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  • Mice  (430)
  • American Association for the Advancement of Science (AAAS)  (430)
  • American Physical Society
  • Annual Reviews
  • Cambridge University Press
  • Oxford University Press
  • 2005-2009
  • 1990-1994  (236)
  • 1980-1984  (194)
  • 1993  (137)
  • 1990  (99)
  • 1983  (111)
  • 1980  (83)
Collection
Keywords
Publisher
  • American Association for the Advancement of Science (AAAS)  (430)
  • American Physical Society
  • Annual Reviews
  • Cambridge University Press
  • Oxford University Press
    • +
Years
  • 2005-2009
  • 1990-1994  (236)
  • 1980-1984  (194)
Year
  • 1
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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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  • 2
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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
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    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
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    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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  • 5
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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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  • 6
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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
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  • 7
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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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
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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
    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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    "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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
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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
    Print ISSN: 0036-8075
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  • 11
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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
    Print ISSN: 0036-8075
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  • 12
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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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  • 13
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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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  • 14
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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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 15
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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)
    Details
    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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 16
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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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 17
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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)
    Details
    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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  • 18
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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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  • 19
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    Human sickle hemoglobin in transgenic mice (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    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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  • 20
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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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  • 21
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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)
    Details
    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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 22
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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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  • 23
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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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  • 24
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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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  • 25
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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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    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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    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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    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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    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)
    Details
    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)
    Details
    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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    Tumor resistance to alkylating agents conferred by mechanisms operative only in vivo (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    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)
    Details
    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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    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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  • 40
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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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  • 41
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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)
    Details
    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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  • 42
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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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  • 43
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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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  • 44
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    Pseudotypes in HIV-infected mice (1990)
    American Association for the Advancement of Science (AAAS)
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    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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  • 45
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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)
    Details
    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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  • 46
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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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  • 47
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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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  • 48
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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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  • 49
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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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  • 50
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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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  • 51
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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)
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    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
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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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    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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  • 54
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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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    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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    Self-nonself discrimination by T cells (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-06-15
    Description: The alpha beta T cell receptor (TCR) recognizes antigens that are presented by major histocompatibility complex (MHC)-encoded cell surface molecules by binding to both the antigen and the MHC molecules. Discrimination of self from nonself antigens and MHC molecules is achieved by negative and positive selection of T cells in the thymus: potentially harmful T cells with receptors that bind to self antigens plus self MHC molecules are deleted before they can mount immune responses. In contrast, the maturation of useful T cells with receptors that bind foreign antigens plus self MHC molecules requires the binding of their receptor to MHC molecules on thymic epithelium in the absence of foreign antigen. The binding of the TCR to either class I or class II MHC molecules directs differentiation of the selected cells into either CD4-8+ (killer) or CD4+8- (helper) T cells, respectively.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉von Boehmer, H -- Kisielow, P -- New York, N.Y. -- Science. 1990 Jun 15;248(4961):1369-73.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Basel Institute for Immunology, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1972594" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CD4-Positive T-Lymphocytes/immunology ; Cell Differentiation ; Cell Survival ; Female ; H-2 Antigens/immunology ; Histocompatibility Antigens/immunology ; *Immune Tolerance ; Killer Cells, Natural/immunology ; Male ; Mice ; Mice, Transgenic ; Phenotype ; Receptors, Antigen, T-Cell/genetics/immunology ; T-Lymphocytes/*immunology ; T-Lymphocytes, Helper-Inducer/immunology ; T-Lymphocytes, Regulatory/immunology
