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  • Mice  (84)
  • American Association for the Advancement of Science (AAAS)  (84)
  • American Institute of Physics (AIP)
  • Oxford University Press
  • 1995-1999
  • 1990-1994
  • 1985-1989  (84)
  • 1987  (84)
Collection
Keywords
Publisher
  • American Association for the Advancement of Science (AAAS)  (84)
  • American Institute of Physics (AIP)
  • Oxford University Press
  • Springer  (6)
Years
  • 1995-1999
  • 1990-1994
  • 1985-1989  (84)
Year
  • 1
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    Mapping the main immunogenic region and toxin-binding site of the nicotinic acetylcholine receptor (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-01-02
    Description: The alpha-chain of the nicotinic acetylcholine receptor carries the binding sites both for cholinergic ligands and for most experimentally induced or naturally occurring antibodies to the native receptor. By means of expression cloning in Escherichia coli, fusion proteins were derived from specific fragments of a complementary DNA encoding the mouse alpha-chain, allowing the mapping of the toxin-binding site to residues 160-216 and the main immunogenic region to residues 6-85. This approach permits the independent study of different functional domains of a complex receptor molecule and should be generally applicable to other proteins for which complementary DNA clones are available.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barkas, T -- Mauron, A -- Roth, B -- Alliod, C -- Tzartos, S J -- Ballivet, M -- New York, N.Y. -- Science. 1987 Jan 2;235(4784):77-80.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2432658" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antibodies, Monoclonal/immunology ; Binding Sites ; Binding, Competitive ; Bungarotoxins/metabolism ; Cloning, Molecular ; Epitopes ; Humans ; Immunosorbent Techniques ; Ligands ; Mice ; Receptors, Nicotinic/genetics/*immunology ; Recombinant Fusion Proteins/immunology ; Species Specificity ; Structure-Activity Relationship
    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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    Differential expression of c-myb mRNA in murine B lymphomas by a block to transcription elongation (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-09-18
    Description: Expression of c-myb proto-oncogene messenger RNA (mRNA) and protein has been detected principally in tumors and in normal tissue of hematopoietic origin. In each hematopoietic lineage examined, expression of the c-myb gene is markedly downregulated during hematopoietic maturation. However, the mechanism by which differential expression of the c-myb gene is regulated is not known. In murine B-lymphoid tumor cell lines, the amount of steady-state c-myb mRNA is 10 to more than 100 times greater in pre-B cell lymphomas than in B cell lymphomas and plasmacytomas. The downregulation of c-myb mRNA correlates with events at the pre-B cell-B cell junction. Differential expression of c-myb mRNA levels detected between a pre-B cell lymphoma and a mature B cell lymphoma is now shown to be mediated by a block to transcription elongation in the first intron of the c-myb locus. In addition, this developmentally regulated difference in transcriptional activity is correlated with alterations in higher order chromatin structure as reflected by changes in the patterns of hypersensitivity to deoxyribonuclease I at the 5' end of the c-myb transcription unit. Regulation of transcription elongation may provide a more sensitive mechanism for rapidly increasing and decreasing mRNA levels in response to external stimuli than regulation of the initiation of transcription.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bender, T P -- Thompson, C B -- Kuehl, W M -- New York, N.Y. -- Science. 1987 Sep 18;237(4821):1473-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3498214" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes ; Chromosome Mapping ; *Gene Expression Regulation ; Introns ; Lymphoma/*genetics ; Mice ; Nucleic Acid Hybridization ; *Peptide Chain Elongation, Translational ; *Proto-Oncogenes ; RNA, Messenger/*metabolism ; *Transcription, Genetic
    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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    Oncogenes in radioresistant, noncancerous skin fibroblasts from a cancer-prone family (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-08-28
    Description: Li-Fraumeni syndrome is manifested in a variety of neoplasms that are transmitted in a dominantly inherited pattern. The noncancerous skin fibroblasts of family members exhibit a unique characteristic of being resistant to the killing effect of ionizing radiation. A three- to eightfold elevation in expression of c-myc and an apparent activation of c-raf-1 gene have been observed in these noncancerous skin fibroblasts. These results may provide insight into the heritable defect underlying the familial predisposition to a variety of cancers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chang, E H -- Pirollo, K F -- Zou, Z Q -- Cheung, H Y -- Lawler, E L -- Garner, R -- White, E -- Bernstein, W B -- Fraumeni, J W Jr -- Blattner, W A -- CA45158/CA/NCI NIH HHS/ -- CO7488/CO/NCI NIH HHS/ -- New York, N.Y. -- Science. 1987 Aug 28;237(4818):1036-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3616624" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Transformation, Neoplastic/radiation effects ; Cells, Cultured ; Fibroblasts/*radiation effects ; Humans ; Mice ; Mice, Nude ; Neoplastic Syndromes, Hereditary/*genetics ; Oncogenes/*radiation effects ; Pedigree ; *Radiation Tolerance ; Skin/cytology/*radiation effects ; Syndrome
    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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    erbB-2 is a potent oncogene when overexpressed in NIH/3T3 cells (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-07-10
    Description: A wide variety of human tumors contain an amplified or overexpressed erbB-2 gene, which encodes a growth factor receptor-like protein. When erbB-2 complementary DNA was expressed in NIH/3T3 cells under the control of the SV40 promoter, the gene lacked transforming activity despite expression of detectable levels of the erbB-2 protein. A further five- to tenfold increase in its expression under influence of the long terminal repeat of Moloney murine leukemia virus was associated with activation of erbB-2 as a potent oncogene. The high levels of the erbB-2 product associated with malignant transformation of NIH/3T3 cells were observed in human mammary tumor cells that overexpressed this gene. These findings demonstrate a new mechanism for acquisition of oncogenic properties by genes encoding growth factor receptor-like proteins and provide a functional basis for the role of their overexpression in the development of human malignancies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Di Fiore, P P -- Pierce, J H -- Kraus, M H -- Segatto, O -- King, C R -- Aaronson, S A -- New York, N.Y. -- Science. 1987 Jul 10;237(4811):178-82.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2885917" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Breast Neoplasms/genetics ; Cell Line ; *Cell Transformation, Neoplastic/genetics ; DNA/genetics ; Fibroblasts/*metabolism ; Gene Expression Regulation ; Genes, Viral ; Humans ; Mice ; Moloney murine leukemia virus/genetics ; Promoter Regions, Genetic ; Proto-Oncogene Proteins/biosynthesis/genetics/*physiology ; Rats ; Receptor, Epidermal Growth Factor ; Receptor, ErbB-2 ; Receptors, Cell Surface/genetics ; Recombinant Fusion Proteins/biosynthesis/genetics/physiology ; Simian virus 40/genetics ; Tumor Stem Cell Assay
