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  • Articles  (196)
  • Mice  (99)
  • Rats  (73)
  • Fisheries
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  • 1995-1999
  • 1990-1994  (196)
  • 1950-1954
  • 1990  (196)
  • Physics  (196)
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  • Articles  (196)
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  • 1995-1999
  • 1990-1994  (196)
  • 1950-1954
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  • 1
    Electronic Resource
    Electronic Resource
    Studies on organ weights in naproxen treated rats after intermittent exposure to simulated high altitude (1990)
    Springer
    International journal of biometeorology 34 (1990), S. 90-92 
    Details
    ISSN: 1432-1254
    Keywords: Rats ; Naproxen ; Hypoxia ; Organ weight
    Source: Springer Online Journal Archives 1860-2000
    Topics: Geography , Physics
    Notes: Abstract Rats were exposed intermittently for 8h per day over 6 days at simulated high altitude of 20 000 feet. One group of altitude-exposed animals was treated with naproxen, a prostaglandin inhibiting drug. Significant reduction in body weight gain was observed in both altitude-exposed and drug-treated altitude-exposed animals compared to the control group. Right and left ventricular weights and weights of the adrenal glands were increased significantly in altitude-exposed and altitude-exposed drug-treated animals. The weight of the spleen was increased significantly in altitude-exposed animals whereas no such increase of splenic weight was observed in drug-treated altitude-exposed group of animals. On the other hand, the weight of the liver was decreased significantly in both cases. In drug-treated altitude-exposed animals, the unaltered splenic weight was thought to be due to inhibition of the erythropoietic activity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01093453
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  • 2
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    A cytosolic protein catalyzes the release of GDP from p21ras (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-04-06
    Description: The rate of release of guanine nucleotides from the ras proteins (Ras) is extremely slow in the presence of Mg2+. It seemed likely, therefore that a factor might exist to accelerate the release of guanosine diphosphate (GDP), and hence the exchange of GDP for guanosine triphosphate (GTP). Such a factor has now been discovered in rat brain cytosol. Brain cytosol was found to catalyze, by orders of magnitude, the release of guanine nucleotides from recombinant v-H-Ras protein bound with [alpha-32P]GDP. This effect occurred even in the presence of a large excess of Mg2+, but was destroyed by heat or by incubation of the cytosol for an hour at 37 degrees C in the absence of phosphatase inhibitors. The effect was observed with either v-H-Ras or c-H-Ras, but not with p25rab3A, a small G protein with about 30% similarity to Ras. The effect could not be mimicked by addition of recombinant Ras-GAP or purified GEF, a guanine nucleotide exchange factor involved in the regulation of eukaryotic protein synthesis. By gel filtration chromatography, the factor appears to possess a molecular size between 100,000 and 160,000 daltons. This protein (Ras-guanine nucleotide-releasing factor, or Ras-GRF) may be involved in the activation of p21ras.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wolfman, A -- Macara, I G -- CA 43551/CA/NCI NIH HHS/ -- ES 01247/ES/NIEHS NIH HHS/ -- GM 41220/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1990 Apr 6;248(4951):67-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biophysics, University of Rochester Medical Center, NY 14642.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2181667" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding, Competitive ; Brain/metabolism ; Cholic Acids ; Cytosol/*metabolism ; Guanine Nucleotides/*metabolism ; Guanosine 5'-O-(3-Thiotriphosphate) ; Guanosine Diphosphate/*metabolism ; Guanosine Triphosphate/analogs & derivatives/metabolism ; Hot Temperature ; Immunosorbent Techniques ; Kinetics ; Magnesium Chloride/pharmacology ; Molecular Weight ; Proto-Oncogene Proteins/*metabolism ; Proto-Oncogene Proteins p21(ras) ; Rats ; Thionucleotides/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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  • 3
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    New transplant method evades immune attack (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-09-14
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Skerrett, P J -- New York, N.Y. -- Science. 1990 Sep 14;249(4974):1248.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2119053" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Diabetes Mellitus, Experimental/*surgery ; Graft Enhancement, Immunologic ; Immune Tolerance ; *Islets of Langerhans Transplantation ; Rats ; T-Lymphocytes/immunology ; Thymus Gland/surgery ; Transplantation, Heterotopic
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    Induction of cellular senescence in immortalized cells by human chromosome 1 (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-02-09
    Description: The control of cellular senescence by specific human chromosomes was examined in interspecies cell hybrids between diploid human fibroblasts and an immortal, Syrian hamster cell line. Most such hybrids exhibited a limited life span comparable to that of the human fibroblasts, indicating that cellular senescence is dominant in these hybrids. Karyotypic analyses of the hybrid clones that did not senesce revealed that all these clones had lost both copies of human chromosome 1, whereas all other human chromosomes were observed in at least some of the immortal hybrids. The application of selective pressure for retention of human chromosome 1 to the cell hybrids resulted in an increased percentage of hybrids that senesced. Further, the introduction of a single copy of human chromosome 1 to the hamster cells by microcell fusion caused typical signs of cellular senescence. Transfer of chromosome 11 had no effect on the growth of the cells. These findings indicate that human chromosome 1 may participate in the control of cellular senescence and further support a genetic basis for cellular senescence.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sugawara, O -- Oshimura, M -- Koi, M -- Annab, L A -- Barrett, J C -- New York, N.Y. -- Science. 1990 Feb 9;247(4943):707-10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2300822" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cell Survival/*genetics ; Chromosome Mapping ; *Chromosomes, Human, Pair 1 ; Clone Cells ; Cricetinae ; Diploidy ; Fibroblasts/*cytology ; Humans ; Hybrid Cells/*cytology ; Hypoxanthine Phosphoribosyltransferase/genetics ; Karyotyping ; Mice ; Ploidies ; Transfection ; Translocation, Genetic ; X Chromosome
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    Female primatologists confer--without men (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-09-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dusheck, J -- New York, N.Y. -- Science. 1990 Sep 28;249(4976):1494-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2218487" target="_blank"〉PubMed〈/a〉
    Keywords: *Biological Evolution ; Congresses as Topic ; Female ; Humans ; Male ; Men ; United States ; *Women
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    T cell reactivity to MHC molecules: immunity versus tolerance (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-06-15
    Description: The specificity of mature CD8+ and CD4+ T lymphocytes is controlled by major histocompatibility complex (MHC) class I and class II molecules, respectively. The MHC class specificity of T cells is stringent in many assays, but is less evident when cells are supplemented with exogenous lymphokines. The repertoire of T cells is shaped through contact with MHC molecules in the thymus and involves a complex process of positive selection and negative selection (tolerance). Tolerance of immature T cells to MHC molecules can reflect either clonal deletion or anergy and results from intrathymic contact with several cell types, including epithelial cells and cells with antigen-presenting function. Unlike immature T cells, mature T cells are relatively resistant to tolerance induction. In certain situations partial unresponsiveness of mature T cells can be achieved by exposing T cells to foreign MHC molecules expressed on atypical antigen-presenting cells. Tolerance is rarely complete, however, and the precise requirements for tolerizing mature T cells are still unclear.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sprent, J -- Gao, E K -- Webb, S R -- AI21487/AI/NIAID NIH HHS/ -- CA25803/CA/NCI NIH HHS/ -- CA38355/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1990 Jun 15;248(4961):1357-63.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Research Institute of Scripps Clinic, La Jolla, CA 92037.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1694041" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen-Presenting Cells/immunology ; Bone Marrow/immunology ; CD4-Positive T-Lymphocytes/immunology ; Clone Cells/immunology ; Epitopes/immunology ; Histocompatibility Antigens/*immunology ; Histocompatibility Antigens Class II/immunology ; *Immune Tolerance ; *Immunity ; Interleukin-2/physiology ; Mice ; Mice, Transgenic ; Receptors, Antigen, T-Cell/immunology ; T-Lymphocytes/*immunology ; T-Lymphocytes, Regulatory/immunology ; Thymus Gland/immunology
    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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  • 7
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    Posttranslational glutamylation of alpha-tubulin (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-01-05
    Description: The high degree of tubulin heterogeneity in neurons is controlled mainly at the posttranslational level. Several variants of alpha-tubulin can be posttranslationally labeled after incubation of cells with [3H]acetate or [3H]glutamate. Peptides carrying the radioactive moiety were purified by high-performance liquid chromatography. Amino acid analysis, Edman degradation sequencing, and mass spectrometric analysis of these peptides led to the characterization of a posttranslational modification consisting of the successive addition of glutamyl units on the gamma-carboxyl group of a glutamate residue (Glu445). This modification, localized within a region of alpha-tubulin that is important in the interactions of tubulin with microtubule-associated proteins and calcium, could play a role in regulating microtubule dynamics.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Edde, B -- Rossier, J -- Le Caer, J P -- Desbruyeres, E -- Gros, F -- Denoulet, P -- New York, N.Y. -- Science. 1990 Jan 5;247(4938):83-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratoire de Biochimie Cellulaire, College de France, Paris.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1967194" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acids/analysis ; Animals ; Brain/*metabolism ; Chromatography, High Pressure Liquid ; Glutamates/*metabolism ; Glutamic Acid ; Mass Spectrometry ; Mice ; Neurons/*metabolism ; Peptide Fragments/analysis ; *Protein Processing, Post-Translational ; Tubulin/*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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  • 8
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    Clonal deletion versus clonal anergy: the role of the thymus in inducing self tolerance (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-06-15
    Description: During development in the thymus, T cells are rendered tolerant to self antigens. It is now apparent that thymocytes bearing self-reactive T cell receptors can be tolerized by processes that result in physical elimination (clonal deletion) or functional inactivation (clonal anergy). As these mechanisms have important clinical implications for transplantation and autoimmunity, current investigations are focused on understanding the cellular and molecular interactions that generate these forms of tolerance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ramsdell, F -- Fowlkes, B J -- New York, N.Y. -- Science. 1990 Jun 15;248(4961):1342-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Cellular and Molecular Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1972593" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Surface/immunology ; Autoantigens/immunology ; Autoimmunity/immunology ; Bone Marrow/immunology ; CD4-Positive T-Lymphocytes/immunology ; Chickens ; Chimera ; Clone Cells/*immunology ; H-2 Antigens/immunology ; Histocompatibility Antigens/immunology ; Histocompatibility Antigens Class II/immunology ; *Immune Tolerance ; Mice ; Mice, Transgenic ; Minor Lymphocyte Stimulatory Antigens ; Receptors, Antigen, T-Cell/*immunology ; T-Lymphocytes/*immunology ; T-Lymphocytes, Regulatory/immunology ; Thymus Gland/*immunology ; Xenopus
    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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  • 9
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    The dominant W42 spotting phenotype results from a missense mutation in the c-kit receptor kinase (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-01-12
    Description: The murine white spotting locus (W) is allelic with the proto-oncogene c-kit, which encodes a transmembrane tyrosine protein kinase receptor for an unknown ligand. Mutations at the W locus affect various aspects of hematopoiesis and the proliferation and migration of primordial germ cells and melanoblasts during development to varying degrees of severity. The W42 mutation has a particularly severe effect in both the homozygous and the heterozygous states. The molecular basis of the W42 mutation was determined. The c-kit protein products in homozygous mutant mast cells were expressed normally but displayed a defective tyrosine kinase activity in vitro. Nucleotide sequence analysis of mutant complementary DNAs revealed a missense mutation that replaces aspartic acid with asparagine at position 790 in the c-kit protein product. Aspartic acid-790 is a conserved residue in all protein kinases. These results provide an explanation for the dominant nature of the W42 mutation and provide insight into the mechanism of c-kit-mediated signal transduction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tan, J C -- Nocka, K -- Ray, P -- Traktman, P -- Besmer, P -- P01-CA-16599/CA/NCI NIH HHS/ -- R01-CA-32926/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1990 Jan 12;247(4939):209-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Biology Program, Sloan Kettering Institute, New York, NY 10021.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1688471" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cells, Cultured ; DNA/genetics ; Gene Expression ; Homozygote ; Liver/analysis/cytology/embryology ; Mast Cells/metabolism ; Mice ; Molecular Sequence Data ; *Mutation ; *Phenotype ; Polymerase Chain Reaction ; Protein-Tyrosine Kinases/*genetics ; Proto-Oncogene Proteins/*genetics ; Proto-Oncogene Proteins c-kit ; RNA/analysis ; Receptors, Cell Surface/genetics ; Signal Transduction
    Print ISSN: 0036-8075
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  • 10
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    Use of prior vaccinations for the development of new vaccines (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-07-27
    Description: There is currently a need for vaccine development to improve the immunogenicity of protective epitopes, which themselves are often poorly immunogenic. Although the immunogenicity of these epitopes can be enhanced by linking them to highly immunogenic carriers, such carriers derived from current vaccines have not proven to be generally effective. One reason may be related to epitope-specific suppression, in which prior vaccination with a protein can inhibit the antibody response to new epitopes linked to the protein. To circumvent such inhibition, a peptide from tetanus toxoid was identified that, when linked to a B cell epitope and injected into tetanus toxoid-primed recipients, retained sequences for carrier but not suppressor function. The antibody response to the B cell epitope was enhanced. This may be a general method for taking advantage of previous vaccinations in the development of new vaccines.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Etlinger, H M -- Gillessen, D -- Lahm, H W -- Matile, H -- Schonfeld, H J -- Trzeciak, A -- New York, N.Y. -- Science. 1990 Jul 27;249(4967):423-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Central Research Unit F. Hoffmann-La Roche, Basel, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1696030" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antigens, Protozoan/*immunology ; B-Lymphocytes/immunology ; Epitopes/*immunology ; Humans ; Mice ; Mice, Inbred BALB C ; Molecular Sequence Data ; Peptide Fragments/immunology ; Plasmodium falciparum/*immunology ; T-Lymphocytes/immunology ; T-Lymphocytes, Helper-Inducer/immunology ; T-Lymphocytes, Regulatory/immunology ; Tetanus Toxoid/*immunology ; *Vaccination ; Vaccines/*immunology
    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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  • 11
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    Acceleration of diabetes in young NOD mice with a CD4+ islet-specific T cell clone (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-09-21
    Description: Nonobese diabetic (NOD) mice develop an autoimmune form of diabetes, becoming hyperglycemic after 3 months of age. This process was accelerated by injecting young NOD mice with CD4+ islet-specific T cell clones derived from NOD mice. Overt diabetes developed in 10 of 19 experimental animals by 7 weeks of age, with the remaining mice showing marked signs of the disease in progress. Control mice did not become diabetic and had no significant pancreatic infiltration. This work demonstrates that a CD4 T cell clone is sufficient to initiate the disease process in the diabetes-prone NOD mouse.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Haskins, K -- McDuffie, M -- P01 DK40144/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1990 Sep 21;249(4975):1433-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Barbara Davis Center for Childhood Diabetes, University of Colorado Health Sciences Center, Denver 80262.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2205920" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD4/analysis/*immunology ; Clone Cells ; Diabetes Mellitus, Experimental/*immunology/pathology ; Female ; Islets of Langerhans/*immunology/pathology ; Male ; Mice ; Mice, Inbred Strains ; Mice, Mutant Strains ; T-Lymphocytes/*immunology/transplantation
    Print ISSN: 0036-8075
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  • 12
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    Autophosphorylation of protein kinase C at three separated regions of its primary sequence (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-07-27
    Description: The major autophosphorylation sites of the rat beta II isozyme of protein kinase C were identified. The modified threonine and serine residues were found in the amino-terminal peptide, the carboxyl-terminal tail, and the hinge region between the regulatory lipid-binding domain and the catalytic kinase domain. Because this autophosphorylation follows an intrapeptide mechanism, extraordinary flexibility of the protein is necessary to phosphorylate the three regions. Comparison of the sequences surrounding the modified residues showed no obvious recognition motif nor any similarity to substrate phosphorylation sites, suggesting that proximity to the active site may be the primary criterion for their phosphorylation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Flint, A J -- Paladini, R D -- Koshland, D E Jr -- DK09765/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1990 Jul 27;249(4967):408-11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Biology, University of California, Berkeley 94720.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2377895" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Binding Sites ; Brain/enzymology ; Cloning, Molecular ; Isoenzymes/genetics/*metabolism ; Molecular Sequence Data ; Peptide Fragments/isolation & purification/metabolism ; Phosphorylation ; Protein Conformation ; Protein Kinase C/genetics/*metabolism ; Rats ; Recombinant Proteins/metabolism ; Signal Transduction ; Trypsin
    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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  • 13
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    Dominant negative regulation of the mouse alpha-fetoprotein gene in adult liver (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-12-21