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  • 57
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    Activation of polyphosphoinositide hydrolysis in T cells by H-2 alloantigen but not MLS determinants (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-07-13
    Description: Murine minor lymphocyte-stimulating (Mls) determinants are cell surface antigens that stimulate strong primary T cell responses; the responding T cells display restricted T cell receptor (TCR) V beta gene usage. Interaction of T cells with mitogens or major histocompatibility complex (MHC) antigens activated the polyphosphoinositide (PI) signaling pathway, but this pathway was not triggered by Mls recognition. However, interleukin-2 (IL-2) secretion and proliferation to all three stimuli were comparable. Thus, although recognition of both allo-H-2 and Mls determinants is thought to be mediated by the TCR, these antigens appear to elicit biochemically distinct signal transduction pathways.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉O'Rourke, A M -- Mescher, M F -- Webb, S R -- New York, N.Y. -- Science. 1990 Jul 13;249(4965):171-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Membrane Biology, Medical Biology Institute, La Jolla, CA 92037.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2164711" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Surface/*immunology ; H-2 Antigens/*immunology ; Hybridomas ; Hydrolysis ; Lymphocyte Activation ; Mice ; Mice, Inbred AKR ; Mice, Inbred CBA ; Minor Lymphocyte Stimulatory Antigens ; Phosphatidylinositols/*metabolism ; Receptors, Antigen, T-Cell/genetics/immunology ; Signal Transduction ; T-Lymphocytes/*metabolism
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    Type 1 neurofibromatosis gene: identification of a large transcript disrupted in three NF1 patients (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-07-13
    Description: Von Recklinghausen neurofibromatosis (NF1) is a common autosomal dominant disorder characterized by abnormalities in multiple tissues derived from the neural crest. No reliable cellular phenotypic marker has been identified, which has hampered direct efforts to identify the gene. The chromosome location of the NF1 gene has been previously mapped genetically to 17q11.2, and data from two NF1 patients with balanced translocations in this region have further narrowed the candidate interval. The use of chromosome jumping and yeast artificial chromosome technology has now led to the identification of a large (approximately 13 kilobases) ubiquitously expressed transcript (denoted NF1LT) from this region that is definitely interrupted by one and most likely by both translocations. Previously identified candidate genes, which failed to show abnormalities in NF1 patients, are apparently located within introns of NF1LT, on the antisense strand. A new mutation patient with NF1 has been identified with a de novo 0.5-kilobase insertion in the NF1LT gene. These observations, together with the high spontaneous mutation rate of NF1 (which is consistent with a large locus), suggest that NF1LT represents the elusive NF1 gene.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wallace, M R -- Marchuk, D A -- Andersen, L B -- Letcher, R -- Odeh, H M -- Saulino, A M -- Fountain, J W -- Brereton, A -- Nicholson, J -- Mitchell, A L -- NS23410/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1990 Jul 13;249(4965):181-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Ann Arbor, MI.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2134734" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Amino Acid Sequence ; Animals ; Base Sequence ; Blotting, Northern ; Blotting, Southern ; Cell Line ; Cloning, Molecular ; DNA, Neoplasm/genetics ; Gene Expression Regulation, Neoplastic ; Humans ; Hybrid Cells ; Male ; Mice ; Molecular Sequence Data ; Mutation ; Neurofibromatosis 1/*genetics ; Protein Biosynthesis ; RNA, Neoplasm/*genetics ; Transcription, Genetic ; *Translocation, Genetic ; Tumor Cells, Cultured
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    Peripheral clonal elimination of functional T cells (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-12-21
    Description: A major mechanism for generating tolerance in developing T cells is the intrathymic clonal deletion of T cells that have receptors for those self antigens that are presented on hematopoietic cells. The mechanisms of tolerance induction to antigens not expressed in the thymus remain unclear. Tolerance to self antigens can be generated extrathymically through the induction of clonal nonresponsiveness in T cells with self-reactive receptors. A second mechanism of extrathymic tolerance was identified: clonal elimination of mature T cells with self-reactive receptors that had previously displayed functional reactivity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jones, L A -- Chin, L T -- Longo, D L -- Kruisbeek, A M -- New York, N.Y. -- Science. 1990 Dec 21;250(4988):1726-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Biological Response Modifiers Program, 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/2125368" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/immunology ; Antigens, CD4/analysis ; Antigens, CD8 ; Antigens, Differentiation, T-Lymphocyte/analysis ; Clone Cells ; *Immune Tolerance ; Kinetics ; *Lymphocyte Depletion ; Mice ; Mice, Inbred DBA ; Mice, Inbred Strains ; Spleen/immunology ; T-Lymphocytes/cytology/*immunology ; Thymus Gland/immunology
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    The staphylococcal enterotoxins and their relatives (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-05-11
    Description: Staphylococcal enterotoxins and a group of related proteins made by Streptococci cause food poisoning and shock in man and animals. These proteins share an ability to bind to human and mouse major histocompatibility complex proteins. The complex ligand so formed has specificity for a particular part of T cell receptors, V beta, and by engaging V beta can stimulate many T cells. It is likely that some or all of the pathological effects of these toxins are caused by their ability to activate quickly so many T cells. It is also possible that encounters with such toxins have caused mice, at least, to evolve mechanisms for varying their T cell V beta repertoires, such that they are less susceptible to attack by the toxins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marrack, P -- Kappler, J -- New York, N.Y. -- Science. 1990 May 11;248(4956):705-11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Medicine, Denver, CO.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2185544" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Enterotoxins/genetics/*immunology ; Histocompatibility Antigens Class II/immunology ; Humans ; Mice ; Molecular Sequence Data ; Staphylococcus/*immunology/pathogenicity ; T-Lymphocytes/*immunology
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    Limit of T cell tolerance to self proteins by peptide presentation (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-03-30
    Description: Cytotoxic T lymphocytes (CTLs) recognize foreign peptides bound to major histocompatibility complex (MHC) class I molecules. MHC molecules can also bind endogenous self peptides, to which T cells are tolerant. Normal mice contained CTLs specific for self peptides that were from proteins of ubiquitous or tissue-restricted expression. In vivo, these endogenous self peptides are not naturally presented in sufficient density by somatic cells expressing MHC class I molecules. They can, however, be presented if added exogenously. Thus, our data imply that CTLs are only tolerant of those endogenous self peptide sequences that are presented by MHC class I-positive cells in a physiological manner.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schild, H -- Rotzschke, O -- Kalbacher, H -- Rammensee, H G -- New York, N.Y. -- Science. 1990 Mar 30;247(4950):1587-9.〈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/2321019" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autoimmunity ; Cell Line ; Histocompatibility Antigens Class I/*immunology ; *Major Histocompatibility Complex ; Mice ; Mice, Inbred C57BL ; Peptide Fragments/*immunology ; T-Lymphocytes, Cytotoxic/*immunology
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    Inhibition of factor VIIa-tissue factor coagulation activity by a hybrid protein (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-06-25
    Description: Lipoprotein-associated coagulation inhibitor (LACI) appears to inhibit tissue factor (TF)-induced blood coagulation by forming a quaternary inhibitory complex containing factor Xa, LACI, factor VIIa, and TF. A genetically engineered hybrid protein consisting of the light chain of factor Xa and the first Kunitz-type inhibitor domain of LACI is shown to directly inhibit the activity of the factor VIIa-TF catalytic complex. Unlike inhibition of factor VIIa-TF activity by native LACI, inhibition by the hybrid protein is not dependent on factor Xa. In an assay of TF-induced coagulation, 50% TF inhibition occurs with hybrid protein at 35 nanograms per milliliter, whereas LACI at 2.5 micrograms per milliliter is required for an equivalent effect. gamma-Carboxylation of glutamic acid residues in the factor Xa light chain portion of the hybrid protein is required for inhibitory activity, indicating that the first Kunitz-type domain of LACI alone is not sufficient for inhibition of factor VIIa-TF.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Girard, T J -- MacPhail, L A -- Likert, K M -- Novotny, W F -- Miletich, J P -- Broze, G J Jr -- New York, N.Y. -- Science. 1990 Jun 15;248(4961):1421-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Hematology/Oncology, 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/1972598" target="_blank"〉PubMed〈/a〉