    Print ISSN: 0036-8075
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  • 5
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    Virus-induced increases in plasma corticosterone (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-12-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dunn, A J -- Powell, M L -- Gaskin, J M -- MH25486/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1987 Dec 4;238(4832):1423-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, College of Medicine, University of Florida, Gainesville 32610.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3685987" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Corticosterone/*blood ; Female ; Hypophysectomy ; Lymphocytes/physiology ; Male ; Mice ; Mice, Inbred Strains ; Models, Biological ; Newcastle Disease/*blood ; Pituitary-Adrenal System/*physiopathology ; Postoperative Complications/blood ; Stress, Physiological/blood
    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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  • 6
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    Transformation by oncogenes encoding protein kinases induces the metastatic phenotype (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-10-09
    Description: Oncogenes encoding serine/threonine or tyrosine kinases were introduced into the established rodent fibroblast cell line NIH 3T3 and tested for tumorigenic and metastatic behavior in T cell-deficient nude mice. Transforming oncogenes of the ras family were capable of converting fibroblast cell lines to fully metastatic tumors. Cell lines transformed by the kinase oncogenes mos, raf, src, fes, and fms formed experimental metastases and (in some cases) these genes were more efficient at metastatic conversion than a mutant ras gene. In contrast, cells transformed by either of two nuclear oncogenes, myc or p53, were tumorigenic when injected subcutaneously but were virtually nonmetastatic after intravenous injection. These data demonstrate that, in addition to ras, a structurally divergent group of kinase oncogenes can induce the metastatic phenotype.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Egan, S E -- Wright, J A -- Jarolim, L -- Yanagihara, K -- Bassin, R H -- Greenberg, A H -- New York, N.Y. -- Science. 1987 Oct 9;238(4824):202-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Manitoba Institute of Cell Biology, University of Manitoba, Winnipeg, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3659911" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Transformation, Neoplastic ; Cells, Cultured ; *Genes ; Mice ; *Neoplasm Metastasis ; *Oncogenes ; Phenotype ; Protein Kinases/*genetics
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  • 7
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    A defined medium for a fastidious Spiroplasma (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-07-31
    Description: A defined medium (H-1) was developed for cultivation of the suckling mouse cataract agent, Spiroplasma mirum, a fastidious member of the class Mollicutes that causes cataracts and chronic brain infection in inoculated neonate mice. The H-1 medium was used to show the importance of sphingomyelin as a growth factor for the culture of the spiroplasma in vitro. The growth of Spiroplasma mirum and the pathology it induces in sphingomyelin-rich tissues in vivo may be related to this dependency.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hackett, K J -- Ginsberg, A S -- Rottem, S -- Henegar, R B -- Whitcomb, R F -- New York, N.Y. -- Science. 1987 Jul 31;237(4814):525-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3603039" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cataract/microbiology ; *Culture Media ; Mice ; Spiroplasma/classification/*growth & development
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  • 8
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    Rheumatoid factor secretion from human Leu-1+ B cells (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-04-03
    Description: A human B cell subpopulation identifiable by the expression of the cell surface antigen Leu-1 (CD5) is responsible for most of the immunoglobulin M rheumatoid factor secreted in vitro after the cells are stimulated with Staphylococcus aureus. The ability of B cells bearing the Leu-1 marker (Leu-1+) to secrete rheumatoid factor is present early in development and extends to adulthood, since Leu-1+ B cells from cord blood and from peripheral blood lymphocytes of both normal adults and patients with certain autoimmune conditions secrete rheumatoid factor in comparable amounts. The neonatal enrichment of Leu-1+ B cells, the presence of Leu-1+ B cells in increased frequencies in patients with autoimmune disease, and the involvement of Leu-1+ B cells in autoantibody secretion suggest both developmental and functional homologies between this human B cell subpopulation and the murine Ly-1 B cell subpopulation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hardy, R R -- Hayakawa, K -- Shimizu, M -- Yamasaki, K -- Kishimoto, T -- New York, N.Y. -- Science. 1987 Apr 3;236(4797):81-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3105057" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Differentiation, B-Lymphocyte ; Antigens, Differentiation, T-Lymphocyte ; Antigens, Surface/*immunology ; Autoimmune Diseases/*immunology ; B-Lymphocytes/*classification/immunology ; Cell Separation ; Fetal Blood/cytology ; Flow Cytometry ; Humans ; Immunoglobulin M/secretion ; Leukocyte Count ; Mice ; Rheumatoid Factor/*secretion
    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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  • 9
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    A Mab to a unique cerebellar neuron generated by immunosuppression and rapid immunization (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-07-03
    Description: The cerebellar cortex is perhaps the best characterized structure in the mammalian central nervous system. Although the major cerebellar cell classes are well known, a new class of cerebellar cortical neuron has now been identified with a monoclonal antibody (Mab) generated by a procedure for rapid immunization and selective immunosuppression of antibody responses. This procedure generates a high frequency of immunoglobulin G-class antibodies of desired specificity, and has allowed the generation of two antibodies that recognize subsets of cerebellar cortical neurons. One of these antibodies defines a previously unrecognized class of cerebellar neuron. The distribution and antigenic characteristics of this neuron suggest that it has a distinct role in cerebellar circuitry.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hockfield, S -- R01 EY06511/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 1987 Jul 3;237(4810):67-70.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3603010" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn/immunology ; Antibodies, Monoclonal/*immunology ; Cerebellar Cortex/cytology/*immunology ; Immune Tolerance ; Mice ; Mice, Inbred BALB C/immunology ; Rats