    Description: Transcription of the mouse alpha-fetoprotein gene is activated in the developing fetal liver and gut and repressed in both tissues shortly after birth. With germline transformation in mice, a cis-acting element was identified upstream of the transcription initiation site of the alpha-fetoprotein gene that was responsible for repression of the gene in adult liver. This negative element acts as a repressor in a position-dependent manner.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vacher, J -- Tilghman, S M -- CA44976/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1990 Dec 21;250(4988):1732-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Biology, Princeton University, NJ 08544.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1702902" target="_blank"〉PubMed〈/a〉
    Keywords: Aging ; Animals ; Animals, Newborn ; Chromosome Deletion ; Cloning, Molecular ; DNA-Binding Proteins/metabolism ; Enhancer Elements, Genetic ; Fetus ; *Gene Expression Regulation ; Hepatocyte Nuclear Factor 1 ; Hepatocyte Nuclear Factor 1-alpha ; Hepatocyte Nuclear Factor 1-beta ; Liver/growth & development/*metabolism ; Mice ; *Nuclear Proteins ; Transcription Factors/metabolism ; Transcription, Genetic ; alpha-Fetoproteins/*genetics
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 14
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    "Superantigens" may shed light on immune puzzle (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-05-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hoffman, M -- New York, N.Y. -- Science. 1990 May 11;248(4956):685-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2333520" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Bacterial/*immunology ; Antigens, Viral/immunology ; Bacterial Toxins/*immunology ; Humans ; Immune System/*physiology ; Lymphocytes/*immunology ; Mice ; T-Lymphocytes/immunology
    Print ISSN: 0036-8075
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  • 15
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    RAG-1 and RAG-2, adjacent genes that synergistically activate V(D)J recombination (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-06-22
    Description: The vast repertoire of immunoglobulins and T cell receptors is generated, in part, by V(D)J recombination, a series of genomic rearrangements that occur specifically in developing lymphocytes. The recombination activating gene, RAG-1, which is a gene expressed exclusively in maturing lymphoid cells, was previously isolated. RAG-1 inefficiently induced V(D)J recombinase activity when transfected into fibroblasts, but cotransfection with an adjacent gene, RAG-2, has resulted in at least a 1000-fold increase in the frequency of recombination. The 2.1-kilobase RAG-2 complementary DNA encodes a putative protein of 527 amino acids whose sequence is unrelated to that of RAG-1. Like RAG-1, RAG-2 is conserved between species that carry out V(D)J recombination, and its expression pattern correlates precisely with that of V(D)J recombinase activity. In addition to being located just 8 kilobases apart, these convergently transcribed genes are unusual in that most, if not all, of their coding and 3' untranslated sequences are contained in single exons. RAG-1 and RAG-2 might activate the expression of the V(D)J recombinase but, more likely, they directly participate in the recombination reaction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Oettinger, M A -- Schatz, D G -- Gorka, C -- Baltimore, D -- GM39458/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1990 Jun 22;248(4962):1517-23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research, Cambridge, MA 02142.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2360047" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Biological Evolution ; Cattle ; Cell Line ; Chickens ; Cricetinae ; DNA/*genetics ; DNA Nucleotidyltransferases/*genetics ; *DNA-Binding Proteins ; Dogs ; Female ; *Gene Rearrangement, B-Lymphocyte ; *Gene Rearrangement, T-Lymphocyte ; *Homeodomain Proteins ; Humans ; Male ; Mice ; Molecular Sequence Data ; *Multigene Family ; Nuclear Proteins ; Nucleic Acid Hybridization ; Opossums ; Proteins/*genetics ; Rabbits ; Recombination, Genetic/*genetics ; Restriction Mapping ; Transfection ; Turtles ; VDJ Recombinases
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  • 16
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    Presentation of exogenous antigen with class I major histocompatibility complex molecules (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-08-24
    Description: Soluble antigens (Ags) in the extracellular fluids are excluded from the class I major histocompatibility complex (MHC)-restricted pathway of Ag presentation in most cells. However, an exogenous Ag can be internalized, processed, and presented in association with class I MHC molecules on specialized Ag-presenting cells (APCs). These APCs express class II molecules and can simultaneously present exogenous Ags to both class I and class II MHC-restricted T cells. These APCs may be important participants in the regulation of host immune responses. This APC activity may explain several phenomena of cytotoxic T lymphocyte (CTL) priming in vivo and might be exploited for eliciting CTL responses to protein vaccines.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rock, K L -- Gamble, S -- Rothstein, L -- AI-20248/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1990 Aug 24;249(4971):918-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Harvard Medical School, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2392683" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen-Presenting Cells/*immunology ; Azides/pharmacology ; Cell Line ; Histocompatibility Antigens Class I/*immunology ; Histocompatibility Antigens Class II/immunology ; Mice ; Mice, Inbred C57BL ; Ovalbumin/*immunology ; Spleen/immunology ; T-Lymphocytes/drug effects/immunology ; T-Lymphocytes, Cytotoxic/immunology
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  • 17
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    Genetic differences in the ethanol sensitivity of GABAA receptors expressed in Xenopus oocytes (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-07-20
    Description: Animal lines selected for differences in drug sensitivity can be used to help determine the molecular basis of drug action. Long-sleep (LS) and short-sleep (SS) mice differ markedly in their genetic sensitivity to ethanol. To investigate the molecular basis for this difference, mRNA from brains of LS and SS mice was expressed in Xenopus oocytes and the ethanol sensitivity of gamma-aminobutyric acid A (GABAA)- and N-methyl D-aspartate (NMDA)-activated ion channels was tested. Ethanol facilitated GABA responses in oocytes injected with mRNA from LS mice but antagonized responses in oocytes injected with mRNA from SS animals. Ethanol inhibited NMDA responses equally in the two lines. Thus, genes coding for the GABAA receptor or associated proteins may be critical determinants of individual differences in ethanol sensitivity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wafford, K A -- Burnett, D M -- Dunwiddie, T V -- Harris, R A -- AA03527/AA/NIAAA NIH HHS/ -- AA06399/AA/NIAAA NIH HHS/ -- New York, N.Y. -- Science. 1990 Jul 20;249(4966):291-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of Colorado Health Sciences Center, Denver.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1695761" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aspartic Acid/analogs & derivatives/pharmacology ; Brain/*metabolism ; Chloride Channels ; Chlorides/*physiology ; Diazepam/pharmacology ; Ethanol/*pharmacology ; Female ; Ion Channels/drug effects/physiology ; Membrane Proteins/*physiology ; Mice ; Mice, Inbred Strains ; Microinjections ; N-Methylaspartate ; Oocytes/*drug effects/*physiology ; RNA, Messenger/administration & dosage/genetics ; Receptors, GABA-A/drug effects/*genetics ; Xenopus ; gamma-Aminobutyric Acid/pharmacology
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  • 18
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    Defective presentation of endogenous antigen by a cell line expressing class I molecules (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-04-20
    Description: Cytotoxic T lymphocytes (CTLs) recognize class I major histocompatibility complex (MHC) molecules associated with antigenic peptides derived from endogenously synthesized proteins. Binding to such peptides is a requirement for class I assembly in the endoplasmic reticulum (ER). A mutant human cell line, T2, assembles and transports to its surface some, but not all, class I MHC molecules. The class I molecules expressed on the surface of T2 do not present peptides derived from cytosolic antigens, although they can present exogenously added peptides to CTL. The transported class I molecules may interact weakly with an unknown retaining factor in the ER such that they can assemble despite the relative shortage of peptides.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hosken, N A -- Bevan, M J -- AI-19335/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1990 Apr 20;248(4953):367-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Research Institute of Scripps Clinic, La Jolla, CA 92037.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2326647" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen-Presenting Cells/*immunology ; Antigens/immunology ; Antigens, Viral/immunology ; B-Lymphocytes/immunology ; Capsid/immunology ; Cell Line ; Endoplasmic Reticulum/immunology ; Gene Expression ; H-2 Antigens/genetics/immunology ; HLA Antigens/genetics ; Histocompatibility Antigens Class I/*immunology ; Histocompatibility Antigens Class II/genetics ; Humans ; Mice ; Mutation ; Ovalbumin/immunology ; Peptides/immunology ; T-Lymphocytes, Cytotoxic/immunology ; Transfection ; Tumor Cells, Cultured ; Viral Core Proteins/immunology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 19
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    Expression of interleukin-10 activity by Epstein-Barr virus protein BCRF1 (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-11-09
    Description: Cytokine synthesis inhibitory factor (CSIF; interleukin-10), a product of mouse TH2 T cell clones that inhibits synthesis of cytokines by mouse TH1 T cell clones, exhibits extensive sequence similarity to an uncharacterized open reading frame in the Epstein-Barr virus BCRF1. Recombinant BCRF1 protein mimics the activity of interleukin-10, suggesting that BCRF1 may have a role in the interaction of the virus with the host's immune system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hsu, D H -- de Waal Malefyt, R -- Fiorentino, D F -- Dang, M N -- Vieira, P -- de Vries, J -- Spits, H -- Mosmann, T R -- Moore, K W -- New York, N.Y. -- Science. 1990 Nov 9;250(4982):830-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, DNAX Research Institute, Palo Alto, CA 94304.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2173142" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; DNA, Viral/genetics ; Electrophoresis, Polyacrylamide Gel ; *Gene Expression Regulation, Viral ; Herpesvirus 4, Human/genetics/*immunology ; Humans ; Interleukin-10 ; Interleukins/*biosynthesis ; Killer Cells, Natural/immunology ; Mice ; Radioimmunoprecipitation Assay ; T-Lymphocytes/immunology ; Viral Proteins/genetics/*immunology
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  • 20
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    Expanded HIV-1 cellular tropism by phenotypic mixing with murine endogenous retroviruses (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-02-16
    Description: In view of the current interest in in vivo murine models for acquired immunodeficiency syndrome (AIDS), the interaction between human immunodeficiency virus type 1 (HIV-1) and endogenous murine leukemia virus (MuLV)-related retroviruses was investigated with a human leukemic T cell line (PF-382x) that acquired xenotropic MuLV (X-MuLV) after in vivo passage in immunosuppressed mice. Despite similar levels of membrane CD4 expression and HIV-1 125I-labeled gp 120 binding, a dramatic acceleration in the time course of HIV-1 infection was observed in PF-382x compared to its X-MuLV-negative counterpart (PF-382). Moreover, PF-382 cells coinfected by X-MuLV and HIV-1 generated a progeny of phenotypically mixed viral particles, enabling HIV-1 to productively infect a panel of CD4- human cells, including B lymphoid cells and purified normal peripheral blood CD4-/CD8+ T lymphocytes. Mixed viral phenotypes were also produced by human CD4+ T cells coinfected with an amphotropic MuLV-related retrovirus (A-MuLV) and HIV-1. These data show that endogenous MuLV acquired by human cells transplanted into mice can significantly interact with HIV-1, thereby inducing important alterations of HIV-1 biological properties.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lusso, P -- di Marzo Veronese, F -- Ensoli, B -- Franchini, G -- Jemma, C -- DeRocco, S E -- Kalyanaraman, V S -- Gallo, R C -- New York, N.Y. -- Science. 1990 Feb 16;247(4944):848-52.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Tumor Cell Biology, National Cancer Institute, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2305256" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/immunology ; Animals ; Antibodies, Monoclonal ; Antigens, CD4/analysis ; Cell Line ; Cell Transformation, Viral ; Disease Models, Animal ; HIV-1/*genetics/physiology ; Hematopoietic Stem Cells/cytology/microbiology ; Humans ; Mice ; Phenotype ; Retroviridae/*genetics ; Viral Proteins/analysis ; Virus Replication
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  • 21
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    Two G protein oncogenes in human endocrine tumors (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-08-10
    Description: Somatic mutations in a subset of growth hormone (GH)-secreting pituitary tumors convert the gene for the alpha polypeptide chain (alpha s) of Gs into a putative oncogene, termed gsp. These mutations, which activate alpha s by inhibiting its guanosine triphosphatase (GTPase) activity, are found in codons for either of two amino acids, each of which is completely conserved in all known G protein alpha chains. The likelihood that similar mutations would activate other G proteins prompted a survey of human tumors for mutations that replace either of these two amino acids in other G protein alpha chain genes. The first gene so far tested, which encodes the alpha chain of Gi2, showed mutations that replaced arginine-179 with either cysteine or histidine in 3 of 11 tumors of the adrenal cortex and 3 of 10 endocrine tumors of the ovary. The mutant alpha i2 gene is a putative oncogene, referred to as gip2. In addition, gsp mutations were found in 18 of 42 GH-secreting pituitary tumors and in an autonomously functioning thyroid adenoma. These findings suggest that human tumors may harbor oncogenic mutations in various G protein alpha chain genes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lyons, J -- Landis, C A -- Harsh, G -- Vallar, L -- Grunewald, K -- Feichtinger, H -- Duh, Q Y -- Clark, O H -- Kawasaki, E -- Bourne, H R -- New York, N.Y. -- Science. 1990 Aug 10;249(4969):655-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Human Genetics, Cetus Corporation, Emeryville CA 94608.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2116665" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; DNA, Neoplasm/genetics ; Endocrine System Diseases/*genetics ; Female ; GTP Phosphohydrolases/genetics/metabolism ; GTP-Binding Proteins/*genetics/metabolism ; Humans ; Male ; Molecular Sequence Data ; *Mutation ; Neoplasms/*genetics ; Oligonucleotide Probes ; *Oncogenes ; Pituitary Neoplasms/*genetics ; Polymerase Chain Reaction
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  • 22
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    Characterization of naturally occurring minor histocompatibility peptides including H-4 and H-Y (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-07-20
    Description: Minor histocompatibility (H) antigens can be peptides derived from cellular proteins that are presented on the cell surface by major histocompatibility complex (MHC) class I molecules. This is similar to viral antigens, because in both cases cytotoxic T lymphocytes (CTLs) recognize artificially produced peptides loaded on target cells. Naturally processed minor H peptides were found to be similar to those artificial CTL-epitopes, as far as size and hydrophobicity is concerned. The peptides studied were isolated from a transfectant that expressed a model CTL-defined antigen, beta-galactosidase, from male cells that express H-Y, which has been known operationally since 1955, and from cells that express H-4, known since 1961.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rotzschke, O -- Falk, K -- Wallny, H J -- Faath, S -- Rammensee, H G -- New York, N.Y. -- Science. 1990 Jul 20;249(4966):283-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max-Planck-Institut fur Biologie, Abteilung Immungenetik, Tubingen, Federal Republic of Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1695760" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Epitopes/isolation & purification ; Female ; H-Y Antigen/*analysis/immunology ; Male ; Mice ; Mice, Inbred Strains ; Minor Histocompatibility Antigens/*analysis/immunology ; Molecular Sequence Data ; Peptides/chemical synthesis ; Species Specificity ; Spleen/immunology ; T-Lymphocytes, Cytotoxic/*immunology
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  • 23
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    Protection from chemotherapy-induced alopecia in a rat model (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-09-28
    Description: Alopecia (hair loss) is among the most distressing side effects of cancer chemotherapy. Little progress has been made, however, in its prevention or treatment, partly because of the lack of suitable experimental model. In recent work on the treatment of myelogenous leukemia in the rat, the following observations were made: (i) treatment of 8-day-old rats with cytosine arabinoside consistently produced alopecia, and (ii) ImuVert, a biologic response modifier derived from the bacterium Serratia marcescens, uniformly produced complete protection against the alopecia. In subsequent experiments, both cyclophosphamide and doxorubicin also produced alopecia in this model, and the doxorubicin-induced alopecia was prevented by treatment with ImuVert. The potential relevance of these observations to chemotherapy-induced alopecia in the clinical setting should be examined.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hussein, A M -- Jimenez, J J -- McCall, C A -- Yunis, A A -- DK07114/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1990 Sep 28;249(4976):1564-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of Miami School of Medicine, FL 33101.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2218498" target="_blank"〉PubMed〈/a〉
    Keywords: Alopecia/chemically induced/*prevention & control ; Animals ; Biological Products ; Cytarabine/therapeutic use/*toxicity ; Disease Models, Animal ; Immunologic Factors/*therapeutic use ; Leukemia, Experimental/*drug therapy ; Rats ; Rats, Inbred F344 ; Skin/drug effects/pathology
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  • 24
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    Autoradiographic imaging of phosphoinositide turnover in the brain (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-08-17
    Description: With [3H]cytidine as a precursor, phosphoinositide turnover can be localized in brain slices by selective autoradiography of the product [3H]cytidine diphosphate diacylglycerol, which is membrane-bound. In the cerebellum, glutamatergic stimulation elicits an increase of phosphoinositide turnover only in Purkinje cells and the molecular layer. In the hippocampus, both glutamatergic and muscarinic cholinergic stimulation increase phosphoinositide turnover, but with distinct localizations. Cholinergic stimulation affects CA1, CA3, CA4, and subiculum, whereas glutamatergic effects are restricted to the subiculum and CA3. Imaging phosphoinositide turnover in brain slices, which are amenable to electrophysiologic studies, will permit a dynamic localized analysis of regulation of this second messenger in response to synaptic stimulation of specific neuronal pathways.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hwang, P M -- Bredt, D S -- Snyder, S H -- DA-00074/DA/NIDA NIH HHS/ -- GM-07309/GM/NIGMS NIH HHS/ -- MH-18501/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1990 Aug 17;249(4970):802-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1975122" target="_blank"〉PubMed〈/a〉
    Keywords: Alanine/analogs & derivatives/pharmacology ; Animals ; Autoradiography ; Brain/*metabolism ; Carbachol/pharmacology ; Cerebellum/drug effects/metabolism ; Cycloleucine/analogs & derivatives/pharmacology ; Cytidine/metabolism ; Cytidine Diphosphate Diglycerides/metabolism ; Glutamates/physiology ; Glutamic Acid ; Hippocampus/drug effects/metabolism ; Neomycin/pharmacology ; Phosphatidylinositols/*metabolism ; Pirenzepine/pharmacology ; Purkinje Cells/metabolism ; Rats ; Receptors, Muscarinic/drug effects/physiology ; Tissue Distribution
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  • 25
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    Recovery of mitogenic activity of a growth factor mutant with a nuclear translocation sequence (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-09-28