    Keywords: 1-Carboxyglutamic Acid/metabolism ; Amino Acid Sequence ; Animals ; Binding Sites ; Calcium/metabolism ; Cell Line ; Cloning, Molecular ; Factor VII/antagonists & inhibitors/metabolism/*pharmacology ; Factor VIIa/*antagonists & inhibitors/metabolism ; Factor Xa/metabolism/*pharmacology ; Fibroblasts/metabolism ; Glutamates/metabolism ; Glutamic Acid ; Lipoproteins/metabolism/*pharmacology ; Mice ; Molecular Sequence Data ; Papillomaviridae ; Protease Inhibitors/*pharmacology ; Protein Sorting Signals ; Recombinant Fusion Proteins/*pharmacology ; Thromboplastin/antagonists & inhibitors/metabolism/*pharmacology ; Transfection
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  • 63
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    Induction of neonatal tolerance to Mlsa antigens by CD8+ T cells (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-06-29
    Description: Antigen-specific tolerance of T cells to minor lymphocyte stimulatory (Mls) antigens can be induced in mice by neonatal injection of foreign lymphohematopoietic cells. Although immune responses to Mlsa antigens are controlled by B cells, CD8+ T cells were the most effective cell type for induction of Mlsa tolerance. Tolerance was evident in both thymus and lymph nodes and could be induced by as few as 2 x 10(4) CD8+ T cells; these cells were 50 to 100 times as potent as CD4+ cells or B cells in causing functional tolerance and deletion of V beta 6+ T cells. Thus, intrathymic contact with antigens expressed on CD8+ T cells may play an important role in controlling the normal development of tolerance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Webb, S R -- Sprent, J -- CA 25803/CA/NCI NIH HHS/ -- CA 38355/CA/NCI NIH HHS/ -- CA 41993/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1990 Jun 29;248(4963):1643-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Research Institute of Scripps Clinic, La Jolla 92037.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1973003" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Antigens, CD8 ; Antigens, Differentiation, T-Lymphocyte/*immunology ; Antigens, Surface/*immunology ; B-Lymphocytes/immunology ; Hematopoietic Stem Cell Transplantation ; Hematopoietic Stem Cells/immunology ; *Immune Tolerance ; Lymphocyte Depletion ; Mice ; Mice, Inbred Strains ; Minor Lymphocyte Stimulatory Antigens ; Receptors, Antigen, T-Cell/immunology ; Spleen/immunology ; T-Lymphocytes/*immunology
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    The calcium channel blocker nifedipine attenuates slow excitatory amino acid neurotoxicity (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-03-23
    Description: High concentrations of potent N-methyl-D-aspartate (NMDA) agonists can trigger degeneration of cultured mouse cortical neurons after an exposure of only a few minutes; in contrast, selective non-NMDA agonists or low levels of NMDA agonists require exposures of several hours to induce comparable damage. The dihydropyridine calcium channel antagonist nifedipine was used to test whether this slow neurotoxicity is mediated by a calcium influx through voltage-gated channels. Nifedipine had little effect on the widespread neuronal degeneration induced by brief exposure to high concentrations of NMDA but substantially attenuated the neurotoxicity produced by 24-hour exposure to submaximal concentrations of alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate, kainate, or quinolinate. Calcium ion influx through dihydropyridine-sensitive, voltage-dependent calcium channels may be an important step in the neuronal injury induced by the prolonged activation of NMDA or non-NMDA glutamate receptors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weiss, J H -- Hartley, D M -- Koh, J -- Choi, D W -- MH09823/MH/NIMH NIH HHS/ -- NS12151/NS/NINDS NIH HHS/ -- NS26907/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1990 Mar 23;247(4949 Pt 1):1474-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology and Neurological Sciences, Stanford University Medical School, CA 94305.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2157282" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aspartic Acid/*analogs & derivatives/toxicity ; Calcium Channels/*drug effects ; Drug Antagonism ; Ibotenic Acid/analogs & derivatives/toxicity ; In Vitro Techniques ; Ion Channel Gating ; Kainic Acid/toxicity ; Mice ; N-Methylaspartate ; Neurons/*drug effects/metabolism ; Nifedipine/*pharmacology ; Quinolinic Acid ; Quinolinic Acids/toxicity ; Receptors, Glutamate ; Receptors, N-Methyl-D-Aspartate ; Receptors, Neurotransmitter/*drug effects ; alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Human brain disease recreated in mice (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-12-14
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J -- New York, N.Y. -- Science. 1990 Dec 14;250(4987):1509-10.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2274781" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain Diseases/*genetics/microbiology ; Creutzfeldt-Jakob Syndrome/*genetics/microbiology ; Gerstmann-Straussler-Scheinker Disease/*genetics/*microbiology ; Humans ; Mice ; Mice, Transgenic ; Mutation ; Prions/*genetics ; Transfection
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    Animal carcinogen testing challenged (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-11-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J -- New York, N.Y. -- Science. 1990 Nov 9;250(4982):743-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2237420" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Carcinogenicity Tests ; Cell Division ; Humans ; Mice ; Mutagenesis ; Neoplasms/chemically induced ; Rats
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 67
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    Methylation of an immediate-early inducible gene as a mechanism for B cell tolerance induction (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-11-09
    Description: Stage-specific gene regulation is important in determining cell function during development. Immature B cells expressing membrane-bound immunoglobulin M (mIgM) are sensitive to antigen-induced tolerance, whereas mature B cells are activated by antigen. Previous studies have established an association between Egr-1 gene induction and antigen receptor (mIgM)-mediated activation of mature B cells. Here it is shown that the immature B cell line WEHI-231 and tolerance-sensitive bone marrow-derived B cells do not express Egr-1. It is further shown that lack of inducible expression in these cells is due to specific methylation of the Egr-1 gene. Thus, covalent inactivation of an activation-associated gene may explain tolerance sensitivity at specific stages of B cell development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Seyfert, V L -- McMahon, S B -- Glenn, W D -- Yellen, A J -- Sukhatme, V P -- Cao, X M -- Monroe, J G -- AI 23568/AI/NIAID NIH HHS/ -- CA 09940/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1990 Nov 9;250(4982):797-800.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia 19104-6084.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2237429" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/*immunology ; Blotting, Southern ; Cell Line ; DNA/*metabolism ; *Gene Expression Regulation ; *Immune Tolerance ; Immunoglobulin M/immunology ; Methylation ; Mice ; Promoter Regions, Genetic ; Restriction Mapping ; Transcription, Genetic ; Transcriptional Activation
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Mapping terra incognita (humani corporis) (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-10-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Culliton, B J -- New York, N.Y. -- Science. 1990 Oct 12;250(4978):210-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2218525" target="_blank"〉PubMed〈/a〉
    Keywords: Anatomy/history ; Animals ; Chromosome Mapping ; Chromosomes, Human, Pair 1 ; Chromosomes, Human, Pair 3 ; Genetics/history ; History, 16th Century ; History, 20th Century ; Hominidae/anatomy & histology/*genetics ; *Human Genome Project ; Humans ; Mice ; Mice, Inbred Strains/genetics ; Pedigree
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Kaposi's sarcoma puzzle begins to yield (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-04-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J -- New York, N.Y. -- Science. 1990 Apr 27;248(4954):442-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2184517" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/*complications ; Animals ; Gene Products, tat/physiology ; Growth Substances/*physiology ; Humans ; Interleukin-6/physiology ; Mice ; Sarcoma, Kaposi/*etiology ; tat Gene Products, Human Immunodeficiency Virus
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    Concerns raised about mouse models for AIDS (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-02-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J -- New York, N.Y. -- Science. 1990 Feb 16;247(4944):809.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2305253" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/drug therapy/*microbiology ; Animals ; *Disease Models, Animal ; HIV-1/pathogenicity/*physiology ; Humans ; Mice ; Virus Replication
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    Suppression of HIV infection in AZT-treated SCID-hu mice (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-02-02
    Description: The SCID-hu mouse, engrafted with human hematolymphoid organs, is permissive for infection with the human immunodeficiency virus (HIV). This mouse model was used to test compounds for antiviral efficacy. Two weeks after infection with HIV, 100 percent (40/40) of SCID-hu mice were positive for HIV by the polymerase chain reaction. When first treated with 3'-azido-3'-deoxythymidine (AZT), none (0/17) were HIV-positive by this assay. However, AZT-treated SCID-hu mice did have a few infected cells; after AZT treatment was stopped, viral spread was detected by polymerase chain reaction in such mice. Thus, the SCID-hu mouse provides a means to directly compare new antiviral compounds with AZT and to further improve antiviral efficacy.〈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 Feb 2;247(4942):564-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉HIV Group, SyStemix, Palo Alto, CA 94303.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2300816" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; DNA, Viral/genetics/isolation & purification ; HIV/drug effects/genetics/isolation & purification ; HIV Infections/*drug therapy ; Humans ; Mice ; Mice, Mutant Strains ; Nucleic Acid Hybridization ; Polymerase Chain Reaction ; Spleen/microbiology ; Thymus Gland/microbiology/transplantation ; Transplantation, Heterologous ; Zidovudine/*therapeutic use