    Print ISSN: 0036-8075
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  • 10
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    Conservation of the Duchenne muscular dystrophy gene in mice and humans (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-10-16
    Description: A portion of the Duchenne muscular dystrophy (DMD) gene transcript from human fetal skeletal muscle and mouse adult heart was sequenced, representing approximately 25 percent of the total, 14-kb DMD transcript. The nucleic acid and predicted amino acid sequences from the two species are nearly 90 percent homologous. The amino acid sequence that is predicted from this portion of the DMD gene indicates that the protein product might serve a structural role in muscle, but the abundance and tissue distribution of the messenger RNA suggests that the DMD protein is not nebulin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hoffman, E P -- Monaco, A P -- Feener, C C -- Kunkel, L M -- 2T 32 GM07753-07/GM/NIGMS NIH HHS/ -- HD18658/HD/NICHD NIH HHS/ -- R01 NS23740/NS/NINDS NIH HHS/ -- T32 GM007753/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1987 Oct 16;238(4825):347-50.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Genetics, Children's Hospital, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3659917" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; DNA/*genetics ; DNA, Recombinant ; Exons ; Humans ; Male ; Mice ; Molecular Sequence Data ; Muscle Proteins/genetics ; Muscles/analysis/embryology ; Muscular Dystrophies/*genetics ; Muscular Dystrophy, Animal/*genetics ; Myocardium/analysis ; Nucleic Acid Hybridization ; RNA, Messenger/genetics ; X Chromosome
    Print ISSN: 0036-8075
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  • 11
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    The raf oncogene is associated with a radiation-resistant human laryngeal cancer (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-08-28
    Description: In order to identify the genetic factors associated with the radiation-resistant human laryngeal carcinoma cell line (SQ-20B), tumor cell DNA was transfected into NIH/3T3 cells. A high incidence (six out of six) of raf sequences was found in transfected NIH/3T3 clones and the tumorigenic potential of SQ-20B DNA could be linked to genomic fragments that represent most of the kinase domain of human c-raf-1. An apparently unaltered 3.5-kilobase pair (kb) human c-raf transcript was identified in SQ-20B cells but was not observed in the transfected NIH/3T3 cell clones. Two new transcripts (4.2 kb and 2.6 kb) were found in tumorigenic clones; the large transcript was missing in a very poorly tumorigenic clone. Cytogenetic analysis indicated that the normal autosomes of chromosome 3 were absent in SQ-20B karyotypes and had formed apparently stable marker chromosomes. Unlike the recipient NIH/3T3 cell line, 30 percent of the transformed clone-1 metaphases had minute and double-minute chromosomes representative of amplified DNA sequences. The frequency of the c-raf-1 identification by NIH/3T3 transfection of SQ-20B DNA suggests the presence of some genetic abnormality within this locus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kasid, U -- Pfeifer, A -- Weichselbaum, R R -- Dritschilo, A -- Mark, G E -- CA425969/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1987 Aug 28;237(4818):1039-41.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3616625" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; DNA, Neoplasm/genetics ; Humans ; Karyotyping ; Laryngeal Neoplasms/*genetics/radiotherapy ; Mice ; Mice, Nude ; Nucleic Acid Hybridization ; Oncogenes/*radiation effects ; Proto-Oncogenes/radiation effects ; *Radiation Tolerance
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  • 12
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    Ouabain resistance conferred by expression of the cDNA for a murine Na+, K+-ATPase alpha subunit (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-08-21
    Description: The molecular basis for the marked difference between primate and rodent cells in sensitivity to the cardiac glycoside ouabain has been established by genetic techniques. A complementary DNA encoding the entire alpha 1 subunit of the mouse Na+- and K+-dependent adenosine triphosphatase (ATPase) was inserted into the expression vector pSV2. This engineered DNA molecule confers resistance against 10(-4) M ouabain to monkey CV-1 cells. Deletion of sequences encoding the carboxyl terminus of the alpha 1 subunit abolish the activity of the complementary DNA. The ability to assay the biological activity of this ATPase in a transfection protocol permits the application of molecular genetic techniques to the analysis of structure-function relationships for the enzyme that establishes the internal Na+/K+ environment of most animal cells. The full-length alpha 1 subunit complementary DNA will also be useful as a dominant selectable marker for somatic cell genetic studies utilizing ouabain-sensitive cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kent, R B -- Emanuel, J R -- Ben Neriah, Y -- Levenson, R -- Housman, D E -- CA-07919/CA/NCI NIH HHS/ -- CA-26712/CA/NCI NIH HHS/ -- CA-38992/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1987 Aug 21;237(4817):901-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3039660" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Cercopithecus aethiops ; DNA/genetics ; Drug Resistance ; Gene Expression Regulation ; Macromolecular Substances ; Mice ; Ouabain/*pharmacology ; Sodium-Potassium-Exchanging ATPase/antagonists & inhibitors/*genetics ; Species Specificity ; Structure-Activity Relationship ; Transfection
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  • 13
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    Chemical identification of a tumor-derived angiogenic factor (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-05-15
    Description: Neoplasms produce substances that induce blood vessel formation (angiogenesis). Fractions from ethanol extracts of the Walker 256 carcinoma were isolated by silica column chromatography and C18 reversed-phase high-performance liquid chromatography. Two of the isolated fractions induced neovascularization when tested in the rabbit corneal micropocket assay. One of the fractions was identified as nicotinamide by desorption-electron impact mass spectrometry, nuclear magnetic resonance spectroscopy, and gas chromatography-mass spectrometry. The second active fraction contained nicotinamide as part of a more complex, as yet unidentified, molecular arrangement. Microgram quantities of commercial nicotinamide induced neovascularization in the corneal micropocket assay and in the chick chorioallantoic membrane assay.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kull, F C Jr -- Brent, D A -- Parikh, I -- Cuatrecasas, P -- New York, N.Y. -- Science. 1987 May 15;236(4803):843-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2437656" target="_blank"〉PubMed〈/a〉
    Keywords: Angiogenesis Inducing Agents/*isolation & purification/pharmacology ; Animals ; Carcinoma 256, Walker/*physiopathology ; Cells, Cultured ; Chick Embryo ; Cornea/blood supply ; Endothelium/cytology/drug effects ; Gas Chromatography-Mass Spectrometry ; Growth Substances/*isolation & purification ; Magnetic Resonance Spectroscopy ; Mass Spectrometry ; Mice ; Neovascularization, Pathologic ; Niacinamide/isolation & purification/pharmacology