    Description: Heparin-binding growth factor-1 (HBGF-1) is an angiogenic polypeptide mitogen for mesoderm- and neuroectoderm-derived cells in vitro and remains biologically active after truncation of the amino-terminal domain (HBGF-1 alpha) of the HBGF-1 beta precursor. Polymerase chain reaction mutagenesis and prokaryotic expression systems were used to prepare a mutant of HBGF-1 alpha lacking a putative nuclear translocation sequence (amino acid residues 21 to 27; HBGF-1U). Although HBGF-1U retains its ability to bind to heparin, HBGF-1U fails to induce DNA synthesis and cell proliferation at concentrations sufficient to induce intracellular receptor-mediated tyrosine phosphorylation and c-fos expression. Attachment of the nuclear translocation sequence from yeast histone 2B at the amino terminus of HBGF-1U yields a chimeric polypeptide (HBGF-1U2) with mitogenic activity in vitro and indicates that nuclear translocation is important for this biological response.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Imamura, T -- Engleka, K -- Zhan, X -- Tokita, Y -- Forough, R -- Roeder, D -- Jackson, A -- Maier, J A -- Hla, T -- Maciag, T -- HL 32348/HL/NHLBI NIH HHS/ -- HL 35627/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1990 Sep 28;249(4976):1567-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Biology, Jerome H. Holland Laboratory for the Biomedical Sciences, American Red Cross, Rockville, MD 20855.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1699274" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Binding, Competitive ; Cattle ; Cell Division/drug effects ; Cell Line ; Cell Nucleus/metabolism ; Cells, Cultured ; DNA Replication/drug effects ; Endothelium, Vascular/drug effects/metabolism ; Fibroblast Growth Factor 1/*genetics/metabolism/pharmacology ; Kinetics ; Mice ; Mitogens/pharmacology ; Molecular Sequence Data ; *Mutation ; Oligonucleotide Probes ; Receptors, Mitogen/metabolism ; Receptors, Vascular Endothelial Growth Factor ; Recombinant Proteins/metabolism/pharmacology ; Transcription, Genetic/drug effects
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  • 26
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    D1 and D2 dopamine receptor-regulated gene expression of striatonigral and striatopallidal neurons (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-12-07
    Description: The striatum, which is the major component of the basal ganglia in the brain, is regulated in part by dopaminergic input from the substantia nigra. Severe movement disorders result from the loss of striatal dopamine in patients with Parkinson's disease. Rats with lesions of the nigrostriatal dopamine pathway caused by 6-hydroxydopamine (6-OHDA) serve as a model for Parkinson's disease and show alterations in gene expression in the two major output systems of the striatum to the globus pallidus and substantia nigra. Striatopallidal neurons show a 6-OHDA-induced elevation in their specific expression of messenger RNAs (mRNAs) encoding the D2 dopamine receptor and enkephalin, which is reversed by subsequent continuous treatment with the D2 agonist quinpirole. Conversely, striatonigral neurons show a 6-OHDA-induced reduction in their specific expression of mRNAs encoding the D1 dopamine receptor and substance P, which is reversed by subsequent daily injections of the D1 agonist SKF-38393. This treatment also increases dynorphin mRNA in striatonigral neurons. Thus, the differential effects of dopamine on striatonigral and striatopallidal neurons are mediated by their specific expression of D1 and D2 dopamine receptor subtypes, respectively.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gerfen, C R -- Engber, T M -- Mahan, L C -- Susel, Z -- Chase, T N -- Monsma, F J Jr -- Sibley, D R -- New York, N.Y. -- Science. 1990 Dec 7;250(4986):1429-32.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Cell Biology, National Institute of Mental Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2147780" target="_blank"〉PubMed〈/a〉
    Keywords: 2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine/pharmacology ; Animals ; Cerebral Cortex/physiology ; Corpus Striatum/drug effects/*metabolism ; Ergolines/pharmacology ; Gene Expression Regulation ; Globus Pallidus/drug effects/*metabolism ; Hydroxydopamines/pharmacology ; Models, Neurological ; Neurons/drug effects/*metabolism ; Oligonucleotide Probes ; Oxidopamine ; Quinpirole ; RNA, Messenger/drug effects/*genetics ; Rats ; Receptors, Dopamine/*genetics ; Receptors, Dopamine D1 ; Receptors, Dopamine D2 ; Substantia Nigra/drug effects/*metabolism ; Thalamus/physiology
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    Light pulses that shift rhythms induce gene expression in the suprachiasmatic nucleus (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-06-08
    Description: Lighting cycles synchronize (entrain) mammalian circadian rhythms by altering activity of cells in the suprachiasmatic nucleus (SCN) of the hypothalamus, a circadian pacemaker. Exposure of hamsters and rats to light pulses at those phases of the circadian rhythm during which light can shift the rhythm caused increased immunoreactivity for the product of the immediate-early gene c-fos in cells in the region of the SCN that receives retinal fibers. Light pulses also increased messenger RNA for the Fos protein and for the immediate-early protein NGFI-A in the rat SCN. Similar increases in mRNA for NGFI-A were seen in the SCN of hamsters. Thus cells in this portion of the SCN undergo alterations in gene expression in response to retinal illumination, but only at times in the circadian cycle when light is capable of influencing entrainment.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rusak, B -- Robertson, H A -- Wisden, W -- Hunt, S P -- New York, N.Y. -- Science. 1990 Jun 8;248(4960):1237-40.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychology, Dalhousie University, Halifax, Nova Scotia, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2112267" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Circadian Rhythm ; Cricetinae ; Darkness ; *Gene Expression ; Light ; Nerve Growth Factors/*genetics ; Proto-Oncogene Proteins/*genetics ; Proto-Oncogene Proteins c-fos ; *Proto-Oncogenes ; RNA, Messenger/*analysis/genetics ; Rats ; Suprachiasmatic Nucleus/*physiology/radiation effects ; Transcription, Genetic
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    Hypertriglyceridemia as a result of human apo CIII gene expression in transgenic mice (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-08-17
    Description: Primary and secondary hypertriglyceridemia is common in the general population, but the biochemical basis for this disease is largely unknown. With the use of transgenic technology, two lines of mice were created that express the human apolipoprotein CIII gene. One of these mouse lines with 100 copies of the gene was found to express large amounts of the protein and to be severely hypertriglyceridemic. The other mouse line with one to two copies of the gene expressed low amounts of the protein, but nevertheless manifested mild hypertriglyceridemia. Thus, overexpression of apolipoprotein CIII can be a primary cause of hypertriglyceridemia in vivo and may provide one possible etiology for this common disorder in humans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ito, Y -- Azrolan, N -- O'Connell, A -- Walsh, A -- Breslow, J L -- HL 36461/HL/NHLBI NIH HHS/ -- HL33435/HL/NHLBI NIH HHS/ -- HL33714/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1990 Aug 17;249(4970):790-3.〈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/2167514" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apolipoprotein C-III ; Apolipoproteins C/blood/*genetics ; Chylomicrons/blood ; Cloning, Molecular ; DNA Restriction Enzymes/metabolism ; DNA, Recombinant/metabolism ; *Gene Expression ; Humans ; Hypertriglyceridemia/blood/*genetics ; Lipoproteins, VLDL/blood ; Mice ; Mice, Inbred C57BL ; Mice, Inbred CBA ; Mice, Transgenic ; Nucleic Acid Hybridization ; RNA, Messenger/genetics ; Triglycerides/blood
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    Human sickle hemoglobin in transgenic mice (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-02-02
    Description: DNA molecules that contain the human alpha- and beta s-globin genes inserted downstream of erythroid-specific, deoxyribonuclease I super-hypersensitive sites were coinjected into fertilized mouse eggs and a transgenic mouse line was established that synthesizes human sickle hemoglobin (Hb S). These animals were bred to beta-thalassemic mice to reduce endogenous mouse globin levels. When erythrocytes from these mice were deoxygenated, greater than 90 percent of the cells displayed the same characteristic sickled shapes as erythrocytes from humans with sickle cell disease. Compared to controls the mice have decreased hematocrits, elevated reticulocyte counts, lower hemoglobin concentrations, and splenomegaly, which are all indications of the anemia associated with human sickle cell disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ryan, T M -- Townes, T M -- Reilly, M P -- Asakura, T -- Palmiter, R D -- Brinster, R L -- Behringer, R R -- HD-09172/HD/NICHD NIH HHS/ -- HL-35559/HL/NHLBI NIH HHS/ -- HL43508/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1990 Feb 2;247(4942):566-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, School of Medicine, University of Alabama, Birmingham 35294.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2154033" target="_blank"〉PubMed〈/a〉
    Keywords: Anemia, Sickle Cell/blood/genetics ; Animals ; DNA/genetics ; DNA Transposable Elements ; Erythrocytes/ultrastructure ; Genes ; Globins/*genetics ; Hemoglobin, Sickle/*genetics/isolation & purification ; Humans ; Mice ; Mice, Transgenic ; Microscopy, Electron ; Microscopy, Electron, Scanning
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    Cloning of an interleukin-3 receptor gene: a member of a distinct receptor gene family (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-01-19
    Description: Interleukin-3 (IL-3) binds to its receptor with high and low affinities, induces tyrosine phosphorylation, and promotes the proliferation and differentiation of hematopoietic cells. A binding component of the IL-3 receptor was cloned. Fibroblasts transfected with the complementary DNA bound IL-3 with a low affinity [dissociation constant (Kd) of 17.9 +/- 3.6 nM]. No consensus sequence for a tyrosine kinase was present in the cytoplasmic domain. Thus, additional components are required for a functional high affinity IL-3 receptor. A sequence comparison of the IL-3 receptor with other cytokine receptors (erythropoietin, IL-4, IL-6, and the beta chain IL-2 receptor) revealed a common motif of a distinct receptor gene family.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Itoh, N -- Yonehara, S -- Schreurs, J -- Gorman, D M -- Maruyama, K -- Ishii, A -- Yahara, I -- Arai, K -- Miyajima, A -- New York, N.Y. -- Science. 1990 Jan 19;247(4940):324-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, DNAX Research Institute of Molecular and Cellular Biology, Palo Alto, CA 94304.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2404337" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; *Cloning, Molecular ; DNA/genetics ; DNA Probes ; Escherichia coli/genetics ; Fibroblasts/metabolism ; Interleukin-3/metabolism ; Mice ; Molecular Sequence Data ; Nucleic Acid Hybridization ; Plasmids ; Protein-Tyrosine Kinases/metabolism ; Receptors, Immunologic/*genetics/metabolism ; Receptors, Interleukin-3 ; Sequence Homology, Nucleic Acid ; Transfection
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    Molecular cloning and expression of a complementary DNA for inositol 1,4,5-trisphosphate 3-kinase (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-04-06
    Description: A complementary DNA (cDNA) clone that encodes inositol 1,4,5-trisphosphate 3-kinase was isolated from a rat brain cDNA expression library with the use of monoclonal antibodies. This clone had an open reading frame that would direct the synthesis of a protein consisting of 449 amino acids and with a molecular mass of 49,853 daltons. The putative protein revealed a potential calmodulin-binding site and six regions with amino acid compositions (PEST regions) common to proteins that are susceptible to calpain. Expression of the cDNA in COS cells resulted in an approximately 150-fold increase in inositol 1,4,5-trisphosphate 3-kinase activity of these cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Choi, K Y -- Kim, H K -- Lee, S Y -- Moon, K H -- Sim, S S -- Kim, J W -- Chung, H K -- Rhee, S G -- New York, N.Y. -- Science. 1990 Apr 6;248(4951):64-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Biochemistry, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2157285" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Binding Sites ; Brain/enzymology ; Calcium/metabolism ; Calmodulin/metabolism ; Calpain/antagonists & inhibitors/pharmacology ; Cell Line ; *Cloning, Molecular ; Codon ; DNA/*genetics ; *Gene Expression ; Molecular Sequence Data ; Molecular Weight ; Phosphotransferases/*genetics/metabolism ; *Phosphotransferases (Alcohol Group Acceptor) ; Plasmids ; Rats ; Transfection
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    Toxoplasma gondii: fusion competence of parasitophorous vacuoles in Fc receptor-transfected fibroblasts (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-08-10
    Description: After actively entering its host cells, the protozoan parasite Toxoplasma gondii resides in an intracellular vacuole that is completely unable to fuse with other endocytic or biosynthetic organelles. The fusion blocking requires entry of viable organisms but is irreversible: fusion competence of the vacuole is not restored if the parasite is killed after entry. The fusion block can be overcome, however, by altering the parasite's route of entry. Thus, phagocytosis of viable antibody-coated T. gondii by Chinese hamster ovary cells transfected with macrophage-lymphocyte Fc receptors results in the formation of vacuoles that are capable of both fusion and acidification. Phagocytosis and fusion appear to involve a domain of the Fc receptor cytoplasmic tail distinct from that required for localization at clathrin-coated pits. These results suggest that the mechanism of fusion inhibition is likely to reflect a modification of the vacuole membrane at the time of its formation, as opposed to the secretion of a soluble inhibitor by the parasite.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Joiner, K A -- Fuhrman, S A -- Miettinen, H M -- Kasper, L H -- Mellman, I -- New York, N.Y. -- Science. 1990 Aug 10;249(4969):641-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, 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/2200126" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Fibroblasts/parasitology/physiology/ultrastructure ; Fluorescent Antibody Technique ; Lysosomes/physiology/ultrastructure ; Macrophages/immunology ; Membrane Fusion ; Mice ; Mice, Inbred BALB C ; Phagocytosis ; Receptors, Fc/genetics/*physiology ; Toxoplasma/growth & development/*physiology ; *Transfection ; Vacuoles/*parasitology/physiology/ultrastructure
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    Effect of phospholipase C-gamma overexpression on PDGF-induced second messengers and mitogenesis (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-05-04
    Description: Platelet-derived growth factor (PDGF) stimulates phospholipase C (PLC) activity and the phosphorylation of the gamma isozyme of PLC (PLC-gamma) in vitro and in living cells. The role of PLC-gamma in the phosphoinositide signaling pathway was addressed by examining the effect of overexpression of PLC-gamma on cellular responses to PDGF. Overexpression of PLC-gamma correlated with PDGF-induced tyrosine phosphorylation of PLC-gamma and with PDGF-induced breakdown of phosphatidylinositol 4,5-bisphosphate (PIP2). However, neither bradykinin- nor lysophosphatidic acid-induced phosphoinositide metabolism was enhanced in the transfected cells, suggesting that the G protein-coupled phosphoinositide responses to these ligands are mediated by other PLC isozymes. The enhanced PDGF-induced generation of inositol trisphosphate (IP3) did not enhance intracellular calcium signaling or influence PDGF-induced DNA synthesis. Thus, enzymes other than PLC-gamma may limit PDGF-induced calcium signaling and DNA synthesis. Alternatively, PDGF-induced calcium signaling and DNA synthesis may use biochemical pathways other than phosphoinositide metabolism for signal transduction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Margolis, B -- Zilberstein, A -- Franks, C -- Felder, S -- Kremer, S -- Ullrich, A -- Rhee, S G -- Skorecki, K -- Schlessinger, J -- New York, N.Y. -- Science. 1990 May 4;248(4955):607-10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Rorer Biotechnology, King of Prussia, PA 19406.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2333512" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/physiology ; Cattle ; Cell Division/*drug effects ; Cells, Cultured ; DNA Replication/drug effects ; Genetic Vectors ; Inositol Phosphates/metabolism ; Isoenzymes/biosynthesis/*genetics/metabolism ; Kinetics ; Mice ; Platelet-Derived Growth Factor/*pharmacology ; Second Messenger Systems/*drug effects ; Transfection ; Type C Phospholipases/biosynthesis/*genetics/metabolism
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    T cells responsive to myelin basic protein in patients with multiple sclerosis (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-02-09
    Description: Gene mutation in vivo in human T lymphocytes appears to occur preferentially in dividing cells. Individuals with multiple sclerosis (MS) are assumed to have one or more populations of diving T cells that are being stimulated by autoantigens. Mutant T cell clones from MS patients were isolated and tested for reactivity to myelin basic protein, an antigen that is thought to participate in the induction of the disease. The hypoxanthine guanine phosphoribosyltransferase (hprt) clonal assay was used to determine mutant frequency values in MS patients with chronic progressive disease. Eleven of 258 thioguanine-resistant (hprt-) T cell clones from five of the six MS patients who were tested proliferated in response to human myelin basic protein without prior in vitro exposure to this antigen. No wild-type clones from these patients, nor any hprt- or wild-type clones from three healthy individuals responded to myelin basic protein. Thus, T cell clones that react with myelin basic protein can be isolated from the peripheral blood of MS patients.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Allegretta, M -- Nicklas, J A -- Sriram, S -- Albertini, R J -- CA30688-07/CA/NCI NIH HHS/ -- NS00849/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1990 Feb 9;247(4943):718-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Genetics Laboratory, University of Vermont, Burlington 05401.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1689076" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Autoantigens/immunology ; Cell Division ; Clone Cells/immunology ; Female ; Humans ; Hypoxanthine Phosphoribosyltransferase/genetics ; Male ; Middle Aged ; Multiple Sclerosis/genetics/*immunology ; Mutation ; Myelin Basic Protein/*immunology ; T-Lymphocytes/drug effects/*immunology ; Thioguanine/pharmacology ; X Chromosome
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    Phencyclidine, dizocilpine, and cerebrocortical neurons (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-01-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Allen, H L -- Iversen, L L -- New York, N.Y. -- Science. 1990 Jan 12;247(4939):221.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Merck Sharp & Dohme Research Laboratories, West Point, PA 19486.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2403696" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cerebral Cortex/drug effects/*ultrastructure ; Dibenzocycloheptenes/administration & dosage/*pharmacology ; Dizocilpine Maleate ; Male ; Neurons/drug effects/*ultrastructure ; Phencyclidine/*pharmacology ; Rats ; Vacuoles/drug effects
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    Experts clash over cancer data (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-11-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marshall, E -- New York, N.Y. -- Science. 1990 Nov 16;250(4983):900-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2237436" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aged ; Female ; Humans ; Male ; Middle Aged ; Neoplasms/*mortality ; United States
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    Smokers: black and white (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-07-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schneiderman, M -- Davis, D L -- Wagener, D K -- New York, N.Y. -- Science. 1990 Jul 20;249(4966):228-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2374921" target="_blank"〉PubMed〈/a〉
    Keywords: African Americans ; European Continental Ancestry Group ; Female ; Humans ; Lung Neoplasms/mortality ; Male ; Prevalence ; Smoking/*epidemiology ; United States
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    A mouse model of the aniridia-Wilms tumor deletion syndrome (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-11-09