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    Direct gene transfer into mouse muscle in vivo (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-03-23
    Description: RNA and DNA expression vectors containing genes for chloramphenicol acetyltransferase, luciferase, and beta-galactosidase were separately injected into mouse skeletal muscle in vivo. Protein expression was readily detected in all cases, and no special delivery system was required for these effects. The extent of expression from both the RNA and DNA constructs was comparable to that obtained from fibroblasts transfected in vitro under optimal conditions. In situ cytochemical staining for beta-galactosidase activity was localized to muscle cells following injection of the beta-galactosidase DNA vector. After injection of the DNA luciferase expression vector, luciferase activity was present in the muscle for at least 2 months.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wolff, J A -- Malone, R W -- Williams, P -- Chong, W -- Acsadi, G -- Jani, A -- Felgner, P L -- HD00669-05/HD/NICHD NIH HHS/ -- HD03352/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1990 Mar 23;247(4949 Pt 1):1465-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatrics, Waisman Center, University of Wisconsin, Madison 53706.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1690918" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Avian Sarcoma Viruses/genetics ; Beetles/genetics ; Chloramphenicol O-Acetyltransferase/biosynthesis/genetics ; DNA/genetics ; Escherichia coli/genetics ; *Gene Expression ; Genetic Vectors ; Histocytochemistry ; Luciferases/biosynthesis/genetics ; Mice ; Muscles/*enzymology ; RNA/genetics ; *Transfection ; beta-Galactosidase/biosynthesis/genetics
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Murine developmental control genes (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-07-27
    Description: Various strategies have been used to isolate genes that participate in the regulation of mouse development. Gene families that have been identified on the basis of their homology to motifs within Drosophila control genes or human transcription factor genes, namely homeobox (Hox), paired-box (Pax), and POU genes, can be compared with respect to gene organization, structure, and expression patterns. The functions of these genes can be analyzed molecularly in vitro and in vivo with the use of available mouse mutants or transgenic mice. In addition, it has been possible to generate gain- or loss-of-function mutations by random or targeted introduction of transgenes. Models derived from these studies can reveal the successive steps of developmental control on a genetic level.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kessel, M -- Gruss, P -- New York, N.Y. -- Science. 1990 Jul 27;249(4967):374-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max Planck-Institute of Biophysical Chemistry, Department of Molecular Cell Biology, Gottingen, FRG.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1974085" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Drosophila/genetics ; *Embryonic and Fetal Development ; Gene Expression ; *Genes ; Genes, Homeobox ; Mice ; Mice, Transgenic ; Mutation
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    Analysis of junctional diversity during B lymphocyte development (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-11-09
    Description: Immunoglobulin rearrangement is central to generating antibody diversity because of heterogeneity generated during recombination by deletion or addition of nucleotides at coding joints by the recombinase machinery. Examination of these junctional modifications revealed that the addition of nongermline-encoded nucleotides was more prevalent in adult versus fetal B cells, thus partially limiting the fetal antibody repertoire. In contrast, deletion of nucleotides occurs equivalently in B cells at different stages of development and at different points in B cell ontogeny. Finally, the bias in murine immunoglobulins for one DH segment reading frame occurs at the DHJH intermediate.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Meek, K -- New York, N.Y. -- Science. 1990 Nov 9;250(4982):820-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas 75235.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2237433" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/genetics/immunology ; Animals ; Animals, Newborn ; *Antibody Diversity ; B-Lymphocytes/*immunology ; Blotting, Southern ; Electrophoresis, Polyacrylamide Gel ; Female ; *Gene Rearrangement, B-Lymphocyte ; Immunoglobulin Joining Region/*genetics ; Mice ; Nucleic Acid Hybridization ; Polymerase Chain Reaction ; Pregnancy ; Restriction Mapping
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    Mini-mouse: disruption of the pygmy locus in a transgenic insertional mutant (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-02-23
    Description: A founder transgenic mouse harbored two different integration patterns of a transgene at the same locus, each of which gave rise to a similar autosomal recessive mutation. Mice of the mutant phenotype were of small stature but had normal levels of growth hormone. The disrupted locus was cloned, and a genetic and molecular analysis showed that the insertional mutants were allelic to a spontaneous mutant, pygmy. The mice should be a useful model for the growth hormone-resistant human dwarf syndromes and could lead to a greater understanding of the pathways involved in growth and development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Xiang, X -- Benson, K F -- Chada, K -- GM38731/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1990 Feb 23;247(4945):967-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, Robert Wood Johnson Medical School, University of Medicine and Dentistry of New Jersey, Piscataway 08854.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2305264" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cloning, Molecular ; DNA/genetics ; Disease Models, Animal ; Dwarfism/*genetics ; Female ; Growth Hormone/blood ; Male ; Mice ; Mice, Mutant Strains ; Mice, Transgenic ; Mutation ; Nucleic Acid Hybridization ; Pedigree ; Restriction Mapping
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Differential phosphorylation of c-Abl in cell cycle determined by cdc2 kinase and phosphatase activity (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-04-13
    Description: The product of the c-abl proto-oncogene (c-Abl) is phosphorylated on three sites during interphase and seven additional sites during mitosis. Two interphase and all mitotic c-Abl sites are phosphorylated by cdc2 kinase isolated from either interphase or mitotic cells, with the mitotic cdc2 having an 11-fold higher activity. Inhibition of phosphatases with okadaic acid in interphase cells leads to the phosphorylation of c-Abl mitotic sites, indicating that those sites are preferentially dephosphorylated during interphase. The differential phosphorylation of c-Abl in the cell cycle is therefore determined by an equilibrium between cdc2 kinase and protein phosphatase activities. Treatment of interphase cells with okadaic acid leads to a rounded morphology similar to that observed during mitosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kipreos, E T -- Wang, J Y -- CA43054/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1990 Apr 13;248(4952):217-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, 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/2183353" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; CDC2 Protein Kinase ; *Cell Cycle ; Cells, Cultured ; Ethers, Cyclic/pharmacology ; Interphase/drug effects ; Mice ; Mice, Inbred Strains ; Molecular Sequence Data ; Molecular Weight ; Okadaic Acid ; Peptide Fragments/isolation & purification ; Peptide Mapping ; Phosphoproteins/*metabolism ; Phosphorylation ; Protein-Tyrosine Kinases/*metabolism ; Proto-Oncogene Proteins/isolation & purification/*metabolism ; Proto-Oncogene Proteins c-abl
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    Diet-induced hypercholesterolemia in mice: prevention by overexpression of LDL receptors (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-11-30
    Description: The current studies were designed to determine whether chronic overexpression of low density lipoprotein (LDL) receptors in the liver would protect mice from the increase in plasma LDL-cholesterol that is induced by high-fat diets. A line of transgenic mice was studied that express the human LDL receptor gene in the liver under control of the transferrin promoter. When fed a diet containing cholesterol, saturated fat, and bile acids for 3 weeks, the transgenic mice, in contrast to normal mice, did not develop a detectable increase in plasma LDL. The current data indicate that unregulated overexpression of LDL receptors can protect against diet-induced hypercholesterolemia in mice.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yokode, M -- Hammer, R E -- Ishibashi, S -- Brown, M S -- Goldstein, J L -- HL 20948/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1990 Nov 30;250(4985):1273-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics, University of Texas, Southwestern Medical Center, Dallas 75235.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2244210" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cholesterol, Dietary/adverse effects ; Cholesterol, LDL/*blood ; Dietary Fats/*adverse effects ; Exons ; *Gene Expression ; Humans ; Hypercholesterolemia/etiology/*prevention & control ; Introns ; Lipoproteins/blood ; Lipoproteins, HDL/blood ; Lipoproteins, IDL ; Lipoproteins, VLDL/blood ; Liver/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Nucleic Acid Hybridization ; Promoter Regions, Genetic/genetics ; RNA, Messenger/genetics ; Receptors, LDL/*genetics ; Transferrin/genetics