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  • 14
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    Neuronal pp60c-src contains a six-amino acid insertion relative to its non-neuronal counterpart (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-07-24
    Description: Neuronal cells express a pp60c-src variant that displays an altered electrophoretic mobility and a different V8 peptide pattern relative to pp60c-src expressed in tissues of non-neuronal origin. To determine whether the neuronal form of pp60c-src is encoded by a brain-specific messenger RNA, a mouse brain complementary DNA (cDNA) library was screened with a chicken c-src probe and a 3.8-kilobase c-src cDNA clone was isolated. This clone encodes a 60-kilodalton protein that differs from chicken or human pp60c-src primarily in having six extra amino acids (Arg-Lys-Val-Asp-Val-Arg) within the NH2-terminal 16 kilodaltons of the molecule. S1 nuclease protection analysis confirmed that brain c-src RNA contains an 18-nucleotide insertion at the position of the extra six amino acids. This insertion occurs at a position that corresponds to a splice junction in the chicken and human c-src genes. The isolated c-src cDNA clone encodes a protein that displays an identical V8 peptide pattern to that observed in pp60c-src isolated from tissues of neuronal origin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Martinez, R -- Mathey-Prevot, B -- Bernards, A -- Baltimore, D -- P0I CA38497/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1987 Jul 24;237(4813):411-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2440106" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Brain/enzymology ; Chickens ; Cloning, Molecular ; DNA/metabolism ; DNA Restriction Enzymes ; DNA Transposable Elements ; Humans ; Isoenzymes/*genetics ; Mice ; Neurons/*enzymology ; Protein Kinases/*genetics ; Proto-Oncogene Proteins/*genetics ; Proto-Oncogene Proteins pp60(c-src) ; Sequence Homology, Nucleic Acid ; Species Specificity
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  • 15
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    Cloned gene of Rickettsia rickettsii surface antigen: candidate vaccine for Rocky Mountain spotted fever (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-01-02
    Description: Two major protective antigens of Rickettsia rickettsii have been previously described. In this study, we cloned the gene encoding one of these antigens into Escherichia coli and tested the effectiveness of the recombinant-made product as a vaccine for Rocky Mountain spotted fever. A clone bank of R strain R. rickettsii DNA was made in E. coli K-12 by using the plasmid vector pBR322. Transformants were screened for their ability to make rickettsial antigens by reactivity with rabbit antibodies to R. rickettsii. One of the transformants, EM24(pGAM21), made a product reactive with two monoclonal antibodies that recognize a 155-kilodalton protein of R. rickettsii. One of the monoclonal antibodies was a member of a class of antibodies that react to heat-sensitive epitopes and protect mice injected with a potentially lethal dose of viable R. rickettsii. The cloned product contained this protective heat-sensitive epitope. In order to obtain enhanced expression, the gene was subcloned downstream of the lactose promoter on the plasmid vector pUC8. A sonic lysate of E. coli harboring the pUC8 subclone was used successfully as a vaccine to protect mice injected with a lethal dose of the viable R. rickettsii.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McDonald, G A -- Anacker, R L -- Garjian, K -- New York, N.Y. -- Science. 1987 Jan 2;235(4784):83-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3099387" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens/*genetics ; Antigens, Bacterial/*genetics ; Bacterial Proteins/genetics/immunology ; Bacterial Vaccines/*genetics ; Cloning, Molecular ; Genes, Bacterial ; Mice ; Rickettsia rickettsii/*genetics/immunology ; Rocky Mountain Spotted Fever/*prevention & control ; Vaccines, Synthetic/*genetics/immunology
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  • 16
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    Mapping patterns of c-fos expression in the central nervous system after seizure (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-07-10
    Description: A dramatic and specific induction of c-fos was observed in identifiable neuronal populations in vivo after administration of the convulsant Metrazole. This effect was time- and dose-dependent and was abolished by prior treatment with the anticonvulsant drugs diazepam or pentobarbital. About 60 minutes after administration of Metrazole, c-fos messenger RNA reached a maximum and declined to basal levels after 180 minutes. A further decrease below that in normal brain was observed before a return to basal levels after 16 hours. While Metrazole still elicited seizures during this period, reinduction of c-fos was largely refractory. At 90 minutes, c-fos protein was observed in the nuclei of neurons in the dentate gyrus, and in the pyriform and cingulate cortices. Subsequently, c-fos protein appeared throughout the cortex, hippocampus, and limbic system. Thus, seizure activity results in increased c-fos gene expression in particular subsets of neurons.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Morgan, J I -- Cohen, D R -- Hempstead, J L -- Curran, T -- New York, N.Y. -- Science. 1987 Jul 10;237(4811):192-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3037702" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Brain Chemistry/drug effects ; DNA-Binding Proteins/biosynthesis/genetics ; Diazepam/pharmacology ; Fluorescent Antibody Technique ; Gene Expression Regulation ; Mice ; Mice, Inbred BALB C ; Neurons/metabolism ; Pentobarbital/pharmacology ; Pentylenetetrazole/antagonists & inhibitors/toxicity ; Proto-Oncogene Proteins/*biosynthesis/genetics ; Proto-Oncogene Proteins c-fos ; Receptors, GABA-A/drug effects ; Seizures/chemically induced/*metabolism
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  • 17
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    Selective inactivation of influenza C esterase: a probe for detecting 9-O-acetylated sialic acids (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-06-05
    Description: The influenza C virus (INF-C) hemagglutinin recognizes 9-O-acetyl-N-acetylneuraminic acid. The same protein contains the receptor-destroying enzyme (RDE), which is a 9-O-acetyl-esterase. The RDE was inactivated by the serine esterase inhibitor di-isopropyl fluorophosphate (DFP). [3H]DFP-labeling localized the active site to the heavy chain of the glycoprotein. DFP did not alter the hemagglutination or fusion properties of the protein, but markedly decreased infectivity of the virus, demonstrating that the RDE is important for primary infection. Finally, DFP-treated INF-C bound specifically and irreversibly to cells expressing 9-O-acetylated sialic acids. This provides a probe for a molecule that was hitherto very difficult to study.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Muchmore, E A -- Varki, A -- 1-K12-AM01408/AM/NIADDK NIH HHS/ -- R01 GM32373/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1987 Jun 5;236(4806):1293-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3589663" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Animals ; Binding Sites ; Biological Assay ; Hemagglutination Tests ; Influenzavirus C/drug effects/*enzymology ; Isoflurophate/metabolism/*pharmacology ; Mice ; Orthomyxoviridae/*enzymology ; Protein Binding ; Sialic Acids/*analysis ; Viral Proteins/metabolism