    Description: Deletion of chromosome 11p13 in humans produces the WAGR syndrome, consisting of aniridia (an absence or malformation of the iris), Wilms tumor (nephroblastoma), genitourinary malformations, and mental retardation. An interspecies backcross between Mus musculus/domesticus and Mus spretus was made in order to map the homologous chromosomal region in the mouse genome and to define an animal model of this syndrome. Nine evolutionarily conserved DNA clones from proximal human 11p were localized on mouse chromosome 2 near Small-eyes (Sey), a semidominant mutation that is phenotypically similar to aniridia. Analysis of Dickie's Small-eye (SeyDey), a poorly viable allele that has pleiotropic effects, revealed the deletion of three clones, f3, f8, and k13, which encompass the aniridia (AN2) and Wilms tumor susceptibility genes in man. Unlike their human counterparts, SeyDey/+ mice do not develop nephroblastomas. These findings suggest that the Small-eye defect is genetically equivalent to human aniridia, but that loss of the murine homolog of the Wilms tumor gene is not sufficient for tumor initiation. A comparison among Sey alleles suggests that the AN2 gene product is required for induction of the lens and nasal placodes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Glaser, T -- Lane, J -- Housman, D -- 2 T32 GMO7753-11/GM/NIGMS NIH HHS/ -- GM27882/GM/NIGMS NIH HHS/ -- T32 GM007753/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1990 Nov 9;250(4982):823-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Cancer Research, Massachusetts Institute of Technology, Cambridge 02139.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2173141" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aniridia/*genetics ; Blotting, Southern ; Chromosome Deletion ; Chromosome Mapping ; DNA/analysis ; *Disease Models, Animal ; Eye/embryology/pathology ; Female ; Genes, Wilms Tumor/*genetics ; Genetic Markers ; Kidney Neoplasms/*genetics ; Male ; Mice ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Muridae ; Mutation ; Phenotype ; Polymorphism, Genetic ; Syndrome ; Wilms Tumor/*genetics
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    Thymic epithelium tolerizes for histocompatibility antigens (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-03-23
    Description: The role of thymic epithelium in the establishment of tissue tolerance was analyzed with a murine chimeric system. All T cells differentiated from birth onward in a thymus comprising allogeneic epithelium and syngeneic hematopoietic cells. Embryonic thymic rudiments that contained no hematopoietic cells from C3H (H-2k) donors were grafted to newborn athymic (nude) BALB/c (H-2d) mice. Chimeras that had normal T cell numbers and function rejected third-party skin grafts, but permanently accepted grafts syngeneic to the thymic epithelium. In vitro functional assays did not always correlate with the state of tolerance in vivo. Thus, pure thymic epithelium induces tolerance to histocompatibility antigens.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Salaun, J -- Bandeira, A -- Khazaal, I -- Calman, F -- Coltey, M -- Coutinho, A -- Le Douarin, N M -- New York, N.Y. -- Science. 1990 Mar 23;247(4949 Pt 1):1471-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Instit d'Embryologie cellulaire et moleculaire du CNRS, College de France, Nogent-sur-Marne.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2321009" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chimera ; Epithelium/immunology ; Graft Rejection/immunology ; Graft Survival/*immunology ; Histocompatibility Antigens/*immunology ; Immune Tolerance/immunology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Mice, Nude ; Thymus Gland/*immunology
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    Identification of a specialized adenylyl cyclase that may mediate odorant detection (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-12-07
    Description: The mammalian olfactory system may transduce odorant information via a G protein-mediated adenosine 3',5'-monophosphate (cAMP) cascade. A newly discovered adenylyl cyclase, termed type III, has been cloned, and its expression was localized to olfactory neurons. The type III protein resides in the sensory neuronal cilia, which project into the nasal lumen and are accessible to airborne odorants. The enzymatic activity of the type III adenylyl cyclase appears to differ from nonsensory cyclases. The large difference seen between basal and stimulated activity for the type III enzyme could allow considerable modulation of the intracellular cAMP concentration. This property may represent one mechanism of achieving sensitivity in odorant perception.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bakalyar, H A -- Reed, R R -- 5T32CA09339/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1990 Dec 7;250(4986):1403-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology and Genetics, Howard Hughes Medical Institute, Johns Hopkins University School of Medicine, Baltimore, MD 21205.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2255909" target="_blank"〉PubMed〈/a〉
    Keywords: Adenylyl Cyclases/genetics/*physiology ; Amino Acid Sequence ; Animals ; Brain/enzymology/physiology ; Cell Line ; Clone Cells ; Cloning, Molecular ; Gene Library ; Glycosylation ; Isoenzymes/genetics/*physiology ; Macromolecular Substances ; Molecular Sequence Data ; Molecular Weight ; Neurons, Afferent/enzymology/physiology ; Nose/enzymology/physiology ; *Odors ; Protein Conformation ; Rats ; *Signal Transduction
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    Endogenous cholecystokinin reduces feeding in young rats (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-03-30
    Description: The hypothesis that endogenous cholecystokinin (CCK) released from the small intestine during feeding causes satiety was tested in rat pups, 9 to 12 days old. Intragastric administration of soybean trypsin inhibitor, a procedure that releases CCK from the small intestine, decreased the subsequent intake of a test meal. This effect was reversed by prior treatment with MK-329, a selective antagonist of CCK at alimentary-type CCK (CCK-A) receptors. Thus, endogenous, small intestinal CCK can cause satiety in the neonatal rat and this effect involves CCK-A receptors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weller, A -- Smith, G P -- Gibbs, J -- MH00149/MH/NIMH NIH HHS/ -- MH40010/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1990 Mar 30;247(4950):1589-91.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychiatry, Cornell University Medical College, White Plains, NY.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2321020" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Benzodiazepinones/pharmacology ; Cholecystokinin/antagonists & inhibitors/*physiology ; Devazepide ; Eating/*physiology ; Intestine, Small/*metabolism ; Rats ; Rats, Inbred Strains ; Receptors, Cholecystokinin/drug effects/*physiology
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    Hair analysis (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-11-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Martinez, F -- Poet, T S -- Watson, R R -- New York, N.Y. -- Science. 1990 Nov 23;250(4984):1070.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2251495" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cocaine/metabolism/pharmacokinetics ; Hair/*chemistry/metabolism ; Humans ; Male ; Mice ; Morphine/metabolism/pharmacokinetics ; *Substance Abuse Detection
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    Correction of CD18-deficient lymphocytes by retrovirus-mediated gene transfer (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-06-15
    Description: Leukocyte adhesion deficiency (LAD) is an inherited disorder of leukocyte function caused by derangements in CD18 expression. The genetic and functional abnormalities in a lymphocyte cell line from a patient with LAD have been corrected by retrovirus-mediated transduction of a functional CD18 gene. Lymphocytes from patients with LAD were exposed to CD18-expressing retrovirus and enriched for cells that express CD11a and CD18 (LFA-1) on the cell surface. Molecular and functional analyses of these cells revealed (i) one copy of proviral sequence per cell, (ii) viral-directed CD18 RNA that exceeded normal endogenous levels, (iii) normal quantities of CD11a and CD18 protein on the cell surface, and (iv) reconstitution of LFA-1-dependent adhesive function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wilson, J M -- Ping, A J -- Krauss, J C -- Mayo-Bond, L -- Rogers, C E -- Anderson, D C -- Todd, R F -- R01 AI19031/AI/NIAID NIH HHS/ -- R01 AI23521/AI/NIAID NIH HHS/ -- R01 CA39064/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1990 Jun 15;248(4961):1413-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Internal Medicine, Ann Arbor, MI.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1972597" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD ; Antigens, CD18 ; Antigens, Differentiation/genetics/immunology ; Cell Aggregation ; Cell Line ; Cell Line, Transformed ; Gene Expression ; Genetic Therapy ; Genetic Vectors ; Herpesvirus 4, Human ; Humans ; *Leukocyte-Adhesion Deficiency Syndrome ; Lymphocyte Function-Associated Antigen-1 ; Lymphocytes/immunology ; Membrane Glycoproteins ; Mice ; Nucleic Acid Hybridization ; Receptors, Leukocyte-Adhesion/genetics/immunology ; Retroviridae/*genetics ; Tetradecanoylphorbol Acetate/pharmacology ; *Transfection
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    Identification of mutations in the COL4A5 collagen gene in Alport syndrome (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-06-08
    Description: X-linked Alport syndrome is a hereditary glomerulonephritis in which progressive loss of kidney function is often accompanied by progressive loss of hearing. Ultrastructural defects in glomerular basement membranes (GBM) of Alport syndrome patients implicate an altered structural protein as the cause of nephritis. The product of COL4A5, the alpha 5(IV) collagen chain, is a specific component of GBM within the kidney, and the gene maps to the same X chromosomal region as does Alport syndrome. Three structural aberrations were found in COL4A5, in intragenic deletion, a Pst I site variant, and an uncharacterized abnormality, which appear to cause nephritis and deafness, with allele-specific severity, in three Alport syndrome kindreds in Utah.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barker, D F -- Hostikka, S L -- Zhou, J -- Chow, L T -- Oliphant, A R -- Gerken, S C -- Gregory, M C -- Skolnick, M H -- Atkin, C L -- Tryggvason, K -- DK 36200/DK/NIDDK NIH HHS/ -- DK 39497/DK/NIDDK NIH HHS/ -- M01 RR 00064/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1990 Jun 8;248(4960):1224-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Informatics, University of Utah School of Medicine, Salt Lake City 84132.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2349482" target="_blank"〉PubMed〈/a〉
    Keywords: Blotting, Southern ; Cloning, Molecular ; Collagen/*genetics ; DNA/genetics/isolation & purification ; Exons ; Female ; *Genes ; Humans ; Male ; Molecular Weight ; *Mutation ; Nephritis, Hereditary/*genetics ; Pedigree ; Restriction Mapping ; X Chromosome
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    Regional variation of extracellular space in the hippocampus (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-08-10
    Description: The factors responsible for the unusual susceptibility of the hippocampus to seizures and ischemic cell damage are not well understood. The CA1 pyramidal subfield of the hippocampus is particularly vulnerable to seizure activity and damage after ischemia. The possibility was examined that regional differences exist in extracellular volume, which might influence neuronal excitability and response to injury in the hippocampus. CA1 stratum pyramidale exhibited an exceptionally low extracellular volume fraction (EVF) of 0.12, whereas the EVFs of CA3 and dentate were considerably higher--0.18 and 0.15, respectively. The EVF of CA1 stratum pyramidale was reversibly reduced by 30 percent when the extracellular potassium concentration was raised from 3.5 to 8.5 mM, a procedure that induced spontaneous electrographic seizures in CA1. Thus there are regional variations in the properties of the extracellular space in the hippocampus that might underlie the propensity of the CA1 region to develop seizures and to suffer damage after ischemia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McBain, C J -- Traynelis, S F -- Dingledine, R -- NS17771/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1990 Aug 10;249(4969):674-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of North Carolina, Chapel Hill 27599.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2382142" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Diffusion ; Extracellular Space/drug effects/*physiology ; Hippocampus/anatomy & histology/*physiology/physiopathology ; In Vitro Techniques ; Iontophoresis ; Organ Specificity ; Potassium/pharmacology ; Pyramidal Tracts/drug effects/*physiology ; Quaternary Ammonium Compounds/metabolism ; Rats ; Rats, Inbred Strains ; Seizures/physiopathology
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    Autoimmune diseases: the failure of self tolerance (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-06-15
    Description: The ability to discriminate between self and nonself antigens is vital to the functioning of the immune system as a specific defense against invading microorganisms. Failure of the immune system to "tolerate" self tissues can result in pathological autoimmune states leading to debilitating illness and sometimes death. The induction of autoimmunity involves genetic and environmental factors that have focused the attention of researchers on the trimolecular complex formed by major histocompatibility complex molecules, antigen, and T cell receptors. Detailed molecular characterization of these components points to potential strategies for disease intervention.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sinha, A A -- Lopez, M T -- McDevitt, H O -- New York, N.Y. -- Science. 1990 Jun 15;248(4961):1380-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, Stanford University School of Medicine, CA 94305.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1972595" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autoantibodies/immunology ; Autoantigens/immunology ; Autoimmune Diseases/chemically induced/*immunology ; B-Lymphocytes/immunology ; Bacterial Infections/immunology ; Biological Factors/physiology ; CD4-Positive T-Lymphocytes/immunology ; Cytokines ; Gene Rearrangement, T-Lymphocyte ; Histocompatibility Antigens Class I/immunology ; Histocompatibility Antigens Class II/immunology ; Humans ; *Immune Tolerance ; Major Histocompatibility Complex ; Mice ; Polymorphism, Genetic ; Polymorphism, Restriction Fragment Length ; Receptors, Antigen, T-Cell/genetics/immunology ; T-Lymphocytes, Regulatory/immunology ; *Virus Diseases/immunology
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    Requirement for cotolerogenic gene products in the clonal deletion of I-E reactive T cells (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-02-23
    Description: T cells that express the T cell receptor V beta 5.2 domain react with the class II major histocompatibility complex (MHC) molecule I-E, and V beta 5.2+ T cells are deleted in mouse strains that express I-E glycoproteins. By examination of genetically defined recombinant inbred (RI) mouse strains, it was found that the deletion was dependent on the expression of I-E and one of a limited number of non-MHC gene products (cotolerogens). The gene encoding one of these cotolerogens maps to chromosome 12 and is linked to the endogenous provirus Mtv-9. These observations suggest that the I-E-mediated and minor lymphocyte-stimulating antigen (Mls)-mediated deletions of alpha beta T cells from the repertoire are similar; both require the expression of a class II MHC glycoprotein and a second non-MHC gene product.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Woodland, D -- Happ, M P -- Bill, J -- Palmer, E -- AI-22259/AI/NIAID NIH HHS/ -- AI-22295/AI/NIAID NIH HHS/ -- AR-37070/AR/NIAMS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1990 Feb 23;247(4945):964-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Basic Sciences, National Jewish Center for Immunology and Respiratory Medicine, Denver, CO 80206.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1968289" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CD4-Positive T-Lymphocytes/immunology ; Clone Cells ; Gene Expression ; Histocompatibility Antigens Class II/genetics/*immunology ; Hybridomas/immunology ; Immune Tolerance ; Mice ; Mice, Inbred C3H ; Mice, Inbred DBA ; Mice, Transgenic ; Phenotype ; Receptors, Antigen, T-Cell/*genetics/immunology ; Spleen/immunology ; T-Lymphocytes/*immunology ; T-Lymphocytes, Regulatory/immunology
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    Inheritance of proliferative breast disease in breast cancer kindreds (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-12-21
    Description: Previous studies have emphasized that genetic susceptibility to breast cancer is rare and is expressed primarily as premenopausal breast cancer, bilateral breast cancer, or both. Proliferative breast disease (PBD) is a significant risk factor for the development of breast cancer and appears to be a precursor lesion. PBD and breast cancer were studied in 103 women from 20 kindreds that were selected for the presence of two first degree relatives with breast cancer and in 31 control women. Physical examination, screening mammography, and four-quadrant fine-needle breast aspirates were performed. Cytologic analysis of breast aspirates revealed PBD in 35% of clinically normal female first degree relatives of breast cancer cases and in 13% of controls. Genetic analysis suggests that genetic susceptibility causes both PBD and breast cancer in these kindreds. This study supports the hypothesis that this susceptibility is responsible for a considerable portion of breast cancer, including unilateral and postmenopausal breast cancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Skolnick, M H -- Cannon-Albright, L A -- Goldgar, D E -- Ward, J H -- Marshall, C J -- Schumann, G B -- Hogle, H -- McWhorter, W P -- Wright, E C -- Tran, T D -- CA-28854/CA/NCI NIH HHS/ -- CA-42014/CA/NCI NIH HHS/ -- CA-48711/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1990 Dec 21;250(4988):1715-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Utah Regional Cancer Center, University of Utah Medical Center, Salt Lake City 84132.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2270486" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aged ; Breast Diseases/*genetics/pathology ; Breast Neoplasms/*genetics/pathology ; Female ; Genetic Predisposition to Disease ; Humans ; Male ; Menopause ; Middle Aged ; Pedigree
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    Induction of chronic myelogenous leukemia in mice by the P210bcr/abl gene of the Philadelphia chromosome (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-02-16
    Description: In tumor cells from virtually all patients with chronic myelogenous leukemia, the Philadelphia chromosome, a fusion of chromosomes 9 and 22, directs the synthesis of the P210bcr/abl protein. The protein-tyrosine kinase activity and hybrid structure of P210bcr/abl are similar to the oncogene product of the Abelson murine leukemia virus, P160gag/v-abl, which induces acute lymphomas. To determine whether P210bcr/abl can induce chronic myelogenous leukemia, murine bone marrow was infected with a retrovirus encoding P210bcr/abl and transplanted into irradiated syngeneic recipients. Transplant recipients developed several hematologic malignancies; prominent among them was a myeloproliferative syndrome closely resembling the chronic phase of human chronic myelogenous leukemia. Tumor tissue from diseased mice harbored the provirus encoding P210bcr/abl. These results demonstrate that P210bcr/abl expression can induce chronic myelogenous leukemia. Retrovirus-mediated expression of the protein provides a murine model system for further analysis of the disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Daley, G Q -- Van Etten, R A -- Baltimore, D -- 2T 32 GM07753-07/GM/NIGMS NIH HHS/ -- CA38497/CA/NCI NIH HHS/ -- T32 GM007753/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1990 Feb 16;247(4944):824-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research, Massachusetts Institute of Technology, Cambridge 02142.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2406902" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bone Marrow/microbiology/pathology ; Cell Line ; DNA, Neoplasm/isolation & purification ; DNA, Viral/isolation & purification ; Fusion Proteins, bcr-abl/*genetics ; Humans ; Leukemia, Experimental/genetics/pathology ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/*genetics/pathology ; Mice ; Myeloproliferative Disorders/microbiology/pathology ; *Philadelphia Chromosome ; Retroviridae/genetics ; Spleen/microbiology ; Transduction, Genetic