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    HIV research in the SCID mouse: biosafety considerations (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-11-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Milman, G -- New York, N.Y. -- Science. 1990 Nov 23;250(4984):1152.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2251504" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Containment of Biohazards ; *Disease Models, Animal ; *Hiv ; *HIV Infections ; Immunologic Deficiency Syndromes/*microbiology ; Mice ; Mice, Mutant Strains
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    The role of the T cell receptor in positive and negative selection of developing T cells (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-06-15
    Description: Although many combinations of alpha beta T cell receptors are available to the T cells in any given organism, far fewer are actually used by mature T cells. The combinations used are limited by two selective processes, positive selection of T cells bearing receptors that will be useful to the host, and clonal elimination or inactivation of T cells bearing receptors that will be damaging to the host. The ways in which these two apparently contradictory processes occur, and the hypotheses that have been suggested to reconcile them, are discussed.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Blackman, M -- Kappler, J -- Marrack, P -- AI 17134/AI/NIAID NIH HHS/ -- AI 18785/AI/NIAID NIH HHS/ -- AI 22295/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1990 Jun 15;248(4961):1335-41.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Institute, Department of Medicine, National Jewish Center for Immunology and Respiratory, Medicine, Denver, CO.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1972592" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/immunology ; Autoantigens/immunology ; CD4-Positive T-Lymphocytes/immunology ; Clone Cells ; H-2 Antigens/immunology ; Histocompatibility Antigens/immunology ; *Immune Tolerance ; Mice ; Mice, Transgenic ; Receptors, Antigen, T-Cell/genetics/*immunology ; T-Lymphocytes/*immunology ; T-Lymphocytes, Regulatory/immunology ; Thymus Gland/immunology
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    A mouse macrophage factor induces head structures and organizes a body axis in Xenopus (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-08-03
    Description: Soluble peptide factors have been implicated as the agents responsible for embryonic inductions in vertebrates. Here, a protein (PIF) secreted by a mouse macrophage cell line is shown to change the developmental fate of Xenopus embryonic cells. Exposure to PIF causes presumptive ectodermal explants to form anterior neural and mesodermal tissues, including brain and eye, instead of ciliated epidermis. In addition, the induced tissues are organized into a rudimentary embryonic axis. These results suggest that PIF or a closely related molecule is involved in inducing anterior structures and organizing the frog body plan.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sokol, S -- Wong, G G -- Melton, D A -- GM 32921/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1990 Aug 3;249(4968):561-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Biology, Harvard University, Cambridge, MA 02138.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2382134" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blastocyst/cytology/drug effects/*physiology ; Cell Differentiation/drug effects ; Embryo, Nonmammalian/cytology/drug effects/*physiology ; Macrophages/*physiology ; Mice ; Molecular Weight ; Organ Culture Techniques ; Proteins/isolation & purification/*pharmacology/secretion ; Xenopus
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  • 81
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    Normal development of mice deficient in beta 2M, MHC class I proteins, and CD8+ T cells (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-06-08
    Description: Major histocompatibility class I proteins display viral and self antigens to potentially responsive cells and are important for the maturation of T cells; beta 2-microglobulin (beta 2M) is required for their normal expression. Mouse chimeras derived from embryonic stem cells with a disrupted beta 2M gene transmitted the inactivated gene to their progeny. Animals homozygous for the mutated beta 2M gene were obtained at expected frequencies after further breeding. The homozygotes appeared normal, although no class I antigens could be detected on their cells and the animals are grossly deficient in CD4- CD8+ T cells, which normally mediate cytotoxic T cell function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koller, B H -- Marrack, P -- Kappler, J W -- Smithies, O -- AI-18785/AI/NIAID NIH HHS/ -- GM20069/GM/NIGMS NIH HHS/ -- HL37001/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1990 Jun 8;248(4960):1227-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, University of North Carolina, Chapel Hill 27599-7525.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2112266" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD4/genetics ; Antigens, CD8 ; Antigens, Differentiation, T-Lymphocyte/*genetics ; Chimera ; Gene Expression ; Genes ; Genes, MHC Class I ; Histocompatibility Antigens Class I/*genetics ; Lymph Nodes/immunology ; Mice ; Mice, Inbred C57BL ; Mice, Mutant Strains ; *Mutation ; Spleen/immunology ; T-Lymphocytes/*immunology ; beta 2-Microglobulin/*deficiency/genetics
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  • 82
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    Expression of murine CD1 on gastrointestinal epithelium (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-11-02
    Description: Cluster of differentiation 1 (CD1) in humans is a family of major histocompatibility complex (MHC) class I-like molecules expressed on the surface of immature thymocytes, Langerhans cells, and a subpopulation of B cells. The only function identified for human CD1 is as a ligand recognized by a subpopulation of T lymphocytes. In order to study the distribution and function of these molecules in the mouse, a murine CD1 complementary DNA was expressed in mouse fibroblasts and used to produce monoclonal antibodies. These antibodies revealed prominent expression of murine CD1 only on gastrointestinal tract epithelium and in the cytoplasm of hepatocytes. Low levels of expression were also detected on thymocytes and peripheral lymphocytes. The gastrointestinal distribution of murine CD1 suggests that this molecule may be important in epithelial immunity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bleicher, P A -- Balk, S P -- Hagen, S J -- Blumberg, R S -- Flotte, T J -- Terhorst, C -- AR 01805/AR/NIAMS NIH HHS/ -- CA 01310/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1990 Nov 2;250(4981):679-82.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Immunology, Dana-Farber Cancer Institute, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1700477" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal ; Antigens, CD1 ; Antigens, Differentiation/*analysis/immunology/physiology ; Digestive System/*immunology ; Epithelium/immunology ; Mice ; Precipitin Tests ; T-Lymphocytes/immunology
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  • 83
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    gCap39, a calcium ion- and polyphosphoinositide-regulated actin capping protein (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-12-07
    Description: The polymerization of actin filaments is involved in growth, movement, and cell division. It has been shown that actin polymerization is controlled by gelsolin, whose interactions with actin are activated by calcium ion (Ca2+) and inhibited by membrane polyphosphoinositides (PPI). A smaller Ca2(+)- and PPI-regulated protein, gCap39, which has 49% sequence identity with gelsolin, has been identified by cDNA cloning and protein purification. Like gelsolin, gCap39 binds to the fast-growing (+) end of actin filaments. However, gCap39 does not sever actin filaments and can respond to Ca2+ and PPI transients independently, under conditions in which gelsolin is ineffective. The coexistence of gCap39 with gelsolin should allow precise regulation of actin assembly at the leading edge of the cell.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yu, F X -- Johnston, P A -- Sudhof, T C -- Yin, H L -- HL 29113/HL/NHLBI NIH HHS/ -- HL 39644/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1990 Dec 7;250(4986):1413-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, University of Texas Southwestern Medical Center, Dallas 75235-9040.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2255912" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/*metabolism ; Amino Acid Sequence ; Animals ; Cell Line ; DNA/genetics/isolation & purification ; Gene Library ; Humans ; Kidney/metabolism ; Kinetics ; Macrophages/metabolism ; Mice ; Microfilament Proteins/genetics/isolation & purification/*metabolism ; Molecular Sequence Data ; *Nuclear Proteins ; Sequence Homology, Nucleic Acid
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  • 84
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    MHC-linked protection from diabetes dissociated from clonal deletion of T cells (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-07-20
    Description: The I-E molecule of the major histocompatibility complex (MHC) can prevent the spontaneous development of diabetes in nonobese diabetic (NOD) mice. The mechanism of this protection has been investigated by breeding wild-type and promoter-mutated E kappa alpha transgenes onto the NOD genetic background. Animals carrying the various mutated transgenes expressed I-E on different subsets of immunocompetent cells, and thus cells important for the I-E protective effect could be identified. Although the wild-type transgene prevented the infiltration of lymphocytes into pancreatic islets, none of the mutants did. However, all of the transgenes could mediate the intrathymic elimination of T cells bearing antigen receptors with variable regions that recognize I-E. Thus, the I-E molecule does not protect NOD mice from diabetes simply by inducing the deletion of self-reactive T cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bohme, J -- Schuhbaur, B -- Kanagawa, O -- Benoist, C -- Mathis, D -- New York, N.Y. -- Science. 1990 Jul 20;249(4966):293-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratoire de Genetique Moleculaire des Eucaryotes du CNRS, Faculte de Medecine, Strasbourg, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2115690" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Clone Cells ; Crosses, Genetic ; Diabetes Mellitus, Experimental/*immunology/prevention & control ; Genes, MHC Class II ; Histocompatibility Antigens Class II/genetics/*immunology ; Islets of Langerhans/immunology ; *Major Histocompatibility Complex ; Mice ; Mice, Mutant Strains ; Mice, Transgenic ; Mutation ; Promoter Regions, Genetic ; Receptors, Antigen, T-Cell/genetics ; T-Lymphocytes/*immunology ; Thymus Gland/immunology