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  • 18
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    Allelic exclusion in transgenic mice that express the membrane form of immunoglobulin mu (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-05-15
    Description: Antibody-producing cells display a special form of regulation whereby each cell produces immunoglobulin from only one of its two sets of antibody genes. This phenomenon, called allelic exclusion, is thought to be mediated by the product of one heavy chain allele restricting the expression of the other. Heavy chains are synthesized in two molecular forms, secreted and membrane bound. In order to determine whether it is specifically the membrane-bound form of the immunoglobulin M (IgM) heavy chain (mu) that mediates this regulation, transgenic mice were created that carry a human mu chain gene altered so that it can only direct the synthesis of the membrane-bound protein. The membrane-bound form of the human mu chain was made by most of the B cells in these animals as measured by assays of messenger RNA and surface immunoglobulins. Further, the many B cells that express the human gene do not express endogenous mouse IgM, and the few B cells that express endogenous mouse mu do not express the transgene. Thus, the membrane-bound form of the mu chain is sufficient to mediate allelic exclusion. In addition, the molecular structures recognized for this purpose are conserved between human and mouse systems.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nussenzweig, M C -- Shaw, A C -- Sinn, E -- Danner, D B -- Holmes, K L -- Morse, H C 3rd -- Leder, P -- New York, N.Y. -- Science. 1987 May 15;236(4803):816-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3107126" target="_blank"〉PubMed〈/a〉
    Keywords: *Alleles ; Animals ; Antibody-Producing Cells/*immunology ; Gene Expression Regulation ; *Genes ; Humans ; Immunoglobulin M/genetics ; Immunoglobulin mu-Chains/*genetics ; Mice ; Mice, Inbred Strains ; RNA, Messenger/genetics ; Transcription, Genetic
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  • 19
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    Pancreatic neoplasia induced by SV40 T-antigen expression in acinar cells of transgenic mice (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-10-09
    Description: Three lines of transgenic mice were produced that develop pancreatic neoplasms as a consequence of expression of an elastase I-SV40 T-antigen fusion gene in the acinar cells. A developmental analysis suggests at least a two-stage process in the ontogeny of this disease. The first stage is a T antigen-induced, preneoplastic state characterized by a progression from hyperplasia to dysplasia of the exocrine pancreas, by an increased percentage of tetraploid cells, and by an arrest in acinar cell differentiation. The second stage is characterized by the formation of tumor nodules that appear to be monoclonal, because they have discrete aneuploid DNA contents. The cells within the nodules as compared to normal pancreatic tissue have less total RNA by a factor of 5, less pancreas-specific messenger RNA by a factor of about 50, and increased levels of T-antigen messenger RNA. A tumor cell line has been derived that retains both pancreatic and neoplastic properties.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ornitz, D M -- Hammer, R E -- Messing, A -- Palmiter, R D -- Brinster, R L -- GM-07266/GM/NIGMS NIH HHS/ -- HD-09172/HD/NICHD NIH HHS/ -- NS-00956/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1987 Oct 9;238(4824):188-93.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute Laboratory, University of Washington, Seattle 98195.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2821617" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Polyomavirus Transforming/*genetics ; *Cell Transformation, Neoplastic ; DNA Restriction Enzymes ; Genes ; Genes, Viral ; Mice ; Mice, Transgenic ; Pancreatic Elastase/genetics ; Pancreatic Neoplasms/genetics/*microbiology/pathology ; Protein Kinases/*genetics ; RNA, Messenger/genetics ; Simian virus 40/*genetics
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  • 20
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    Zinc selectively blocks the action of N-methyl-D-aspartate on cortical neurons (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-05-01
    Description: Large amounts of zinc are present in synaptic vesicles of mammalian central excitatory boutons and may be released during synaptic activity, but the functional significance of the metal for excitatory neurotransmission is currently unknown. Zinc (10 to 1000 micromolar) was found to have little intrinsic membrane effect on cortical neurons, but invariably produced a zinc concentration-dependent, rapid-onset, reversible, and selective attenuation of the membrane responses to N-methyl-D-aspartate, homocysteate, or quinolinate. In contrast, zinc generally potentiated the membrane responses to quisqualate or alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate and often did not affect the response to kainate. Zinc also attenuated N-methyl-D-aspartate receptor-mediated neurotoxicity but not quisqualate or kainate neurotoxicity. The ability of zinc to specifically modulate postsynaptic neuronal responses to excitatory amino acid transmitters, reducing N-methyl-to-aspartate receptor-mediated excitation while often increasing quisqualate receptor-mediated excitation, is proposed to underlie its normal function at central excitatory synapses and furthermore could be relevant to neuronal cell loss in certain disease states.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Peters, S -- Koh, J -- Choi, D W -- NS07280/NS/NINDS NIH HHS/ -- NS21628/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1987 May 1;236(4801):589-93.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2883728" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aspartic Acid/*analogs & derivatives/pharmacology ; Cell Membrane/physiology ; Cerebral Cortex/*cytology ; Drug Interactions ; Electrophysiology ; Homocysteine/analogs & derivatives/pharmacology ; Ibotenic Acid/analogs & derivatives/pharmacology ; Kainic Acid/pharmacology ; Magnesium/pharmacology ; Membrane Potentials/drug effects ; Mice ; N-Methylaspartate ; Neurons/drug effects/*physiology ; Oxadiazoles/pharmacology ; Quinolinic Acid ; Quinolinic Acids/pharmacology ; Quisqualic Acid ; Receptors, N-Methyl-D-Aspartate ; Receptors, Neurotransmitter/drug effects/physiology ; Zinc/*pharmacology ; alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid
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  • 21
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    Avian v-myc replaces chromosomal translocation in murine plasmacytomagenesis (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-02-13