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    HIV-1 coat protein neurotoxicity prevented by calcium channel antagonists (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-04-20
    Description: Coat protein gp120 from the human immunodeficiency virus type-1 (HIV-1) increased intracellular free calcium and injured rodent retinal ganglion cells and hippocampal neurons in culture. Highly purified recombinant gp120 envelope protein produced these effects in a dose-dependent fashion at picomolar concentrations. Immunoprecipitation with antibody to gp120, but not with control immunoglobulin-containing serum, depleted solutions of the viral envelope protein and also prevented both the rise in intracellular calcium and neuronal toxicity. The gp120-induced increase in intracellular calcium was abrogated by transiently lowering extracellular calcium or by adding the dihydropyridine calcium channel antagonist nimodipine (100 nM). Calcium channel antagonists also prevented gp120-induced neuronal injury. In addition, intracellular stores appeared to contribute substantially to the increase in calcium elicited by gp120. Since increases in intracellular calcium have been associated with neurotoxicity, it is possible that an injurious effect of gp120 on neurons might be related to this mechanism and that treatment with calcium channel antagonists may prove useful in mitigating HIV-1-related neuronal injury.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dreyer, E B -- Kaiser, P K -- Offermann, J T -- Lipton, S A -- EY 05477/EY/NEI NIH HHS/ -- NS 01395/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1990 Apr 20;248(4953):364-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, Children's Hospital, Boston, MA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2326646" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/*metabolism ; Calcium Channel Blockers/*pharmacology ; Cells, Cultured ; HIV Envelope Protein gp120/administration & dosage/antagonists & ; inhibitors/*physiology ; HIV-1/*analysis ; Hippocampus/cytology ; Neurons/*drug effects/metabolism ; Nimodipine/pharmacology ; Rats ; Recombinant Proteins/pharmacology ; Retinal Ganglion Cells/drug effects/metabolism
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    Olfactory recognition: a simple memory system (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-11-30
    Description: Mice have an olfactory (pheromone) recognition memory located at the first relay in the sensory system. It is acquired with one-trial learning, contingent upon norepinephrine activation at mating, and lasts for several weeks. The mechanism involves Hebbian (association-dependent) changes in synaptic efficacy at dendrodendritic synapses in the accessory olfactory bulb. As a result of this memory, males made familiar by mating are recognized by the females, thereby mitigating pregnancy block. Such a memory function is biologically important to the female, as it is required to sustain pregnancy in the presence of her stud male's odors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brennan, P -- Kaba, H -- Keverne, E B -- New York, N.Y. -- Science. 1990 Nov 30;250(4985):1223-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Sub-Department of Animal Behaviour, University of Cambridge, United Kingdom.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2147078" target="_blank"〉PubMed〈/a〉
    Keywords: Amygdala/drug effects/physiology ; Animals ; Female ; Hypothalamus/physiology ; Lidocaine/pharmacology ; Male ; Memory/*physiology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred CBA ; N-Methylaspartate/antagonists & inhibitors/physiology ; Norepinephrine/physiology ; Olfactory Bulb/drug effects/physiology ; Olfactory Pathways/drug effects/physiology ; *Pheromones/urine ; Pregnancy ; Pregnancy, Animal/*physiology ; Receptors, N-Methyl-D-Aspartate/physiology ; Reproduction/physiology ; Smell/*physiology ; Synapses/physiology
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    Transplanted suprachiasmatic nucleus determines circadian period (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-02-23
    Description: The pacemaker role of the suprachiasmatic nucleus in a mammalian circadian system was tested by neural transplantation by using a mutant strain of hamster that shows a short circadian period. Small neural grafts from the suprachiasmatic region restored circadian rhythms to arrhythmic animals whose own nucleus had been ablated. The restored rhythms always exhibited the period of the donor genotype regardless of the direction of the transplant or genotype of the host. The basic period of the overt circadian rhythm therefore is determined by cells of the suprachiasmatic region.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ralph, M R -- Foster, R G -- Davis, F C -- Menaker, M -- HD13162/HD/NICHD NIH HHS/ -- HD18686/HD/NICHD NIH HHS/ -- MH09483/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1990 Feb 23;247(4945):975-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, University of Virginia, Charlottesville 22903.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2305266" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Circadian Rhythm/genetics/*physiology ; Cricetinae ; Immunohistochemistry ; Male ; Mutation ; Nerve Tissue/*transplantation ; Neuropeptide Y/analysis ; Suprachiasmatic Nucleus/embryology/*physiology ; Vasopressins/analysis
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    Autonomous developmental control of human embryonic globin gene switching in transgenic mice (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-11-23
    Description: The mechanisms by which expression of the beta-like globin genes are developmentally regulated are under intense investigation. The temporal control of human embryonic (epsilon) globin expression was analyzed. A 3.7-kilobase (kb) fragment that contained the entire human epsilon-globin gene was linked to a 2.5-kb cassette of the locus control region (LCR), and the developmental time of expression of this construct was studied in transgenic mice. The human epsilon-globin transgene was expressed in yolk sac-derived primitive erythroid cells, but not in fetal liver or bone marrow-derived definitive erythroid cells. The absence of epsilon gene expression in definitive erythroid cells suggests that the developmental regulation of the epsilon-globin gene depends only on the presence of the LCR and the epsilon-globin gene itself (that is, an autonomous negative control mechanism). The autonomy of epsilon-globin gene developmental control distinguishes it from the competitive mechanism of regulation of gamma and beta-globin genes, and therefore, suggests that at least two distinct mechanisms function in human hemoglobin switching.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Raich, N -- Enver, T -- Nakamoto, B -- Josephson, B -- Papayannopoulou, T -- Stamatoyannopoulos, G -- DK 3132/DK/NIDDK NIH HHS/ -- HL 20899/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1990 Nov 23;250(4984):1147-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Medical Genetics, University of Washington, Seattle 98195.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2251502" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bone Marrow/embryology ; Bone Marrow Cells ; Erythroid Precursor Cells/metabolism ; Erythropoiesis ; Fetus/*metabolism ; *Gene Expression Regulation ; Globins/*genetics ; Hemoglobins/biosynthesis ; Humans ; Liver/cytology/embryology ; Mice ; Mice, Transgenic ; Regulatory Sequences, Nucleic Acid ; Yolk Sac/cytology
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    Transcription factor interactions: selectors of positive or negative regulation from a single DNA element (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-09-14
    Description: The mechanism by which a single factor evokes opposite regulatory effects from a specific DNA sequence is not well understood. In this study, a 25-base pair element that resides upstream of the mouse proliferin gene was examined; it conferred on linked promoters either positive or negative glucocorticoid regulation, depending upon physiological context. This sequence, denoted a "composite" glucocorticoid response element (GRE), was bound selectively in vitro both by the glucocorticoid receptor and by c-Jun and c-Fos, components of the phorbol ester-activated AP-1 transcription factor. Indeed, c-Jun and c-Fos served as selectors of hormone responsiveness: the composite GRE was inactive in the absence of c-Jun, whereas it conferred a positive glucocorticoid effect in the presence of c-Jun, and a negative glucocorticoid effect in the presence of c-Jun and relatively high levels of c-Fos. The receptor also interacted selectively with c-Jun in vitro. A general model for composite GRE action is proposed that invokes both DNA binding and protein-protein interactions by receptor and nonreceptor factors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Diamond, M I -- Miner, J N -- Yoshinaga, S K -- Yamamoto, K R -- New York, N.Y. -- Science. 1990 Sep 14;249(4974):1266-72.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Biophysics, University of California, San Francisco 94143-0448.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2119054" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cross-Linking Reagents ; DNA-Binding Proteins/physiology ; Gene Expression Regulation/genetics/*physiology ; Glucocorticoids/physiology ; Glycoproteins/*genetics ; HeLa Cells ; Humans ; Intercellular Signaling Peptides and Proteins ; Mice ; Molecular Sequence Data ; Proto-Oncogene Proteins/physiology ; Proto-Oncogene Proteins c-fos ; Proto-Oncogene Proteins c-jun ; Receptors, Glucocorticoid/metabolism ; Regulatory Sequences, Nucleic Acid/genetics ; Tetradecanoylphorbol Acetate/pharmacology ; Transcription Factors/*physiology ; Transcription, Genetic/drug effects
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    Recognizing self from nonself (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-06-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koshland, D E Jr -- New York, N.Y. -- Science. 1990 Jun 15;248(4961):1273.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2356462" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/immunology ; Humans ; *Immune Tolerance ; Mice ; Mice, Transgenic ; T-Lymphocytes/immunology
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    Induction by antigen of intrathymic apoptosis of CD4+CD8+TCRlo thymocytes in vivo (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-12-21
    Description: In order to examine the mechanisms by which clonal deletion of autoreactive T cells occurs, a peptide antigen was used to induce deletion of antigen-reactive thymocytes in vivo. Mice transgenic for a T cell receptor (TCR) that reacts to this peptide contain thymocytes that progress from the immature to the mature phenotype. Intraperitoneal administration of the peptide antigen to transgenic mice results in a rapid deletion of the immature CD4+ CD8+ TCRlo thymocytes. Apoptosis of cortical thymocytes can be seen within 20 hours of treatment. These results provide direct evidence for the in vivo role of apoptosis in the development of antigen-induced tolerance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Murphy, K M -- Heimberger, A B -- Loh, D Y -- New York, N.Y. -- Science. 1990 Dec 21;250(4988):1720-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Washington University School of Medicine, St. Louis, MO 63110.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2125367" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antigens, CD4/*immunology ; Antigens, CD8 ; Antigens, Differentiation, T-Lymphocyte/*immunology ; Mice ; Mice, Transgenic ; Microscopy, Electron ; Molecular Sequence Data ; Ovalbumin/immunology ; Phagocytosis ; Phenotype ; Receptors, Antigen, T-Cell/genetics/*immunology ; T-Lymphocytes/cytology/*immunology/ultrastructure ; Thymus Gland/cytology/*immunology
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    Tolerance in transgenic mice expressing major histocompatibility molecules extrathymically on pancreatic cells (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-06-15
    Description: Transgenic mice with defined expression of major histocompatibility complex (MHC) proteins provide novel systems for understanding the fundamental question of T cell tolerance to nonlymphoid self components. The MHC class II I-E and I-A and class I H-2K molecules expressed specifically on pancreatic islet or acinar cells serve as model self antigens. In these systems, transgenic proteins are not detected in the thymus or other lymphoid tissues. Yet mice are tolerant to the pancreatic MHC products in vivo; this tolerance is not induced by clonal deletion. These studies have been aided by monoclonal antibodies specific for I-E-reactive T cells and indicate that clonal anergy may be an important mechanism of tolerance to peripheral proteins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Burkly, L C -- Lo, D -- Flavell, R A -- New York, N.Y. -- Science. 1990 Jun 15;248(4961):1364-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Biogen Incorporated, 14 Cambridge Center, MA 02142.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1694042" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen-Presenting Cells/immunology ; Autoantigens/immunology ; CD4-Positive T-Lymphocytes/immunology ; Clone Cells/immunology ; Epitopes/immunology ; H-2 Antigens/immunology ; Histocompatibility Antigens/*immunology ; Histocompatibility Antigens Class II/immunology ; *Immune Tolerance ; Islets of Langerhans/*immunology ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Receptors, Antigen, T-Cell/immunology ; T-Lymphocytes/*immunology ; T-Lymphocytes, Regulatory/immunology ; Thymus Gland/immunology
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    Different tumor-derived p53 mutants exhibit distinct biological activities (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-10-05
    Description: In its wild-type form, the protein p53 can interfere with neoplastic processes. Tumor-derived cells often express mutant p53. Full-length mutant forms of p53 isolated so far from transformed mouse cells exhibit three common properties in vitro: loss of transformation-suppressing activity, gain of pronounced transforming potential, and ability to bind the heat shock protein cognate hsc70. A tumor-derived mouse p53 variant is now described, whose site of mutation corresponds to a hot spot for p53 in human tumors. While absolutely nonsuppressing, it is only weakly transforming and exhibits no detectable hsc70 binding. The data suggest that the ability of a p53 mutant to bind endogenous p53 is not the sole determinant of its oncogenic potential. The data also support the existence of gain-of-function p53 mutants.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Halevy, O -- Michalovitz, D -- Oren, M -- R01 CA40099/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1990 Oct 5;250(4977):113-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemical Immunology, Weizmann Institute of Science, Rehovot, Israel.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2218501" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Transformation, Neoplastic ; Cloning, Molecular ; Humans ; Mice ; *Mutation ; Nuclear Proteins/*genetics ; Plasmids ; Polymerase Chain Reaction ; RNA, Messenger/genetics ; Rats ; Transfection ; Tumor Suppressor Protein p53/*genetics/physiology
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    Flunarizine protects neurons from death after axotomy or NGF deprivation (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-06-15
    Description: Systemically administered flunarizine enhanced neuronal survival in lumbar sensory ganglia in newborn rats after axotomy. Flunarizine-treated rats lost 71 percent fewer neurons than the untreated control rats at the end of 1 week. In cell culture, flunarizine at 30 to 40 microM also prevented neuronal death in nerve growth factor-dependent embryonic sensory and sympathetic neurons after the abrupt withdrawal of neurotrophic support. The drug may cause this effect by acting at an intracellular site, one distinct from its blockade of voltage-dependent calcium channels.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rich, K M -- Hollowell, J P -- HL20604/HL/NHLBI NIH HHS/ -- NS18071/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1990 Jun 15;248(4961):1419-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurosurgery, Washington University School of Medicine, St. Louis, Mo 63110.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2356470" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Cell Survival/drug effects ; Cells, Cultured ; Dose-Response Relationship, Drug ; Flunarizine/administration & dosage/*pharmacology ; Ganglia, Spinal/cytology/embryology ; Ganglia, Sympathetic/cytology/embryology ; Microscopy, Electron, Scanning ; Nerve Crush ; Nerve Growth Factors/administration & dosage/*pharmacology ; Neurons/*cytology/drug effects ; Rats ; Sciatic Nerve/physiology/surgery
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    5-Methylcytosine as an endogenous mutagen in the human LDL receptor and p53 genes (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-09-14
    Description: Direct genomic sequencing revealed that cytosine residues known to have undergone a germ-line mutation in the low density lipoprotein receptor gene or somatic mutations in the p53 tumor suppressor gene were methylated in all normal human tissues analyzed. Thus, these mutations should be scored as transitions from 5-methylcytosine to thymine rather than from cytosine to thymine. Methylated cytosines occur exclusively at CpG dinucleotides, which, although markedly underrepresented in human DNA, are sites for more than 30 percent of all known disease-related point mutations. Thus, 5-methylcytosine functions as an endogenous mutagen and carcinogen in humans, in that methylation seems to increase the potential for mutation at cytosine residues at least by a factor of 10.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rideout, W M 3rd -- Coetzee, G A -- Olumi, A F -- Jones, P A -- R35 CA49758/CA/NCI NIH HHS/ -- T32 CA09569/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1990 Sep 14;249(4974):1288-90.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Urological Cancer Research Laboratory, Kenneth Norris Jr. Comprehensive Cancer Center, University of Southern California, Los Angeles 90033.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1697983" target="_blank"〉PubMed〈/a〉
    Keywords: 5-Methylcytosine ; Base Sequence ; Cytosine/*analogs & derivatives/physiology ; Deoxyribonuclease HpaII ; Deoxyribonucleases, Type II Site-Specific ; Dinucleoside Phosphates/genetics ; Guanosine ; Humans ; Leukocytes ; Male ; Methylation ; Molecular Sequence Data ; *Mutation ; Oncogene Proteins/*genetics ; Phosphoproteins/*genetics ; Polymerase Chain Reaction ; Receptors, LDL/*genetics ; Spermatozoa ; Tumor Suppressor Protein p53
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    Tumor resistance to alkylating agents conferred by mechanisms operative only in vivo (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-03-23
    Description: EMT-6 murine mammary tumors were made resistant to cis-diamminedichloroplatinum (II) (CDDP), carboplatin, cyclophosphamide (CTX), or thiotepa in vivo by treatment of tumor-bearing animals with the drug during a 6-month period. In spite of high levels of in vivo resistance, no significant resistance was observed when the cells from these tumors were exposed to the drugs in vitro. The pharmacokinetics of CDDP and CTX were altered in animals bearing the respective resistant tumors. The resistance of all tumor lines except for the EMT-6/thiotepa decreased during 3 to 6 months in vivo passage in the absence of drugs. These results indicate that very high levels of resistance to anticancer drugs can develop through mechanisms that are expressed only in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Teicher, B A -- Herman, T S -- Holden, S A -- Wang, Y Y -- Pfeffer, M R -- Crawford, J W -- Frei, E 3rd -- P01-CA38497/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1990 Mar 23;247(4949 Pt 1):1457-61.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Dana-Farber Cancer Institute, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2108497" target="_blank"〉PubMed〈/a〉
    Keywords: Alkylating Agents/pharmacokinetics/*therapeutic use ; Animals ; Antineoplastic Agents/pharmacokinetics/*therapeutic use ; Carboplatin ; Cisplatin/therapeutic use ; Cyclophosphamide/therapeutic use ; Drug Resistance ; Kidney/metabolism ; Liver/metabolism ; Mammary Neoplasms, Experimental/*drug therapy/metabolism ; Mice ; Mice, Inbred BALB C ; Organoplatinum Compounds/therapeutic use ; Sulfhydryl Compounds/analysis ; Thiotepa/therapeutic use ; Tissue Distribution ; Tumor Cells, Cultured
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    Erythropoietin retards DNA breakdown and prevents programmed death in erythroid progenitor cells (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-04-20