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  • 85
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    Homology of cytokine synthesis inhibitory factor (IL-10) to the Epstein-Barr virus gene BCRFI (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-06-08
    Description: Complementary DNA clones encoding mouse cytokine synthesis inhibitory factor (CSIF; interleukin-10), which inhibits cytokine synthesis by TH1 helper T cells, were isolated and expressed. The predicted protein sequence shows extensive homology with an uncharacterized open reading frame, BCRFI, in the Epstein-Barr virus genome, suggesting the possibility that this herpes virus exploits the biological activity of a captured cytokine gene to enhance its survival in the host.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Moore, K W -- Vieira, P -- Fiorentino, D F -- Trounstine, M L -- Khan, T A -- Mosmann, T R -- New York, N.Y. -- Science. 1990 Jun 8;248(4960):1230-4.〈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/2161559" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cell Line ; Cloning, Molecular ; Codon/genetics ; *Genes, Viral ; Herpesvirus 4, Human/*genetics ; Interleukin-10 ; Interleukins/*genetics ; Mice ; Molecular Sequence Data ; Nucleic Acid Hybridization ; RNA, Messenger/genetics ; Restriction Mapping ; Sequence Homology, Nucleic Acid ; T-Lymphocytes, Helper-Inducer/immunology ; Transfection
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  • 86
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    Specific expression of a tyrosine kinase gene, blk, in B lymphoid cells (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-01-19
    Description: Several pathways of transmembrane signaling in lymphocytes involve protein-tyrosine phosphorylation. With the exception of p56lck, a tyrosine kinase specific to T lymphoid cells that associates with the T cell transmembrane proteins CD4 and CD8, the kinases that function in these pathways are unknown. A murine lymphocyte complementary DNA that represents a new member of the src family has now been isolated and characterized. This complementary DNA, termed blk (for B lymphoid kinase), specifies a polypeptide of 55 kilodaltons that is related to, but distinct from, previously identified retroviral or cellular tyrosine kinases. The protein encoded by blk exhibits tyrosine kinase activity when expressed in bacterial cells. In the mouse and among cell lines, blk is specifically expressed in the B cell lineage. The tyrosine kinase encoded by blk may function in a signal transduction pathway that is restricted to B lymphoid cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dymecki, S M -- Niederhuber, J E -- Desiderio, S V -- New York, N.Y. -- Science. 1990 Jan 19;247(4940):332-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology and Genetics, 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/2404338" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; B-Lymphocytes/*enzymology ; Base Sequence ; Codon ; DNA/genetics/isolation & purification ; Escherichia coli/enzymology/genetics ; *Gene Expression ; Mice ; Molecular Sequence Data ; Protein-Tyrosine Kinases/*genetics ; Signal Transduction ; src-Family Kinases/*genetics
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  • 87
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    EGF receptor and erbB-2 tyrosine kinase domains confer cell specificity for mitogenic signaling (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-04-06
    Description: The epidermal growth factor (EGF) receptor (EGFR) can efficiently couple with mitogenic signaling pathways when it is transfected into interleukin-3 (IL-3)-dependent 32D hematopoietic cells. When expression vectors for erbB-2, which is structurally related to EGFR, or its truncated counterpart, delta NerbB-2, were introduced into 32D cells, neither was capable of inducing proliferation. This was despite overexpression and constitutive tyrosine kinase activity of their products at levels associated with potent transformation of fibroblast target cells. Thus, EGFR and erbB-2 couple with distinct mitogenic signaling pathways. The region responsible for the specificity of intracellular signal transduction was localized to a 270-amino acid stretch encompassing their respective tyrosine kinase domains. Thus, tissue- or cell-specific regulation of growth factor receptor signaling can occur at a point after the initial interaction of growth factor with receptor. Such specificity in signal transduction may account for the selection of certain oncogenes in some malignancies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Di Fiore, P P -- Segatto, O -- Taylor, W G -- Aaronson, S A -- Pierce, J H -- New York, N.Y. -- Science. 1990 Apr 6;248(4951):79-83.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Cellular and Molecular Biology, 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/2181668" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cell Division ; Cell Line ; DNA/genetics ; DNA, Recombinant ; Fibroblasts/cytology/metabolism ; Gene Expression ; Genetic Vectors ; Hematopoietic Stem Cells/cytology/metabolism ; Immunoblotting ; Mice ; *Mitogens ; Molecular Sequence Data ; Protein-Tyrosine Kinases/genetics/*physiology ; Proto-Oncogene Proteins/genetics/*physiology ; Receptor, Epidermal Growth Factor/genetics/*physiology ; Sequence Homology, Nucleic Acid ; Signal Transduction ; Transfection
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  • 88
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    Organization of the human and mouse low-affinity Fc gamma R genes: duplication and recombination (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-05-11
    Description: Receptors for immunoglobulin G immune complexes (Fc gamma RII and Fc gamma RIII) are expressed on most hematopoietic cells and show much structural and functional diversity. In order to determine the genetic basis for this diversity, a family of genes encoding the human and mouse receptors was isolated and characterized. Humans have five distinct genes for low-affinity Fc gamma Rs, in contrast to two in the mouse. With the use of yeast artificial chromosomes, the genes encoding the human receptors were oriented and linked, which established the structure of this complex locus. Comparison of the human and mouse genes generated a model for the evolutionary amplification of this locus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Qiu, W Q -- de Bruin, D -- Brownstein, B H -- Pearse, R -- Ravetch, J V -- GM 36306/GM/NIGMS NIH HHS/ -- GM 39256/GM/NIGMS NIH HHS/ -- K23 AG022476/AG/NIA NIH HHS/ -- R01 AG031171/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 1990 May 11;248(4956):732-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Molecular Biology, Sloan-Kettering Institute, New York, NY 10021.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2139735" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Differentiation/*genetics/metabolism ; Base Sequence ; Blotting, Southern ; Exons ; Genome, Human ; Humans ; Immunoglobulin G/metabolism ; Introns ; Mice ; Molecular Sequence Data ; *Multigene Family ; Mutation ; Receptors, Fc/*genetics/metabolism ; Receptors, IgG ; Recombination, Genetic ; Restriction Mapping ; Spleen/immunology
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  • 89
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    Two distinct transcription factors that bind the immunoglobulin enhancer microE5/kappa 2 motif (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-01-26
    Description: Activity of the immunoglobulin heavy and kappa light chain gene enhancers depends on a complex interplay of ubiquitous and developmentally regulated proteins. Two complementary DNAs were isolated that encode proteins, denoted ITF-1 and ITF-2, that are expressed in a variety of cell types and bind the microE5/kappa 2 motif found in both heavy and kappa light chain enhancers. The complementary DNAs are the products of distinct genes, yet both ITF-1 and ITF-2 are structurally and functionally similar. The two proteins interact with one another through their putative helix-loop-helix motifs and each possesses a distinct domain that dictates transcription activation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Henthorn, P -- Kiledjian, M -- Kadesch, T -- New York, N.Y. -- Science. 1990 Jan 26;247(4941):467-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Philadelphia, PA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2105528" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/metabolism ; Base Sequence ; Binding Sites ; Cell Line ; Cloning, Molecular ; DNA/genetics/*metabolism ; *Enhancer Elements, Genetic ; *Genes, Immunoglobulin ; Humans ; Immunoglobulin kappa-Chains/genetics ; Immunoglobulin mu-Chains/genetics ; Macromolecular Substances ; Mice ; Molecular Sequence Data ; Plasmids ; Protein Conformation ; Saccharomyces cerevisiae/genetics ; Transcription Factors/*metabolism ; Transcription, Genetic ; Transfection ; Transformation, Genetic
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  • 90
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    PDGF-induced activation of phospholipase C is not required for induction of DNA synthesis (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-06-29