    Description: Deregulation of c-myc expression in association with chromosomal translocations occurs in over 95% of murine plasmacytomas, rat immunocytomas, and human Burkitt lymphomas. Infection with a murine retrovirus (J-3) containing an avian v-myc rapidly induced plasmacytomas in pristane-primed BALB/cAn mice. Only 17% of the induced plasmacytomas that were karyotyped showed the characteristic chromosomal translocations involving the c-myc locus. Instead, all of the translocation-negative tumors demonstrated characteristic J-3 virus integration sites that were actively transcribed. Thus, the high levels of v-myc expression have replaced the requirement for chromosomal translocation in plasmacytomagenesis and accelerated the process of transformation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Potter, M -- Mushinski, J F -- Mushinski, E B -- Brust, S -- Wax, J S -- Wiener, F -- Babonits, M -- Rapp, U R -- Morse, H C 3rd -- New York, N.Y. -- Science. 1987 Feb 13;235(4790):787-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3810165" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Birds ; *Cell Transformation, Neoplastic ; *Genes, Viral ; Mice ; Mice, Inbred BALB C ; Mice, Inbred Strains ; Moloney murine leukemia virus/*genetics ; Nucleic Acid Hybridization ; *Oncogenes ; Plasmacytoma/genetics/*microbiology ; Retroviridae/*genetics ; Transcription, Genetic ; *Translocation, Genetic
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  • 22
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    Three recessive loci required for insulin-dependent diabetes in nonobese diabetic mice (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-07-17
    Description: A polygenic basis for susceptibility to insulin-dependent diabetes in nonobese diabetic (NOD) mice has been established by outcross to a related inbred strain, nonobese normal (NON). Analysis of first and second backcross progeny has shown that at least three recessive genes are required for development of overt diabetes. One, Idd-1s, is tightly linked to the H-2K locus on chromosome 17; another, Idd-2s, is localized proximal to the Thy-1/Alp-1 cluster on chromosome 9. Segregation of a third, Idd-3s, could be shown in a second backcross. Neither Idd-1s nor Idd-2s could individually be identified as the locus controlling insulitis; leukocytic infiltrates in pancreas were common in most asymptomatic BC1 mice. Both F1 and BC1 mice exhibited the unusually high percentage of splenic T lymphocytes characteristic of NOD, suggesting dominant inheritance of this trait. The polygenic control of diabetogenesis in NOD mice, in which a recessive gene linked to the major histocompatibility complex is but one of several controlling loci, suggests that similar polygenic interactions underlie this type of diabetes in humans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Prochazka, M -- Leiter, E H -- Serreze, D V -- Coleman, D L -- AM 14461/AM/NIADDK NIH HHS/ -- AM 27722/AM/NIADDK NIH HHS/ -- AM 36175/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1987 Jul 17;237(4812):286-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2885918" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromosome Mapping ; Diabetes Mellitus, Type 1/*genetics/immunology ; *Genes, Recessive ; Islets of Langerhans/immunology ; Mice ; Mice, Inbred Strains ; Mice, Mutant Strains ; Polymorphism, Genetic ; Polymorphism, Restriction Fragment Length ; T-Lymphocytes/physiology
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  • 23
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    Evolutionary and somatic selection of the antibody repertoire in the mouse (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-11-20
    Description: The repertoire of antibody variable (V) regions has been subject to evolutionary selection, affecting both the diversity of V region genes in the germline and their expression in the B lymphocyte population and its subsets. In ontogeny, contact with an antigen leads to the expansion of B cells expressing antibodies complementary to it. In a defined phase of B cell differentiation, new sets of V regions are generated from the existing repertoire through somatic hypermutation. Cells carrying advantageous antibody mutants are selected into the memory compartment and produce a stable secondary response upon reexposure to the antigen.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rajewsky, K -- Forster, I -- Cumano, A -- New York, N.Y. -- Science. 1987 Nov 20;238(4830):1088-94.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Genetics, University of Cologne, Koln, FRG.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3317826" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies/*genetics ; *Antibody Diversity ; B-Lymphocytes/*physiology ; *Biological Evolution ; *Genes, Immunoglobulin ; Genes, Switch ; Immunity ; Immunoglobulin Isotypes/genetics ; Immunoglobulin Variable Region/genetics ; Mice ; Mutation ; Selection, Genetic
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  • 24
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    Nerve terminal remodeling visualized in living mice by repeated examination of the same neuron (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-11-20
    Description: The distribution of presynaptic endings on the surfaces of autonomic ganglion cells was mapped in living mice after intravenous administration of a styryl pyridinium dye. The staining and imaging techniques did not appear to damage the ganglion cells, or the synapses on them; these procedures could therefore be repeated after an arbitrary period. Observations of the same neurons at intervals of up to 3 weeks indicate that the pattern of preganglionic terminals on many of these nerve cells gradually changes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Purves, D -- Voyvodic, J T -- Magrassi, L -- Yawo, H -- New York, N.Y. -- Science. 1987 Nov 20;238(4830):1122-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy and Neurobiology, Washington University School of Medicine, St. Louis, MO 63110.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3685967" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Coloring Agents ; Fluorescent Dyes ; Ganglia, Parasympathetic/*cytology/physiology ; Membrane Potentials ; Mice ; Nerve Endings/ultrastructure ; Neuronal Plasticity ; Pyridinium Compounds ; Time Factors ; Video Recording
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  • 25
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    Activated oncogenes in B6C3F1 mouse liver tumors: implications for risk assessment (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-09-11