    Description: The mechanism by which erythropoietin controls mammalian erythrocyte production is unknown. Labeling experiments in vitro with [3H]thymidine demonstrated DNA cleavage in erythroid progenitor cells that was accompanied by DNA repair and synthesis. Erythropoietin reduced DNA cleavage by a factor of 2.6. In the absence of erythropoietin, erythroid progenitor cells accumulated DNA cleavage fragments characteristic of those found in programmed cell death (apoptosis) by 2 to 4 hours and began dying by 16 hours. In the presence of erythropoietin, the progenitor cells survived and differentiated into reticulocytes. Thus, apoptosis is a major component of normal erythropoiesis, and erythropoietin controls erythrocyte production by retarding DNA breakdown and preventing apoptosis in erythroid progenitor cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koury, M J -- Bondurant, M C -- DK 31513/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1990 Apr 20;248(4953):378-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Hematology, Vanderbilt University Medical Center, Nashville, TN.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2326648" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; DNA/biosynthesis/*drug effects/metabolism ; DNA Repair ; Erythrocyte Aging/drug effects ; Erythroid Precursor Cells/cytology/drug effects/*metabolism ; Erythropoietin/*pharmacology ; Friend murine leukemia virus ; Leukemia, Erythroblastic, Acute ; Mice ; Molecular Weight
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    An insulin-stimulated protein kinase similar to yeast kinases involved in cell cycle control (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-07-06
    Description: A protein kinase characterized by its ability to phosphorylate microtubule-associated protein-2 (MAP2), is thought to be an early intermediate in an insulin-stimulated phosphorylation cascade and in a variety of other mammalian cell responses to extracellular signals. A complementary DNA that encodes this protein serine-threonine kinase has been cloned, and the protein designated extracellular signal-regulated kinase 1 (ERK1). ERK1 has striking similarity to two protein kinases, KSS1 and FUS3, from yeast. The yeast kinases function in an antagonistic manner to regulate the cell cycle in response to mating factors. Thus, ERK1 and the two yeast kinases constitute a family of evolutionarily conserved enzymes involved in regulating the response of eukaryotic cells to extracellular signals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Boulton, T G -- Yancopoulos, G D -- Gregory, J S -- Slaughter, C -- Moomaw, C -- Hsu, J -- Cobb, M H -- DK 01918/DK/NIDDK NIH HHS/ -- DK 34128/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1990 Jul 6;249(4964):64-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of Texas Southwestern Graduate School of Biomedical Sciences, Dallas 75235.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2164259" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Calcium-Calmodulin-Dependent Protein Kinases ; Cell Cycle/*physiology ; Cell Line ; Central Nervous System/*enzymology ; DNA/*genetics ; Fibroblasts/enzymology ; Humans ; Insulin/pharmacology ; Mitogen-Activated Protein Kinase 3 ; *Mitogen-Activated Protein Kinases ; Molecular Sequence Data ; Phosphorylation ; Protein Kinases/genetics/*metabolism ; Rats ; Receptor, Insulin/metabolism ; Yeasts/enzymology
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    Target control of collateral extension and directional axon growth in the mammalian brain (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-01-12
    Description: Individual neurons in the brain send their axons over considerable distances to multiple targets, but the mechanisms governing this process are unresolved. An amenable system for studying axon outgrowth, branching, and target selection is the mammalian corticopontine projection. This major connection develops from parent corticospinal axons that have already grown past the pons, by a delayed interstitial budding of collateral branches that then grow directly into their target, the basilar pons. When cocultured with explants of developing cortex in three-dimensional collagen matrices, the basilar pons elicits the formation and directional growth of cortical axon collaterals across the intervening matrix. This effect appears to be target-specific and selectively influences neurons in the appropriate cortical layer. These in vitro findings provide evidence that the basilar pons becomes innervated by controlling at a distance the budding and directed ingrowth of cortical axon collaterals through the release of a diffusible, chemotropic molecule.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Heffner, C D -- Lumsden, A G -- O'Leary, D D -- EY07025/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 1990 Jan 12;247(4939):217-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy and Neurobiology, Washington University School of Medicine, St. Louis, MO 63110.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2294603" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/*physiology/ultrastructure ; Cerebral Cortex/growth & development/*ultrastructure ; Culture Techniques ; Fluorescent Dyes ; Motor Cortex/ultrastructure ; Nerve Growth Factors/physiology ; Neural Pathways/growth & development/ultrastructure ; Pons/*physiology/ultrastructure ; Rats ; Spinal Cord/ultrastructure ; Visual Cortex/ultrastructure
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    Alteration of alpha 1 Na+,K(+)-ATPase 86Rb+ influx by a single amino acid substitution (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-08-31
    Description: The sodium- and potassium-dependent adenosine triphosphatase (Na+,K(+)-ATPase) maintains the transmembrane Na+ gradient to which is coupled all active cellular transport systems. The R and S alleles of the gene encoding the Na+,K(+)-ATPase alpha 1 subunit isoform were identified in Dahl salt-resistant (DR) and Dahl salt-sensitive (DS) rats, respectively. Characterization of the S allele-specific Na+,K(+)-ATPase alpha 1 complementary DNA identified a leucine substitution of glutamine at position 276. This mutation alters the hydropathy profile of a region in proximity to T3(Na), the trypsin-sensitive site that is only detected in the presence of Na+. This mutation causes a decrease in the rubidium-86 influx of S allele-specific sodium pumps, thus marking a domain in the Na+,K(+)-ATPase alpha subunit important for K+ transport, and supporting the hypothesis of a putative role of these pumps in hypertension.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Herrera, V L -- Ruiz-Opazo, N -- HL 01967/HL/NHLBI NIH HHS/ -- HL 18318/HL/NHLBI NIH HHS/ -- HL 39267/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1990 Aug 31;249(4972):1023-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Molecular Genetics, Whitaker Cardiovascular Institute, Boston University School of Medicine, MA 02118.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1975705" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cell Membrane/enzymology ; Kidney/enzymology ; Kinetics ; Molecular Sequence Data ; *Mutation ; Polymorphism, Restriction Fragment Length ; Protein Conformation ; Rats ; Rats, Inbred Strains ; Rubidium/*metabolism ; Rubidium Radioisotopes ; Sodium-Potassium-Exchanging ATPase/*genetics/metabolism
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    Molecular characterization of a functional cDNA encoding the rat substance P receptor (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-02-23
    Description: Substance P is a member of the tachykinin peptide family and participates in the regulation of diverse biological processes. The polymerase chain reaction and conventional library screening were used to isolate a complementary DNA (cDNA) encoding the rat substance P receptor from brain and submandibular gland. By homology analysis, this receptor belongs to the G protein-coupled receptor superfamily. The receptor cDNA was expressed in a mammalian cell line and the ligand binding properties of the encoded receptor were pharmacologically defined by Scatchard analysis and tachykinin peptide displacement as those of a substance P receptor. The distribution of the messenger RNA for this receptor is highest in urinary bladder, submandibular gland, striatum, and spinal cord, which is consistent with the known distribution of substance P receptor binding sites. Thus, this receptor appears to mediate the primary actions of substance P in various brain regions and peripheral tissues.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hershey, A D -- Krause, J E -- NS21937/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1990 Feb 23;247(4945):958-62.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy and Neurobiology, Washington University School of Medicine, St. Louis, MO 63110.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2154852" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Brain Chemistry ; Cloning, Molecular ; DNA/*genetics/isolation & purification ; GTP-Binding Proteins/metabolism ; Gene Expression ; Intestine, Small/analysis ; Molecular Sequence Data ; Nucleic Acid Hybridization ; Polymerase Chain Reaction ; RNA, Messenger/analysis ; Rats ; Receptors, Neurokinin-1 ; Receptors, Neurotransmitter/*genetics ; Sequence Homology, Nucleic Acid ; Submandibular Gland/analysis ; Tissue Distribution ; Urinary Bladder/analysis
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Genetics of small populations (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-10-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Carson, H L -- New York, N.Y. -- Science. 1990 Oct 12;250(4978):191.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2218517" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Evolution ; Female ; Genetic Variation ; *Genetics, Population ; Male ; Recombination, Genetic ; Selection, Genetic
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    A cytoplasmic protein inhibits the GTPase activity of H-Ras in a phospholipid-dependent manner (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-11-16
    Description: A cytoplasmic protein has been identified that inhibits the guanosine triphosphatase (GTPase) activity of bacterially synthesized, cellular H-Ras protein. This GTPase inhibiting protein is able to counteract the activity of GTPase activating protein (GAP), which has been postulated to function as a negative regulator of Ras activity. The potential biological importance of the GTPase inhibiting protein is further supported by its interaction with lipids. Phospholipids produced in cells as a consequence of mitogenic stimulation increase the activity of the GTPase inhibiting protein, as well as inhibit the activity of GAP. The interaction of such lipids with each of these two regulatory proteins would, therefore, tend to increase the biological activity of Ras and stimulate cell proliferation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tsai, M H -- Yu, C L -- Stacey, D W -- CA 48662/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1990 Nov 16;250(4983):982-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Cleveland Clinic Foundation 44195.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2237442" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Division ; Dose-Response Relationship, Drug ; GTP Phosphohydrolases/*antagonists & inhibitors ; GTPase-Activating Proteins ; Mice ; Phospholipids/*pharmacology ; Proteins/antagonists & inhibitors ; Proto-Oncogene Proteins p21(ras)/*antagonists & inhibitors ; ras GTPase-Activating Proteins
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Increased activity of calcium leak channels in myotubes of Duchenne human and mdx mouse origin (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-11-02
    Description: Elevated free Ca2+ concentrations found in adult dystrophic muscle fibers result in enhanced protein degradation. Since the difference in concentrations may reflect differences in entry, Ca2+ leak channels in cultures of normal and Duchenne human myotubes, and normal and mdx murine myotubes, have been identified and characterized. The open probability of leak channels is markedly increased in dystrophic myotubes. Other channel properties, such as mean open times, single channel conductance, ion selectivity, and behavior in the presence of pharmacological agents, were similar among myotube types. Compared to the Ca2+ concentrations in normal human and normal mouse myotubes, intracellular resting free Ca2+ concentrations ([Ca2+]i) in myotubes of Duchenne and mdx origin were significantly higher at a time when dystrophin is first expressed in normal tissue. Taken together, these findings suggest that the increased open probability of Ca2+ leak channels contributes to the elevated free intracellular Ca2+ concentration in Duchenne human and mdx mouse myotubes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fong, P Y -- Turner, P R -- Denetclaw, W F -- Steinhardt, R A -- New York, N.Y. -- Science. 1990 Nov 2;250(4981):673-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cell Biology, University of California, Berkeley 94720.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2173137" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/*metabolism ; Calcium Channels/drug effects/*physiology ; Dystrophin/genetics ; Humans ; Membrane Potentials ; Mice ; Muscles/metabolism ; Muscular Dystrophies/*metabolism ; Muscular Dystrophy, Animal/*metabolism ; Nifedipine/pharmacology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Population dynamics of the United States and the Soviet Union (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-03-30
    Description: Population growth in the United States and the Soviet Union is slowing. Since the 1970s, labor force growth in both countries is slowing even more than population growth, and both countries are aging. Economic effects of slowing growth can be compensated for by increased participation in the labor force and increased productivity and by adjustments in the military forces. Economic flexibility and policy choices will determine how successfully the trend to slower population growth will be accommodated.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Torrey, B B -- Kingkade, W W -- New York, N.Y. -- Science. 1990 Mar 30;247(4950):1548-52.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for International Research, U.S. Bureau of the Census, Washington DC 20233.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2321015" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Aged ; Female ; Fertility ; Humans ; Male ; Middle Aged ; *Population Dynamics ; Ussr ; United States
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Tumorigenicity in human melanoma cell lines controlled by introduction of human chromosome 6 (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-02-02
    Description: Chromosome banding analysis of human malignant melanoma has documented the nonrandom alteration of chromosome 6. To determine the relevance of chromosome 6 abnormalities in melanoma, a normal chromosome 6 was directly introduced into melanoma cell lines. The resulting (+6) microcell hybrids were significantly altered in their phenotypic properties in culture and lost their ability to form tumors in nude mice. The loss of the chromosome 6 from melanoma microcell hybrids resulted in the reversion to tumorigenicity of these cells in mice. The introduction of the selectable marker (psv2neo) alone into melanoma cell lines had no effect on tumorigenicity. These results support the idea that one or more genes on chromosome 6 may control the malignant expression of human melanoma.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Trent, J M -- Stanbridge, E J -- McBride, H L -- Meese, E U -- Casey, G -- Araujo, D E -- Witkowski, C M -- Nagle, R B -- CA-19104/CA/NCI NIH HHS/ -- CA-23074/CA/NCI NIH HHS/ -- R37-CA-29476/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1990 Feb 2;247(4942):568-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of Arizona, Arizona Cancer Center, Tucson 85724.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2300817" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Division ; Cell Line ; Chromosome Aberrations ; Chromosome Banding ; *Chromosomes, Human, Pair 6 ; Humans ; Hybrid Cells/cytology ; Karyotyping ; Melanoma/*genetics/pathology ; Mice ; Phenotype ; Transplantation, Heterologous
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    Light-evoked changes in the interphotoreceptor matrix (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-06-29
    Description: The normal function of vertebrate photoreceptor cells depends on multiple interactions and transfer of substances between the photoreceptors and the retinal pigment epithelium (RPE), but the mechanisms of these interactions are poorly understood. Many are thought to be mediated by the interphotoreceptor matrix (IPM), a complex extracellular matrix that surrounds the photoreceptors and lies between them and the RPE. Histochemical, immunocytochemical, and lectin probes for several IPM constituents revealed that components of the IPM in the rat undergo a major shift in distribution or molecular conformation after the transition between light and dark. In the light, various IPM constituents concentrated in bands at the apical and basal regions of the outer segment zone; in the dark, they distributed much more uniformly throughout the zone. The change in IPM distribution was triggered by the light-dark transition; it was not a circadian event, and it was not driven by a systemic factor. The light-evoked change in IPM distribution may facilitate the transfer of substances between the photoreceptors and the RPE.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Uehara, F -- Matthes, M T -- Yasumura, D -- LaVail, M M -- EYO1919/EY/NEI NIH HHS/ -- EYO2162/EY/NEI NIH HHS/ -- EYO6842/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 1990 Jun 29;248(4963):1633-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy, University of California, San Francisco 94143.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2194288" target="_blank"〉PubMed〈/a〉
    Keywords: Albinism ; Animals ; Darkness ; Extracellular Matrix/physiology ; *Fluorescein-5-isothiocyanate/*analogs & derivatives ; Fluoresceins ; Glycoconjugates/analysis ; Immunoenzyme Techniques ; Immunohistochemistry ; In Vitro Techniques ; Light ; Photoreceptor Cells/*physiology/radiation effects ; Pigment Epithelium of Eye/cytology/*physiology ; Rats ; Rats, Inbred F344 ; Retina/cytology/*physiology/radiation effects ; Rod Cell Outer Segment/physiology ; Sialic Acids/analysis ; Wheat Germ Agglutinins
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    Inhibition of leishmanias but not host macrophages by the antitubulin herbicide trifluralin (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-08-24
    Description: The dinitroaniline herbicide trifluralin (alpha, alpha, alpha-trifluoro-2,6-dinitro-N, N-dipropyl-p-toluidine), at micromolar concentrations, selectively inhibited both proliferation and differentiation of the parasitic protozoan Leishmania mexicana amazonensis. In vitro, radioactive trifluralin showed specific binding to leishmania tubulin but not to mammalian tubulin. Because herbicides such as trifluralin are economical and are considered safe for man and domesticated animals, they may serve as useful sources of potential antiparasitic agents.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chan, M M -- Fong, D -- AI 21364/AI/NIAID NIH HHS/ -- CA 49359/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1990 Aug 24;249(4971):924-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, Rutgers, State University of New Jersey, Piscataway 08855.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2392684" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Division/drug effects ; Cell Line ; Leishmania mexicana/drug effects/*growth & development ; Macrophages/drug effects/*physiology ; Protein Binding ; Rats ; Species Specificity ; Toluidines/*pharmacology ; Trifluralin/metabolism/*pharmacology ; Tubulin/metabolism ; *Tubulin Modulators ; Tumor Cells, Cultured/cytology/drug effects
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    Cloning and expression of a developmentally regulated protein that induces mitogenic and neurite outgrowth activity (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-12-21
    Description: A heparin binding mitogenic protein isolated from bovine uterus shares NH2-terminal amino acid sequence with a protein isolated from newborn rat brain. The cDNA's of the bovine, human, and rat genes have been isolated and encode extraordinarily conserved proteins unrelated to known growth or neurotrophic factors, although identity of nearly 50 percent has been found with the predicted sequence of a retinoic acid induced transcript in differentiating mouse embryonal carcinoma cells. Lysates of COS-7 cells transiently expressing this protein were mitogenic for NRK cells and initiated neurite outgrowth from mixed cultures of embryonic rat brain cells. RNA transcripts encoding this protein were widely distributed in tissues and were developmentally regulated. This protein, previously designated as heparin binding growth factor (HBGF)-8, is now renamed pleiotrophin (PTN) to reflect its diverse activities. PTN may be the first member of a family of developmentally regulated cytokines.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Y S -- Milner, P G -- Chauhan, A K -- Watson, M A -- Hoffman, R M -- Kodner, C M -- Milbrandt, J -- Deuel, T F -- CA49712/CA/NCI NIH HHS/ -- HL14147/HL/NHLBI NIH HHS/ -- HL31102/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1990 Dec 21;250(4988):1690-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Jewish Hospital, Washington University Medical Center, St. Louis, MO 63110.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2270483" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Axons/*physiology/ultrastructure ; Base Sequence ; Brain/*metabolism ; *Carrier Proteins ; Cattle ; Cell Division ; Cell Line ; Cloning, Molecular ; Cytokines/*genetics ; Humans ; Mitogens/*genetics ; Molecular Sequence Data ; Organ Specificity ; Rats ; Sequence Homology, Nucleic Acid ; Transfection