    Description: Platelet-derived growth factor (PDGF) induction of DNA synthesis is believed to involve activation of phospholipase C (PLC) and subsequent accumulation of inositol 1,4,5-triphosphate [I(1,4,5)P3], increase in intracellular Ca2+, activation of protein kinase C (PKC), and receptor down regulation. Generation of these events is triggered by the tyrosine protein kinase (TPK) activity of the PDGF receptor. The TPK inhibitor genistein blocked PDGF induction of these events, including DNA synthesis, with the exception of receptor down regulation. PDGF-induced phosphotyrosine phosphorylations, including receptor autophosphorylation, were inhibited by genistein. Removal of genistein and PDGF resulted in DNA synthesis without the occurrence of PLC activation. These findings indicate that these early events, with the exception of receptor down regulation, are not necessary for PDGF-induced DNA synthesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hill, T D -- Dean, N M -- Mordan, L J -- Lau, A F -- Kanemitsu, M Y -- Boynton, A L -- CA 2942/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1990 Jun 29;248(4963):1660-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Research Center of Hawaii, University of Hawaii, Honolulu 96813.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2163545" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/metabolism ; Cells, Cultured ; Chlorides/pharmacology ; DNA Replication/*drug effects ; Dimethyl Sulfoxide/pharmacology ; Enzyme Activation ; Genistein ; Inositol Phosphates/metabolism ; Isoflavones/pharmacology ; Kinetics ; Lithium/pharmacology ; Lithium Chloride ; Mice ; Phosphatidylinositol 4,5-Diphosphate ; Phosphatidylinositols/metabolism ; Phosphorylation ; Platelet-Derived Growth Factor/*pharmacology ; Protein Kinase C/metabolism ; Protein-Tyrosine Kinases/metabolism ; Type C Phospholipases/*metabolism
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  • 91
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    Diversity of Conus neuropeptides (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-07-20
    Description: Conus venoms contain a remarkable diversity of pharmacologically active small peptides. Their targets are ion channels and receptors in the neuromuscular system. The venom of Conus geographus contains high-affinity peptides that act on voltage-sensitive calcium channels, sodium channels, N-methyl-D-aspartate (NMDA) receptors, acetylcholine receptors, and vasopressin receptors; many more peptides with still uncharacterized receptor targets are present in this venom. It now seems that the Conus species (approximately 500 in number) will each use a distinctive assortment of peptides and that the pharmacological diversity in Conus venoms may be ultimately comparable to that of plant alkaloids or secondary metabolites of microorganisms. The cone snails may generate this diverse spectrum of venom peptides by a "fold-lock-cut" synthetic pathway. These peptides are specific enough to discriminate effectively between closely related receptor subtypes and can be used for structure-function correlations.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Olivera, B M -- Rivier, J -- Clark, C -- Ramilo, C A -- Corpuz, G P -- Abogadie, F C -- Mena, E E -- Woodward, S R -- Hillyard, D R -- Cruz, L J -- GM 22737/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1990 Jul 20;249(4966):257-63.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, University of Utah, Salt Lake City 84112.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2165278" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Mice ; Molecular Sequence Data ; Mollusk Venoms/*genetics/isolation & purification/toxicity ; Neuropeptides/*genetics ; Receptors, N-Methyl-D-Aspartate ; Receptors, Neurotransmitter/drug effects ; Sequence Homology, Nucleic Acid ; Sleep/drug effects ; Snails/*physiology ; Species Specificity
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  • 92
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    The role of beta 2-microglobulin in peptide binding by class I molecules (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-12-07
    Description: Efficient transport of class I major histocompatibility complex molecules to the cell surface requires association of the class I heavy chain with endogenous peptide and the class I light chain, beta 2-microglobulin (beta 2M). A mutant cell line deficient in beta 2M transports low amounts of nonpeptide-associated heavy chains to the cell surface that can associate with exogenously provided beta 2M and synthetic peptide antigens. Normal beta 2M-sufficient cells grown in serum-free media devoid of beta 2M also require an exogenous source of beta 2M to efficiently bind synthetic peptide. Thus, class I molecules on normal cells do not spontaneously bind or exchange peptides.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vitiello, A -- Potter, T A -- Sherman, L A -- AI-25280/AI/NIAID NIH HHS/ -- CA-25803/CA/NCI NIH HHS/ -- CA-49394/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1990 Dec 7;250(4986):1423-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cytel Corporation, La Jolla, CA 92037.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2124002" target="_blank"〉PubMed〈/a〉
    Keywords: Abelson murine leukemia virus/genetics ; Animals ; Antibodies ; Biological Transport ; Cell Line ; Cell Membrane/immunology ; Cell Transformation, Neoplastic ; Cytotoxicity, Immunologic ; Histocompatibility Antigens Class I/analysis/*metabolism ; Immunoglobulin Heavy Chains/metabolism ; Kinetics ; Mice ; Mice, Inbred Strains ; T-Lymphocytes, Cytotoxic/immunology ; beta 2-Microglobulin/genetics/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 93
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    Spontaneous neurodegeneration in transgenic mice with mutant prion protein (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-12-14
    Description: Transgenic mice were created to assess genetic linkage between Gerstmann-Straussler-Scheinker syndrome and a leucine substitution at codon 102 of the human prion protein gene. Spontaneous neurologic disease with spongiform degeneration and gliosis similar to that in mouse scrapie developed at a mean age of 166 days in 35 mice expressing mouse prion protein with the leucine substitution. Thus, many of the clinical and pathological features of Gerstmann-Straussler-Scheinker syndrome are reproduced in transgenic mice containing a prion protein with a single amino acid substitution, illustrating that a neurodegenerative process similar to a human disease can be genetically modeled in animals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hsiao, K K -- Scott, M -- Foster, D -- Groth, D F -- DeArmond, S J -- Prusiner, S B -- AG02132/AG/NIA NIH HHS/ -- NS14069/NS/NINDS NIH HHS/ -- NS22786/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1990 Dec 14;250(4987):1587-90.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, University of California, San Francisco 94143.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1980379" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Brain/pathology ; Brain Diseases/*genetics/microbiology/pathology ; Codon ; DNA/genetics ; Disease Models, Animal ; Endopeptidase K ; Gerstmann-Straussler-Scheinker Disease/*genetics/microbiology/pathology ; Leucine ; Mice ; Mice, Transgenic ; Molecular Sequence Data ; *Mutation ; Nucleic Acid Hybridization ; Pedigree ; PrPSc Proteins ; Prions/*genetics ; Serine Endopeptidases/metabolism ; Transfection ; Vacuoles/pathology ; Viral Proteins/*genetics/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 94
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    Expression of gene rrg is associated with reversion of NIH 3T3 transformed by LTR-c-H-ras (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-08-17
    Description: A partial complementary DNA was isolated for a gene (rrg) that is normally expressed in mouse NIH 3T3 cells, but is down-regulated after cellular transformation by long terminal repeat (LTR)-activated c-H-ras (LTR-c-H-ras). This gene was reexpressed in a nontumorigenic persistent revertant cell line created by prolonged treatment of the transformed cells with mouse interferon alpha/beta. Persistent revertants stably transfected with rrg complementary DNA antisense expression vectors appeared transformed, had decreased amounts of rrg messenger RNA, and were tumorigenic in nude mice. Stable transfection with sense constructs did not alter the normal morphology, message level, or nontumorigenicity of the persistent revertant cell line.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Contente, S -- Kenyon, K -- Rimoldi, D -- Friedman, R M -- R01 CA 37351-04A1/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1990 Aug 17;249(4970):796-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Uniformed Services University of the Health Sciences, Bethesda, MD 20814-4799.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1697103" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line, Transformed ; Cloning, Molecular ; DNA/genetics ; *Gene Expression ; *Genes, ras ; Humans ; Interferon Type I/pharmacology ; Mice ; Mice, Nude ; Neoplasms, Experimental/etiology ; Nucleic Acid Hybridization ; Proto-Oncogene Proteins/*genetics ; Proto-Oncogene Proteins p21(ras) ; RNA/analysis/genetics ; RNA, Antisense ; RNA, Messenger/genetics ; Rats ; Transfection
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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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    Neurotrophin-3: a neurotrophic factor related to NGF and BDNF (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-03-23