    Description: The validity of mouse liver tumor end points in assessing the potential hazards of chemical exposure to humans is a controversial but important issue, since liver neoplasia in mice is the most frequent tumor target tissue end point in 2-year carcinogenicity studies. The ability to distinguish between promotion of background tumors versus a genotoxic mechanism of tumor initiation by chemical treatment would aid in the interpretation of rodent carcinogenesis data. Activated oncogenes in chemically induced and spontaneously occurring mouse liver tumors were examined and compared as one approach to determine the mechanism by which chemical treatment caused an increased incidence of mouse liver tumors. Data suggest that furan and furfural caused an increased incidence in mouse liver tumors at least in part by induction of novel weakly activating point mutations in ras genes even though both chemicals did not induce mutations in Salmonella assays. In addition to ras oncogenes, two activated raf genes and four non-ras transforming genes were detected. The B6C3F1 mouse liver may thus provide a sensitive assay system to detect various classes of proto-oncogenes that are susceptible to activation by carcinogenic insult. As illustrated with mouse liver tumors, analysis of activated oncogenes in spontaneously occurring and chemically induced rodent tumors will provide information at a molecular level to aid in the use of rodent carcinogenesis data for risk assessment.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Reynolds, S H -- Stowers, S J -- Patterson, R M -- Maronpot, R R -- Aaronson, S A -- Anderson, M W -- New York, N.Y. -- Science. 1987 Sep 11;237(4820):1309-16.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3629242" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; *Cell Transformation, Neoplastic ; Cells, Cultured ; Liver Neoplasms/*genetics ; Mice ; Mutation ; Nucleic Acid Hybridization ; *Oncogenes ; *Proto-Oncogenes ; Risk
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  • 26
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    Thrombospondin promotes cell-substratum adhesion (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-06-19
    Description: The physiological role of the platelet-secreted protein thrombospondin (TSP) is poorly understood, although it has been postulated to be involved in platelet aggregation and cellular adhesion. In this report, TSP isolated from human platelets was found to promote, in vitro, the cell-substratum adhesion of a variety of cells, including platelets, melanoma cells, muscle cells, endothelial cells, fibroblasts, and epithelial cells. The adhesion-promoting activity of TSP was species independent, specific, and not due to contamination by fibronectin, vitronectin, laminin, or platelet factor 4. The cell surface receptor for TSP is protein in nature and appears distinct from that for fibronectin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tuszynski, G P -- Rothman, V -- Murphy, A -- Siegler, K -- Smith, L -- Smith, S -- Karczewski, J -- Knudsen, K A -- New York, N.Y. -- Science. 1987 Jun 19;236(4808):1570-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2438772" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD36 ; Cattle ; Cell Adhesion/*drug effects ; Fibroblasts/drug effects ; Fibronectins/pharmacology ; Glycoproteins/*pharmacology ; Humans ; Melanoma/metabolism ; Mice ; Platelet Aggregation/drug effects ; Rabbits ; Rats ; Receptors, Mitogen/metabolism ; Swine ; Thrombospondins
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    A cell-cycle constraint on the regulation of gene expression by platelet-derived growth factor (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-11-27
    Description: In density-arrested monolayer cultures of Balb/c 3T3 cells, platelet-derived growth factor (PDGF) stimulates expression of the c-myc and c-fos proto-oncogenes, as well as the functionally uncharacterized genes, JE, KC, and JB. These genes are not coordinately regulated. Under ordinary conditions, c-fos, JE, KC, and JB respond to PDGF only when the cells are in a state of G0 growth arrest at the time of PDGF addition. The c-myc gene is regulated in opposition to the other genes, responding best to PDGF in cycling cultures.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rollins, B J -- Morrison, E D -- Stiles, C D -- CA 20042-09/CA/NCI NIH HHS/ -- GM 31489-04/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1987 Nov 27;238(4831):1269-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Medicine, Dana-Farber Cancer Institute, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3685976" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Cycle/drug effects ; Cell Division/drug effects ; Cells, Cultured ; Gene Expression Regulation/*drug effects ; Interphase ; Mice ; Mice, Inbred BALB C ; Platelet-Derived Growth Factor/*pharmacology ; Proto-Oncogenes/*drug effects ; Transcription, Genetic/*drug effects
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    The molecular basis of the sparse fur mouse mutation (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-07-24
    Description: The ornithine transcarbamylase-deficient sparse fur mouse is an excellent model to study the most common human urea cycle disorder. The mutation has been well characterized by both biochemical and enzymological methods, but its exact nature has not been revealed. A single base substitution in the complementary DNA for ornithine transcarbamylase from the sparse fur mouse has been identified by means of a combination of two recently described techniques for rapid mutational analysis. This strategy is simpler than conventional complementary DNA library construction, screening, and sequencing, which has often been used to find a new mutation. The ornithine transcarbamylase gene in the sparse fur mouse contains a C to A transversion that alters a histidine residue to an asparagine residue at amino acid 117.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Veres, G -- Gibbs, R A -- Scherer, S E -- Caskey, C T -- HD21452/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1987 Jul 24;237(4813):415-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3603027" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; DNA/analysis ; Disease Models, Animal ; *Genes ; Mice ; Mice, Mutant Strains ; *Mutation ; Ornithine Decarboxylase/deficiency/*genetics ; RNA, Messenger/genetics
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  • 29
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    Retroviruses and mouse embryos: a rapid model for neurovirulence and transplacental antiviral therapy (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-06-26
    Description: A murine model in which neurotropic retroviral infection can be studied over short periods of time was developed. Microinjection of Cas-Br-E virus into midgestation mouse embryos caused paralysis and death within 25 days after birth, in contrast to virus-infected neonates which develop disease only after 4 months. To evaluate whether antiviral drugs could cross the placental barrier and influence the course of the disease, the drug 3'-azido-3'-deoxythymidine (AZT) was administered to infected embryos through the drinking water of pregnant females. AZT treatment markedly retarded the onset and course of virus-induced central nervous system disease, permitting animals to survive beyond 4 months of age. These results are evidence for effective antiviral treatment during gestation and in the perinatal period and are of potential significance for the management of maternal transmission of the acquired immune deficiency syndrome (AIDS) virus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sharpe, A H -- Jaenisch, R -- Ruprecht, R M -- CA38497/CA/NCI NIH HHS/ -- HD19015/HD/NICHD NIH HHS/ -- U01-AI24845-01/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1987 Jun 26;236(4809):1671-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3037694" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Antiviral Agents/*therapeutic use ; Central Nervous System Diseases/drug therapy/embryology/*microbiology ; Female ; Fetal Diseases/*drug therapy/microbiology ; Gestational Age ; Maternal-Fetal Exchange ; Mice ; Pregnancy ; *Prenatal Exposure Delayed Effects ; Retroviridae/pathogenicity ; Thymidine/*analogs & derivatives/therapeutic use ; Tumor Virus Infections/*drug therapy/embryology ; Virulence ; Zidovudine