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    Structural mutations of the T cell receptor zeta chain and its role in T cell activation (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-07-13
    Description: T cell hybridomas that express zeta zeta, but not zeta eta, dimers in their T cell receptors (TCRs) produce interleukin-2 (IL-2) and undergo an inhibition of spontaneous growth when activated by antigen, antibodies to the receptor, or antibodies to Thy-1. Hybridomas without zeta and eta were reconstituted with mutated zeta chains. Cytoplasmic truncations of up to 40% of the zeta molecule reconstituted normal surface assembly of TCRs, but antigen-induced IL-2 secretion and growth inhibition were lost. In contrast, cross-linking antibodies to the TCR activated these cells. A point mutation conferred the same signaling phenotype as did the truncations and caused defective antigen-induced tyrosine kinase activation. Thus zeta allows the binding of antigen/major histocompatibility complex (MHC) to alpha beta to effect TCR signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Frank, S J -- Niklinska, B B -- Orloff, D G -- Mercep, M -- Ashwell, J D -- Klausner, R D -- New York, N.Y. -- Science. 1990 Jul 13;249(4965):174-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cell Biology and Metabolism Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2371564" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cross-Linking Reagents ; Dose-Response Relationship, Immunologic ; Hybridomas ; Immunity, Cellular ; Immunoblotting ; Interleukin-2/*biosynthesis ; Ligands ; *Lymphocyte Activation ; Major Histocompatibility Complex ; Mice ; Molecular Sequence Data ; Mutation ; Peptide Fragments/genetics/*immunology ; Precipitin Tests ; Receptors, Antigen, T-Cell/genetics/*immunology ; Signal Transduction ; T-Lymphocytes/*immunology ; Transfection
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    Fetal brain grafts and Parkinson's disease (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-12-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉New York, N.Y. -- Science. 1990 Dec 7;250(4986):1434-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2255915" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenal Medulla/transplantation ; Animals ; Brain Tissue Transplantation/*physiology ; Disease Models, Animal ; Fetal Tissue Transplantation/*physiology ; Humans ; Parkinson Disease/physiopathology/*surgery ; Rats
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    Chronic fatigue as chameleon (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-09-14
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cherfas, J -- New York, N.Y. -- Science. 1990 Sep 14;249(4974):1240.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2399460" target="_blank"〉PubMed〈/a〉
    Keywords: Fatigue Syndrome, Chronic/*etiology/microbiology/psychology ; Female ; Humans ; Male
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    Cell proliferation in carcinogenesis (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-08-31
    Description: Chemicals that induce cancer at high doses in animal bioassays often fail to fit the traditional characterization of genotoxins. Many of these nongenotoxic compounds (such as sodium saccharin) have in common the property that they increase cell proliferation in the target organ. A biologically based, computerized description of carcinogenesis was used to show that the increase in cell proliferation can account for the carcinogenicity of nongenotoxic compounds. The carcinogenic dose-response relationship for genotoxic chemicals (such as 2-acetylaminofluorene) was also due in part to increased cell proliferation. Mechanistic information is required for determination of the existence of a threshold for the proliferative (and carcinogenic) response of nongenotoxic chemicals and the estimation of risk for human exposure.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, S M -- Ellwein, L B -- CA28015/CA/NCI NIH HHS/ -- CA32513/CA/NCI NIH HHS/ -- CA36727/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1990 Aug 31;249(4972):1007-11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha 68198.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2204108" target="_blank"〉PubMed〈/a〉
    Keywords: 2-Acetylaminofluorene/metabolism/toxicity ; Animals ; Carcinogens/pharmacology/*toxicity ; Cell Division/*drug effects ; Humans ; Liver/metabolism ; Liver Neoplasms/chemically induced ; Mice ; Mitotic Index/drug effects ; Rats ; Saccharin/toxicity ; Urinary Bladder Neoplasms/chemically induced
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    Secretion of neurotoxins by mononuclear phagocytes infected with HIV-1 (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-12-14
    Description: Mononuclear phagocytes (microglia, macrophages, and macrophage-like giant cells) are the principal cellular targets for human immunodeficiency virus-1 (HIV-1) in the central nervous system (CNS). Since HIV-1 does not directly infect neurons, the causes for CNS dysfunction in acquired immunodeficiency syndrome (AIDS) remain uncertain. HIV-1-infected human monocytoid cells, but not infected human lymphoid cells, released toxic agents that destroy chick and rat neurons in culture. These neurotoxins were small, heat-stable, protease-resistant molecules that act by way of N-methyl-D-aspartate receptors. Macrophages and microglia infected with HIV-1 may produce neurologic disease through chronic secretion of neurotoxic factors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Giulian, D -- Vaca, K -- Noonan, C A -- NS 25637/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1990 Dec 14;250(4987):1593-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, Baylor College of Medicine, Houston, TX 77030.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2148832" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Assay ; Cell Line ; Cell Survival/*drug effects ; Chick Embryo ; Culture Media/analysis ; HIV-1/*physiology ; Humans ; Intermediate Filaments ; Lymphocytes/microbiology/physiology ; Macrophages/microbiology/physiology ; Monocytes/microbiology/physiology ; N-Methylaspartate/*analogs & derivatives ; Neuroglia/microbiology/physiology ; Neurons/cytology/drug effects/*physiology ; Phagocytes/microbiology/*physiology ; Rats ; Receptors, N-Methyl-D-Aspartate/*physiology ; Spinal Cord/cytology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Behavioral effects of progesterone associated with rapid modulation of oxytocin receptors (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-11-02
    Description: The ventromedial nuclei of the hypothalamus (VMN) are important for the control of feminine mating behavior, and hormone action within these nuclei has been causally related to behavior. Estradiol induces receptors for oxytocin in the VMN and in the area lateral to these nuclei over the course of 1 to 2 days, and progesterone causes, within 30 minutes of its application, a further increase in receptor binding and an expansion of the area covered by these receptors lateral to the VMN. The rapid progesterone effect appears to be a direct and specific effect of this steroid on the receptor or membrane, because it was produced in vitro as well as in vivo and was not mimicked by a variety of other steroids. The effect of progesterone occurred in the posterior part of the VMN, where oxytocin infusion facilitated feminine mating behavior; it did not take place in the anterior part of the VMN, where oxytocin infusion had no effect on mating behavior.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schumacher, M -- Coirini, H -- Pfaff, D W -- McEwen, B S -- HD-05751/HD/NICHD NIH HHS/ -- NS-07080/NS/NINDS NIH HHS/ -- TWO4103/TW/FIC NIH HHS/ -- New York, N.Y. -- Science. 1990 Nov 2;250(4981):691-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Neuroendocrinology, Rockefeller University, New York, NY 10021.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2173139" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Estradiol/pharmacology ; Female ; Oxytocin/pharmacology ; Progesterone/*pharmacology ; Rats ; Receptors, Angiotensin/*drug effects/metabolism ; Receptors, Oxytocin ; Sexual Behavior, Animal/*drug effects ; Ventromedial Hypothalamic Nucleus/*drug effects
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  • 81
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    Soluble human complement receptor type 1: in vivo inhibitor of complement suppressing post-ischemic myocardial inflammation and necrosis (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-07-13
    Description: The complement system is an important mediator of the acute inflammatory response, and an effective inhibitor would suppress tissue damage in many autoimmune and inflammatory diseases. Such an inhibitor might be found among the endogenous regulatory proteins of complement that block the enzymes that activate C3 and C5. Of these proteins, complement receptor type 1 (CR1; CD35) has the most inhibitory potential, but its restriction to a few cell types limits its function in vivo. This limitation was overcome by the recombinant, soluble human CR1, sCR1, which lacks the transmembrane and cytoplasmic domains. The sCR1 bivalently bound dimeric forms of its ligands, C3b and methylamine-treated C4 (C4-ma), and promoted their inactivation by factor I. In nanomolar concentrations, sCR1 blocked complement activation in human serum by the two pathways. The sCR1 had complement inhibitory and anti-inflammatory activities in a rat model of reperfusion injury of ischemic myocardium, reducing myocardial infarction size by 44 percent. These findings identify sCR1 as a potential agent for the suppression of complement-dependent tissue injury in autoimmune and inflammatory diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weisman, H F -- Bartow, T -- Leppo, M K -- Marsh, H C Jr -- Carson, G R -- Concino, M F -- Boyle, M P -- Roux, K H -- Weisfeldt, M L -- Fearon, D T -- New York, N.Y. -- Science. 1990 Jul 13;249(4965):146-51.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, MD 21205.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2371562" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autoimmune Diseases/*immunology/pathology ; Complement Activation ; Complement C3/antagonists & inhibitors ; Complement C3b Inactivator Proteins/pharmacology ; Complement C4b/antagonists & inhibitors ; Complement C5/antagonists & inhibitors ; Complement Inactivator Proteins/*pharmacology/ultrastructure ; Disease Models, Animal ; Myocardial Reperfusion Injury/*immunology/pathology/prevention & control ; Myocardium/*pathology ; Necrosis ; Rats ; Receptors, Complement/*pharmacology/ultrastructure ; Recombinant Proteins/pharmacology
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  • 82
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    Tapping into nerve conversations (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-05-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Williams, S -- New York, N.Y. -- Science. 1990 May 4;248(4955):555.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2333508" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Electrophysiology/*instrumentation ; Hindlimb/innervation ; Microelectrodes ; Nerve Regeneration ; Neurons/*physiology ; Rats ; Spinal Nerves/*physiology
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  • 83
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    Pseudotypes in HIV-infected mice (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-11-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McCune, J M -- Namikawa, R -- Shih, C C -- Rabin, L -- Kaneshima, H -- New York, N.Y. -- Science. 1990 Nov 23;250(4984):1152-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2174574" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Containment of Biohazards ; *Disease Models, Animal ; HIV/*genetics/pathogenicity ; HIV Infections/*microbiology ; Immunologic Deficiency Syndromes/*microbiology ; Leukemia Virus, Murine/*genetics/physiology ; Mice ; Mice, Mutant Strains ; Phenotype
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  • 84
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    Induction of donor-specific unresponsiveness by intrathymic islet transplantation (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-09-14
    Description: The application of isolated pancreatic islet transplantation for treatment of diabetes mellitus has been hampered by the vulnerability of islet allografts to immunologic rejection. Rat islet allografts that were transplanted into the thymus of recipients treated with a single injection of anti-lymphocyte serum survived indefinitely. A state of donor-specific unresponsiveness was achieved that permitted survival of a second donor strain islet allograft transplanted to an extrathymic site. Maturation of T cell precursors in a thymic microenvironment that is harboring foreign alloantigen may induce the selective unresponsiveness. This model provides an approach for pancreatic islet transplantation and a potential strategy for specific modification of the peripheral immune repertoire.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Posselt, A M -- Barker, C F -- Tomaszewski, J E -- Markmann, J F -- Choti, M A -- Naji, A -- DK26007/DK/NIDDK NIH HHS/ -- DK34878/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1990 Sep 14;249(4974):1293-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Surgery, Hospital of the University of Pennsylvania, Philadelphia 19104.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2119056" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antilymphocyte Serum ; Blood Glucose/metabolism ; Diabetes Mellitus, Experimental/*surgery ; Graft Enhancement, Immunologic ; Immune Tolerance ; *Islets of Langerhans Transplantation ; Rats ; Rats, Inbred Lew ; Rats, Inbred WF ; T-Lymphocytes/immunology ; Thymus Gland/surgery ; Transplantation, Heterotopic
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  • 85
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    Immunobiology and pathogenesis of hepatocellular injury in hepatitis B virus transgenic mice (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-04-20
    Description: The role of the immune response to hepatitis B virus (HBV)-encoded antigens in the pathogenesis of liver cell injury has not been defined because of the absence of appropriate experimental models. HBV envelope transgenic mice were used to show that HBV-encoded antigens are expressed at the hepatocyte surface in a form recognizable by major histocompatibility complex (MHC) class I-restricted, CD8+ cytotoxic T lymphocytes specific for a dominant T cell epitope within the major envelope polypeptide and by envelope-specific antibodies. Both interactions led to the death of the hepatocyte in vivo, providing direct evidence that hepatocellular injury in human HBV infection may also be immunologically mediated.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Moriyama, T -- Guilhot, S -- Klopchin, K -- Moss, B -- Pinkert, C A -- Palmiter, R D -- Brinster, R L -- Kanagawa, O -- Chisari, F V -- CA34635/CA/NCI NIH HHS/ -- CA38635/CA/NCI NIH HHS/ -- CA40489/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1990 Apr 20;248(4953):361-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Research Institute of Scripps Clinic, La Jolla, CA 92037.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1691527" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cell Line, Transformed ; Cytotoxicity, Immunologic ; Epitopes/immunology ; Hepatitis B/*immunology ; Hepatitis B Surface Antigens/genetics/*immunology ; Histocompatibility Antigens Class I/immunology ; Liver/*immunology ; Mice ; Mice, Transgenic ; Molecular Sequence Data ; Simian virus 40 ; T-Lymphocytes, Cytotoxic/immunology ; T-Lymphocytes, Regulatory/immunology ; Transfection
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  • 86
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    A dominant mutation that predisposes to multiple intestinal neoplasia in the mouse (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-01-19
    Description: In a pedigree derived from a mouse treated with the mutagen ethylnitrosourea, a mutation has been identified that predisposes to spontaneous intestinal cancer. The mutant gene was found to be dominantly expressed and fully penetrant. Affected mice developed multiple adenomas throughout the entire intestinal tract at an early age.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Moser, A R -- Pitot, H C -- Dove, W F -- CA07175/CA/NCI NIH HHS/ -- CA50585/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1990 Jan 19;247(4940):322-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉McArdle Laboratory for Cancer Research, University of Wisconsin-Madison 53706.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2296722" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoma/complications/*genetics ; Alleles ; Anemia/complications/genetics ; Animals ; Ethylnitrosourea ; Female ; Intestinal Neoplasms/complications/*genetics/pathology ; Male ; Mice ; Mice, Inbred AKR ; Mice, Inbred C57BL ; Mice, Mutant Strains ; *Mutation
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    BEIR V: implications for the nuclear workforce (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-02-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉New York, N.Y. -- Science. 1990 Feb 9;247(4943):620-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2300818" target="_blank"〉PubMed〈/a〉
    Keywords: Female ; Humans ; Male ; Neoplasms, Radiation-Induced/*epidemiology ; Occupational Diseases/*epidemiology ; Radiation Injuries/*epidemiology ; Risk Factors
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  • 88
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    Solution structure of the glucocorticoid receptor DNA-binding domain (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-07-13
    Description: The three-dimensional structure of the DNA-binding domain (DBD) of the glucocorticoid receptor has been determined by nuclear magnetic resonance spectroscopy and distance geometry. The structure of a 71-residue protein fragment containing two "zinc finger" domains is based on a large set of proton-proton distances derived from nuclear Overhauser enhancement spectra, hydrogen bonds in previously identified secondary structure elements, and coordination of two zinc atoms by conserved cysteine residues. The DBD is found to consist of a globular body from which the finger regions extend. A model of the dimeric complex between the DBD and the glucocorticoid response element is proposed. The model is consistent with previous results indicating that specific amino acid residues of the DBD are involved in protein-DNA and protein-protein interactions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hard, T -- Kellenbach, E -- Boelens, R -- Maler, B A -- Dahlman, K -- Freedman, L P -- Carlstedt-Duke, J -- Yamamoto, K R -- Gustafsson, J A -- Kaptein, R -- New York, N.Y. -- Science. 1990 Jul 13;249(4965):157-60.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry, University of Utrecht, The Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2115209" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; DNA/*metabolism ; DNA-Binding Proteins/analysis/*metabolism ; Humans ; Magnetic Resonance Spectroscopy ; Metalloproteins/analysis ; Models, Molecular ; Molecular Sequence Data ; Peptide Fragments/analysis/metabolism ; Protein Conformation ; Rats ; Receptors, Glucocorticoid/*analysis/metabolism ; Regulatory Sequences, Nucleic Acid ; Zinc/analysis
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  • 89
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    Suppression of tumorigenicity of human prostate carcinoma cells by replacing a mutated RB gene (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-02-09