    Description: The development and maintenance of the nervous system depends on proteins known as neurotrophic factors. Although the prototypical neurotrophic factor, nerve growth factor (NGF), has been intensively studied for decades, the discovery and characterization of additional such factors has been impeded by their low abundance. Sequence homologies between NGF and the recently cloned brain-derived neurotrophic factor (BDNF) were used to design a strategy that has now resulted in the cloning of a gene encoding a novel neurotrophic factor, termed neurotrophin-3 (NT-3). The distribution of NT-3 messenger RNA and its biological activity on a variety of neuronal populations clearly distinguish NT-3 from NGF and BDNF, and provide compelling evidence that NT-3 is an authentic neurotrophic factor that has its own characteristic role in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Maisonpierre, P C -- Belluscio, L -- Squinto, S -- Ip, N Y -- Furth, M E -- Lindsay, R M -- Yancopoulos, G D -- New York, N.Y. -- Science. 1990 Mar 23;247(4949 Pt 1):1446-51.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Regeneron Pharmaceuticals, Inc., Tarrytown, New York 10591.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2321006" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Brain-Derived Neurotrophic Factor ; Cells, Cultured ; Cloning, Molecular ; DNA/genetics ; Mice ; Molecular Sequence Data ; Nerve Growth Factors/biosynthesis/*genetics/physiology ; Nerve Tissue Proteins/biosynthesis/*genetics/physiology ; Neurons/physiology ; Polymerase Chain Reaction ; Rats ; Restriction Mapping ; Sequence Homology, Nucleic Acid
    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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  • 96
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    Antigen presentation requires transport of MHC class I molecules from the endoplasmic reticulum (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-02-09
    Description: The role of exocytosis of major histocompatibility complex (MHC) class I molecules in the presentation of antigens to mouse cytotoxic T lymphocytes (CTLs) was examined by use of a recombinant vaccinia virus that expresses the E19 glycoprotein from adenovirus. E19 blocked the presentation of vaccinia and influenza virus proteins to CTLs in a MHC class I allele-specific manner identical to its inhibition of MHC class I transport from the endoplasmic reticulum. This finding indicates that (i) the relevant parameter for antigen presentation is the rate of MHC class I molecule exocytosis, not the level of class I cell surface expression, and (ii) association of class I molecules with antigen is likely to occur within the endoplasmic reticulum.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cox, J H -- Yewdell, J W -- Eisenlohr, L C -- Johnson, P R -- Bennink, J R -- New York, N.Y. -- Science. 1990 Feb 9;247(4943):715-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2137259" target="_blank"〉PubMed〈/a〉
    Keywords: Adenovirus Early Proteins ; Animals ; Antigen-Presenting Cells/drug effects/immunology/*ultrastructure ; Antigens/*immunology ; Antigens, Viral/immunology ; Antiviral Agents ; Biological Transport ; Brefeldin A ; Cell Line ; Cyclopentanes/pharmacology ; Endoplasmic Reticulum/*immunology ; Exocytosis ; Glycoproteins/analysis ; H-2 Antigens/immunology ; Histocompatibility Antigens Class I/immunology/*metabolism ; Mice ; Mice, Inbred A ; Mice, Inbred BALB C ; Mice, Inbred C3H ; Mice, Inbred CBA ; Oncogene Proteins, Viral/analysis ; Orthomyxoviridae Infections/immunology ; Recombinant Proteins/immunology ; T-Lymphocytes, Cytotoxic/*immunology ; Vaccinia virus/immunology
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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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    The role of B cells for in vivo T cell responses to a Friend virus-induced leukemia (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-08-24
    Description: B cells can function as antigen-presenting cells and accessory cells for T cell responses. This study evaluated the role of B cells in the induction of protective T cell immunity to a Friend murine leukemia virus (F-MuLV)-induced leukemia (FBL). B cell-deficient mice exhibited significantly reduced tumor-specific CD4+ helper and CD8+ cytotoxic T cell responses after priming with FBL or a recombinant vaccinia virus containing F-MuLV antigens. Moreover, these mice had diminished T cell responses to the vaccinia viral antigens. Tumor-primed T cells transferred into B cell-deficient mice effectively eradicated disseminated FBL. Thus, B cells appear necessary for efficient priming but not expression of tumor and viral T cell immunity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schultz, K R -- Klarnet, J P -- Gieni, R S -- HayGlass, K T -- Greenberg, P D -- CA 33084/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1990 Aug 24;249(4971):921-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatrics, University of Washington, Seattle 98195.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2118273" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen-Presenting Cells/immunology ; Antigens, CD4/analysis ; Antigens, CD8 ; Antigens, Differentiation, T-Lymphocyte/analysis ; B-Lymphocytes/*immunology ; Friend murine leukemia virus/*immunology ; Genes, MHC Class I ; Immunization, Passive ; Leukemia, Experimental/*immunology/therapy ; Mice ; Mice, Inbred C57BL ; T-Lymphocytes/*immunology ; T-Lymphocytes, Cytotoxic/immunology ; Vaccinia virus/immunology
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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 cell culture model for T lymphocyte clonal anergy (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-06-15
    Description: T lymphocytes respond to foreign antigens both by producing protein effector molecules known as lymphokines and by multiplying. Complete activation requires two signaling events, one through the antigen-specific receptor and one through the receptor for a costimulatory molecule. In the absence of the latter signal, the T cell makes only a partial response and, more importantly, enters an unresponsive state known as clonal anergy in which the T cell is incapable of producing its own growth hormone, interleukin-2, on restimulation. Our current understanding at the molecular level of this modulatory process and its relevance to T cell tolerance are reviewed.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schwartz, R H -- New York, N.Y. -- Science. 1990 Jun 15;248(4961):1349-56.〈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/2113314" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD/immunology ; Antigens, CD4/immunology ; Antigens, CD8 ; Antigens, Differentiation, T-Lymphocyte/immunology ; Cells, Cultured ; Clone Cells/*immunology ; Gene Expression Regulation ; Gene Rearrangement, T-Lymphocyte ; *Immune Tolerance ; Interleukin-2/biosynthesis/genetics ; Mice ; *Models, Biological ; Receptors, Antigen, T-Cell/genetics/immunology ; Second Messenger Systems ; Signal Transduction ; T-Lymphocytes/*immunology ; Thymus Gland/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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  • 99
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    The need for central and peripheral tolerance in the B cell repertoire (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-06-15
    Description: The immune system normally avoids producing antibodies that react with autologous ("self") antigens by censoring self-reactive T and B cells. Unlike the T cell repertoire, antibody diversity is generated within the B cell repertoire in two phases; the first occurs by gene rearrangement in primary lymphoid organs, and the second phase involves antigen-driven hypermutation in peripheral lymphoid organs. The possibility that distinct cellular mechanisms may impose self tolerance at these two different phases of B cell diversification may explain recent findings in transgenic mouse models, in which self-reactive B cells appear to be silenced both by functional inactivation and by physical elimination.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Goodnow, C C -- Adelstein, S -- Basten, A -- New York, N.Y. -- Science. 1990 Jun 15;248(4961):1373-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centenary Institute for Cancer Medicine and Cell Biology, University of Sydney, New South Wales, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2356469" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibody Diversity/immunology ; Autoantibodies/biosynthesis/immunology ; Autoantigens/immunology ; B-Lymphocytes/*immunology ; Binding Sites, Antibody ; Cell Survival ; Down-Regulation ; Gene Rearrangement, B-Lymphocyte ; H-2 Antigens/immunology ; *Immune Tolerance ; Mice ; Mice, Transgenic ; Muramidase/immunology ; Receptors, Antigen, B-Cell/genetics/immunology ; Receptors, Antigen, T-Cell/genetics/immunology ; 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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  • 100
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    Rate and mechanism of nonhomologous recombination during a single cycle of retroviral replication (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-01-08
    Description: Oncogenes discovered in retroviruses such as Rous sarcoma virus were generated by transduction of cellular proto-oncogenes into the viral genome. Several different kinds of junctions between the viral and proto-oncogene sequences have been found in different viruses. A system of retrovirus vectors and a protocol that mimicked this transduction during a single cycle of retrovirus replication was developed. The transduction involved the formation of a chimeric viral-cellular RNA, strand switching of the reverse transcription growing point from an infectious retrovirus to the chimeric RNA, and often a subsequent deletion during the rest of viral DNA synthesis. A short region of sequence identity was frequently used for the strand switching. The rate of this process was about 0.1 to 1 percent of the rate of homologous retroviral recombination.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, J -- Temin, H M -- CA-07175/CA/NCI NIH HHS/ -- CA-22443/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1993 Jan 8;259(5092):234-8.〈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/8421784" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; *Cinnamates ; *DNA Replication ; DNA, Viral/chemistry/genetics ; Drug Resistance/genetics ; Genes, Viral ; Genetic Vectors ; Hygromycin B/analogs & derivatives ; Kinetics ; Mice ; Molecular Sequence Data ; Moloney murine leukemia virus/genetics ; Neomycin ; Plasmids ; *Proto-Oncogenes ; RNA, Viral/analysis/genetics ; *Recombination, Genetic ; Repetitive Sequences, Nucleic Acid ; Retroviridae/*genetics/physiology ; Transfection ; *Virus Replication
    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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