    Description: Introduction of a normal retinoblastoma gene (RB) into retinoblastoma cells was previously shown to suppress several aspects of their neoplastic phenotype, including tumorigenicity in nude mice, thereby directly demonstrating a cancer suppression function of RB. To explore the possibility of a similar activity in a common adult tumor, RB expression was examined in three human prostate carcinoma cell lines. One of these, DU145, contained an abnormally small protein translated from an RB messenger RNA transcript that lacked 105 nucleotides encoded by exon 21. To assess the functional consequences of this mutation, normal RB expression was restored in DU145 cells by retrovirus-mediated gene transfer. Cells that maintained stable exogenous RB expression lost their ability to form tumors in nude mice, although their growth rate in culture was apparently unaltered. These results suggest that RB inactivation can play a significant role in the genesis of a common adult neoplasm and that restoration of normal RB-encoded protein in tumors could have clinical utility.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bookstein, R -- Shew, J Y -- Chen, P L -- Scully, P -- Lee, W H -- 5758/PHS HHS/ -- New York, N.Y. -- Science. 1990 Feb 9;247(4943):712-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, School of Medicine, University of California, San Diego, La Jolla 92093.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2300823" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; DNA/genetics ; Gene Amplification ; Gene Expression ; Humans ; Male ; Mice ; Mice, Nude ; Molecular Sequence Data ; Mutation ; Nucleic Acid Hybridization ; Prostatic Neoplasms/*genetics/pathology ; RNA, Messenger/genetics ; Retinoblastoma/*genetics ; *Suppression, Genetic ; Transfection ; Tumor Cells, Cultured
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  • 90
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    Transport protein genes in the murine MHC: possible implications for antigen processing (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-12-21
    Description: T lymphocyte activation requires recognition by the T cell of peptide fragments of foreign antigen bound to a self major histocompatibility complex (MHC) molecule. Genetic evidence suggests that part of the class II region of the MHC influences the expression, in trans, of MHC class I antigens on the cell surface, by regulating the availability of peptides that bind to and stabilize the class I molecule. Two closely related genes in this region, HAM1 and HAM2, were cloned and had sequence similarities to a superfamily of genes involved in the ATP-dependent transport of a variety of substrates across cell membranes. Thus, these MHC-linked transport protein genes may be involved in transporting antigen, or peptide fragments thereof, from the cytoplasm into a membrane-bounded compartment containing newly synthesized MHC molecules.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Monaco, J J -- Cho, S -- Attaya, M -- GM38774/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1990 Dec 21;250(4988):1723-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, Medical College of Virginia/Virginia Commonwealth University, Richmond 23298-0678.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2270487" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Carrier Proteins/*genetics ; Cell Line ; Cloning, Molecular ; *Major Histocompatibility Complex ; Mice ; Molecular Sequence Data ; *Multigene Family ; Protein Conformation ; Sequence Homology, Nucleic Acid ; T-Lymphocytes/*immunology
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  • 91
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    Recognition of a peptide antigen by heat shock--reactive gamma delta T lymphocytes (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-07-06
    Description: Small synthetic peptides that correspond to different portions of the 65-kilodalton mycobacterial heat shock protein (Hsp65) were used to identify a putative antigenic epitope for gamma delta cells. Weaker gamma delta responses to the equivalent portion of the autologous homolog, mouse Hsp63, were also seen. The stimulatory epitope overlaps with an epitope recognized by arthritogenic alpha beta T cell clones. The data suggest that gamma delta cells have a role in autoimmune disorders and imply that these cells recognize ligands by a mechanism similar to that of alpha beta T lymphocytes, that is, in the form of small processed protein fragments bound to antigen-presenting molecules.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Born, W -- Hall, L -- Dallas, A -- Boymel, J -- Shinnick, T -- Young, D -- Brennan, P -- O'Brien, R -- New York, N.Y. -- Science. 1990 Jul 6;249(4964):67-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, University of Colorado Health Sciences Center, Denver.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1695022" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antigen-Presenting Cells/immunology ; Cross Reactions ; Epitopes/*analysis ; Heat-Shock Proteins/*immunology ; Hybridomas ; Ligands ; Mice ; Molecular Sequence Data ; Mycobacterium/immunology ; Peptide Fragments/*immunology ; T-Lymphocytes/*immunology
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  • 92
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    Shared actions of endotoxin and taxol on TNF receptors and TNF release (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-04-20
    Description: Bacterial lipopolysaccharide (LPS) exerts profound effects on mammalian hosts in part by inducing macrophages to release tumor necrosis factor-alpha (TNF-alpha); the mechanisms involved are unresolved. The microtubule stabilizer taxol shared two actions of LPS on macrophages: it rapidly decreased TNF-alpha receptors and triggered TNF-alpha release. Both actions of taxol were absent in LPS-hyporesponsive C3H/HeJ mice. In recombinant inbred mice, the genes controlling responses to LPS and to taxol were closely linked. Dexamethasone blocked release of TNF-alpha by both stimuli but did not block the decrease in TNF-alpha receptors. Thus, a protein associated with microtubules may be a cellular target of LPS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ding, A H -- Porteu, F -- Sanchez, E -- Nathan, C F -- CA-43610/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1990 Apr 20;248(4953):370-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Cornell University Medical College, New York, NY 10021.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1970196" target="_blank"〉PubMed〈/a〉
    Keywords: Alkaloids/*pharmacology ; Animals ; Crosses, Genetic ; Dexamethasone/pharmacology ; Lipopolysaccharides/*pharmacology ; Macrophages/*drug effects/metabolism ; Mice ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Mice, Mutant Strains ; Paclitaxel ; Receptors, Cell Surface/*drug effects/metabolism ; Receptors, Tumor Necrosis Factor ; Tumor Necrosis Factor-alpha/*metabolism
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    Activin-binding protein from rat ovary is follistatin (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-02-16
    Description: Activin, a member of the transforming growth factor beta protein family, was originally isolated from gonadal fluids and stimulates the release of pituitary follicle-stimulating hormone (FSH). Activin has numerous functions in both normal and neoplastic cells. Various cells synthesize activin and have a specific binding site for this peptide. However, the molecular basis for its actions is unknown. A binding protein for activin was purified from rat ovary and was identical to follistatin, a specific inhibitor of FSH release. It is likely that the binding protein participates in the diverse regulatory actions of activin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nakamura, T -- Takio, K -- Eto, Y -- Shibai, H -- Titani, K -- Sugino, H -- New York, N.Y. -- Science. 1990 Feb 16;247(4944):836-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Frontier Research Program, Institute of Physical and Chemical Research (RIKEN), Saitama, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2106159" target="_blank"〉PubMed〈/a〉
    Keywords: Activins ; Animals ; *Carrier Proteins ; Cells, Cultured ; Female ; Follicle Stimulating Hormone/secretion ; Inhibins/isolation & purification/*metabolism/pharmacology ; Kinetics ; Molecular Weight ; Ovary/*metabolism ; Pituitary Gland/drug effects/secretion ; Protein Binding ; Rats
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 94
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    Inhibition of T cell receptor expression and function in immature CD4+CD8+ cells by CD4 (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-09-28
    Description: Most immature CD4+CD8+ thymocytes express only a small number of T cell receptor (TCR) molecules on their surface, and the TCR molecules they do express are only marginally capable of transducing intracellular signals. TCR expression and function was not intrinsically low in immature CD4+CD8+ thymocytes, but was found to be actively inhibited by CD4-mediated signals. Indeed, release of CD4+CD8+ thymocytes from CD4-mediated signals resulted in significant increases in both TCR expression and signaling function. These results suggest that, in CD4+CD8+ cells developing in the thymus, increased TCR expression and function requires release from CD4-mediated inhibition.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nakayama, T -- June, C H -- Munitz, T I -- Sheard, M -- McCarthy, S A -- Sharrow, S O -- Samelson, L E -- Singer, A -- New York, N.Y. -- Science. 1990 Sep 28;249(4976):1558-61.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Experimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2120773" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/immunology ; Antigens, CD4/*immunology ; Antigens, CD8 ; Antigens, Differentiation, T-Lymphocyte/*immunology ; Cell Membrane/immunology ; Cells, Cultured ; Histocompatibility Antigens Class II/immunology ; Mice ; Mice, Inbred C57BL ; Receptors, Antigen, T-Cell/biosynthesis/*physiology ; T-Lymphocytes/*immunology
    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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  • 95
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    Regulation of alloreactivity in vivo by a soluble form of the interleukin-1 receptor (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-05-11
    Description: In vitro studies have shown that cytokines are involved in the regulation of the immune response, but their role in vivo is less well defined. Specific cytokine antagonists enable the identification of particular cytokines involved in the response and offer a means for modifying it. Systemic administration of a soluble, extracellular portion of the receptor for interleukin-1 (sIL-1R) had profound inhibitory effects on the development of in vivo alloreactivity. Survival of heterotopic heart allografts was prolonged from 12 days in controls to 17 days in mice treated with sIL-1R. Lymph node hyperplasia in response to a localized injection of allogeneic cells was completely blocked by sIL-1R treatment. The inhibition was overcome by simultaneous administration of interleukin-1 (IL-1); thus, sIL-1R acts by neutralizing IL-1. These results implicate IL-1 as a regulator of allograft rejection and demonstrate the in vivo biological efficacy of a soluble cytokine receptor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fanslow, W C -- Sims, J E -- Sassenfeld, H -- Morrissey, P J -- Gillis, S -- Dower, S K -- Widmer, M B -- New York, N.Y. -- Science. 1990 May 11;248(4956):739-42.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immunex Corporation, Seattle, WA 98101.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2139736" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Graft Rejection ; *Graft Survival ; H-2 Antigens/immunology ; Heart Transplantation/*immunology ; Immunosuppression ; Interleukin-1/*immunology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Receptors, Antigen, T-Cell/immunology ; Receptors, Immunologic/*immunology ; Receptors, Interleukin-1 ; Transplantation, Heterotopic ; Transplantation, Homologous
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 96
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    Protection of mice against the Lyme disease agent by immunizing with recombinant OspA (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-10-26
    Description: Lyme borreliosis is a tick-borne illness caused by Borrelia burgdorferi. The gene for outer surface protein A (OspA) from B. burgdorferi strain N40 was cloned into an expression vector and expressed in Escherichia coli. C3H/HeJ mice actively immunized with live transformed E. coli or purified recombinant OspA protein produced antibodies to OspA and were protected from challenge with several strains of B. burgdorferi. Recombinant OspA is a candidate for a vaccine for Lyme borreliosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fikrig, E -- Barthold, S W -- Kantor, F S -- Flavell, R A -- AI 26815/AI/NIAID NIH HHS/ -- DK-07476/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1990 Oct 26;250(4980):553-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Immunobiology, 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/2237407" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Bacterial/immunology ; Bacterial Outer Membrane Proteins/genetics/*immunology ; Borrelia burgdorferi Group/*immunology ; Cloning, Molecular ; Escherichia coli/genetics/immunology ; Glutathione Transferase ; *Immunization ; Lyme Disease/*prevention & control ; Mice ; Mice, Inbred C3H ; Recombinant Fusion Proteins/immunology ; Recombinant Proteins/immunology ; Transformation, Bacterial ; *Vaccines, Synthetic
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 97
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    Phosphorylation of the polymeric immunoglobulin receptor required for its efficient transcytosis (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-05-11
    Description: The endosomal compartment of polarized epithelial cells is a major crossroads for membrane traffic. Proteins entering this compartment from the cell surface are sorted for transport to one of several destinations: recycling to the original cell surface, targeting to lysosomes for degradation, or transcytosis to the opposite surface. The polymeric immunoglobulin receptor (pIgR), which is normally transcytosed from the basolateral to the apical surface, was used as a model to dissect the signals that mediate this sorting event. When exogenous receptor was expressed in Madin-Darby Canine Kidney (MDCK) cells, it was shown that phosphorylation of pIgR at the serine residue at position 664 is required for efficient transcytosis. Replacement of this serine with alanine generated a receptor that is transcytosed only slowly, and appears to be recycled. Conversely, substitution with aspartic acid (which mimics the negative charge of the phosphate group) results in rapid transcytosis. It was concluded that phosphorylation is the signal that directs the pIgR from the endosome into the transcytotic pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Casanova, J E -- Breitfeld, P P -- Ross, S A -- Mostov, K E -- R01-AI-25144/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1990 May 11;248(4956):742-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy, University of California, San Francisco 94143.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2110383" target="_blank"〉PubMed〈/a〉
    Keywords: Alanine ; Animals ; Aspartic Acid ; Cell Line ; Cell Membrane/immunology/metabolism ; Endocytosis ; Immunoglobulin A/metabolism ; Kinetics ; Ligands ; Membrane Glycoproteins/metabolism ; Molecular Weight ; Mutation ; Phosphorylation ; Rats ; Receptors, Immunologic ; Secretory Component/genetics/*metabolism ; Serine
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 98
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    A promoter that drives transgene expression in cerebellar Purkinje and retinal bipolar neurons (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-04-13
    Description: A genomic clone encoding the Purkinje cell-specific L7 protein has been isolated and utilized to drive the expression of beta-galactosidase in mice. Three independent transgenic lines, germ line transformed with an L7-beta-galactosidase fusion gene, exhibit beta-galactosidase expression in both cerebellar Purkinje cells and retinal bipolar neurons. This distribution is the same as that previously determined for the L7 protein by immunohistochemistry. The transgenic murine lines can be used to obtain populations of marked Purkinje and bipolar neurons. Similar L7 promoter constructs can be used to express other foreign genes specifically in these two classes of neurons.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Oberdick, J -- Smeyne, R J -- Mann, J R -- Zackson, S -- Morgan, J I -- 1 F32 NS 08680-01/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1990 Apr 13;248(4952):223-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, Roche Research Center, Nutley, NJ 07110.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2109351" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cerebellum/metabolism ; Cloning, Molecular ; Crosses, Genetic ; Galactosidases/*genetics ; *Gene Expression ; Gene Library ; Mice ; Mice, Transgenic ; Nerve Tissue Proteins/analysis/*genetics ; *Promoter Regions, Genetic ; Purkinje Cells/*metabolism ; Recombinant Fusion Proteins/analysis ; Restriction Mapping ; Retina/*metabolism ; Retinal Ganglion Cells/*metabolism ; beta-Galactosidase/analysis/*genetics
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 99
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    Amyloid beta protein precursor gene and hereditary cerebral hemorrhage with amyloidosis (Dutch) (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-06-01
    Description: Human hereditary cerebral hemorrhage with amyloidosis of the Dutch type (HCHWA-D), an autosomal dominant form of cerebral amyloid angiopathy (CAA), is characterized by extensive amyloid deposition in the small leptomeningeal arteries and cortical arterioles, which lead to an early death of those afflicted in their fifth or sixth decade. Immunohistochemical and biochemical studies have indicated that the amyloid subunit in HCHWA-D is antigenically related to and homologous in sequence with the amyloid beta protein isolated from brains of patients with Alzheimer's disease and Down syndrome. The amyloid beta protein is encoded by the amyloid beta protein precursor (APP) gene located on chromosome 21. Restriction fragment length polymorphisms detected by the APP gene were used to examine whether this gene is a candidate for the genetic defect in HCHWA-D. The data indicate that the APP gene is tightly linked to HCHWA-D and therefore, in contrast to familial Alzheimer's disease, cannot be excluded as the site of mutation in HCHWA-D.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Van Broeckhoven, C -- Haan, J -- Bakker, E -- Hardy, J A -- Van Hul, W -- Wehnert, A -- Vegter-Van der Vlis, M -- Roos, R A -- New York, N.Y. -- Science. 1990 Jun 1;248(4959):1120-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Born Bunge Foundation, Department of Biochemistry, University of Antwerp, Belgium.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1971458" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aged ; Amyloid/*genetics ; Amyloid beta-Protein Precursor ; Amyloidosis/complications/*genetics ; Cerebral Hemorrhage/etiology/*genetics ; Cerebrovascular Disorders/complications/*genetics ; Female ; Genes, Dominant ; Genetic Linkage ; Humans ; Lod Score ; Male ; Middle Aged ; Netherlands ; Pedigree ; Polymorphism, Restriction Fragment Length ; Protein Precursors/*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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  • 100
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    A family of three mouse potassium channel genes with intronless coding regions (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-02-23
    Description: To understand the molecular mechanisms responsible for generating physiologically diverse potassium channels in mammalian cells, mouse genomic clones have been isolated with a potassium channel complementary DNA, MBK1, that is homologous to the Drosophila potassium channel gene, Shaker. A family of three closely related potassium channel genes (MK1, MK2, and MK3) that are encoded at distinct genomic loci has been isolated. Sequence analysis reveals that the coding region of each of these three genes exists as a single uninterrupted exon in the mouse genome. This organization precludes the generation of multiple forms of the protein by alternative RNA splicing, a mechanism known to characterize the Drosophila potassium channel genes Shaker and Shab. Thus, mammals may use a different strategy for generating diverse K+ channels by encoding related genes at multiple distinct genomic loci, each of which produces only a single protein.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chandy, K G -- Williams, C B -- Spencer, R H -- Aguilar, B A -- Ghanshani, S -- Tempel, B L -- Gutman, G A -- AI21366/AI/NIAID NIH HHS/ -- AI24783/AI/NIAID NIH HHS/ -- NS27206/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1990 Feb 23;247(4945):973-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of California, Irvine 92717.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2305265" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; DNA/genetics ; DNA Probes ; Drosophila/genetics ; Exons ; *Introns ; Mice ; Mice, Inbred BALB C ; Molecular Sequence Data ; Nucleic Acid Hybridization ; *Potassium Channels ; Restriction Mapping
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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