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  • 30
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    Islet allograft survival after a single course of treatment of recipient with antibody to L3T4 (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-07-17
    Description: Allografts of pancreatic islets of Langerhans were induced to survive for an indefinite period in diabetic mice if, at the time of engraftment, the mice received a single course of treatment with a monoclonal antibody directed against the L3T4 determinant, a nonpolymorphic cell surface glycoprotein present on the cell surface of the murine T helper-inducer lymphocyte subset. This treatment allowed the survival of islets of Langerhans transplanted across a major histocompatibility barrier without additional immunosuppression. The results demonstrate that the lymphocyte subset defined by the expression of the L3T4 molecules is central to the induction of allograft rejection and provides a model for tolerance induction for organ allograft transplantation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shizuru, J A -- Gregory, A K -- Chao, C T -- Fathman, C G -- DK32075/DK/NIDDK NIH HHS/ -- DK37104/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1987 Jul 17;237(4812):278-80.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2955518" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/therapeutic use ; Antigens, Differentiation, T-Lymphocyte ; Antigens, Surface/*immunology ; Diabetes Mellitus, Experimental/*therapy ; *Graft Survival ; Immune Tolerance ; *Islets of Langerhans Transplantation ; Mice ; T-Lymphocytes, Helper-Inducer/*immunology
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  • 31
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    Reversible inhibition of mammary gland growth by transforming growth factor-beta (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-07-17
    Description: Transforming growth factor-beta (TGF-beta) can stimulate or inhibit growth of cells in vitro, as well as induce the transformed phenotype. Although widely distributed in animal tissue, the effects of TGF-beta in vivo are largely unknown, and a physiological role for the peptide hormone has not been demonstrated. The effect of TGF-beta on developing epithelial tissue in situ was studied by using slow-release plastic pellets containing TGF-beta to treat developing mouse mammary gland. Powerful inhibition of mammary growth and morphogenesis was observed. This growth-inhibited mammary tissue was histologically normal, and the inhibitory effect was fully reversible. Under the conditions of these experiments, TGF-beta displayed many of the characteristics expected of a physiologically active growth-regulatory molecule.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Silberstein, G B -- Daniel, C W -- 1050/PHS HHS/ -- New York, N.Y. -- Science. 1987 Jul 17;237(4812):291-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3474783" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; DNA/biosynthesis ; Drug Implants ; Epithelial Cells ; Extracellular Matrix/physiology ; Mammary Glands, Animal/*growth & development ; Mice ; Peptides/*pharmacology ; Transforming Growth Factors
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  • 32
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    Downregulation of L3T4+ cytotoxic T lymphocytes by interleukin-2 (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-10-16
    Description: Proliferation of activated cytotoxic T lymphocytes (CTLs) that recognize foreign histocompatibility antigens is induced by interleukin-2, a potent immunoregulatory molecule originally described as T cell growth factor. Interleukin-2 (IL-2) is widely used to isolate and induce clonal expansion of CTLs for functional studies in vitro and in vivo. However, in studies with CTLs specific for class I and class II histocompatibility antigens, IL-2 rapidly downregulated the lytic activity of some class II-specific CTLs in a time- and dose-dependent manner. Lytic activity of L3T4+ CTLs specific for the murine class II antigen I-Ek was repeatedly up- and downregulated in vitro by alternate exposure to specific (alloantigen) and nonspecific (recombinant IL-2) signals, respectively. These results demonstrate that some CTLs modulate their functional property (cytolysis) while undergoing IL-2-driven cell proliferation without loss of antigen specificity or ability to revert to a lytic phenotype.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shih, C C -- Truitt, R L -- AI-22312/AI/NIAID NIH HHS/ -- CA-39854/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1987 Oct 16;238(4825):344-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatrics, Medical College of Wisconsin, Children's Hospital of Wisconsin, Milwaukee 53233.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2443976" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antigens, Differentiation, T-Lymphocyte/genetics ; Cell Line ; Clone Cells/immunology ; Cytotoxicity, Immunologic ; Epitopes ; H-2 Antigens/immunology ; Interleukin-2/*physiology ; Isoantigens/immunology ; *Lymphocyte Activation ; Mice ; Phenotype ; T-Lymphocytes, Cytotoxic/*immunology
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    Interferon-gamma and B cell stimulatory factor-1 reciprocally regulate Ig isotype production (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-05-22
    Description: Gamma interferon (IFN-gamma) and B cell stimulatory factor-1 (BSF-1), also known as interleukin-4, are T cell-derived lymphokines that have potent effects on B cell proliferation and differentiation. They are often secreted by distinct T cell clones. It is now shown that IFN-gamma stimulates the expression of immunoglobulin (Ig) of the IgG2a isotype and inhibits the production of IgG3, IgG1, IgG2b, and IgE. By contrast, BSF-1 has powerful effects in promoting switching to the expression of IgG1 and IgE but markedly inhibits IgM, IgG3, IgG2a, and IgG2b. These results indicate that BSF-1 and IFN-gamma as well as the T cells that produce them may act as reciprocal regulatory agents in the determination of Ig isotype responses. The effects of IFN-gamma and BSF-1 on isotype expression are independent.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Snapper, C M -- Paul, W E -- New York, N.Y. -- Science. 1987 May 22;236(4804):944-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3107127" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal ; Antigen-Antibody Complex ; B-Lymphocytes/drug effects/*immunology ; Cricetinae ; Growth Substances/*pharmacology ; Immunoglobulin Isotypes/*biosynthesis ; Interferon-gamma/immunology/*pharmacology ; Interleukin-4 ; Kinetics ; Lymphocyte Activation ; Lymphokines/*pharmacology ; Mice ; Mice, Inbred DBA ; Recombinant Proteins/*pharmacology
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    Two pairs of recombination signals are sufficient to cause immunoglobulin V-(D)-J joining (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-11-20
    Description: The minimum sequence requirements for antigen receptor V-(D)-J joining were studied by constructing recombination-substrates containing synthetic recombination signals and introducing them into a recombination-competent pre-B cell line. Two sets of heptamer (CACTGTG) and nonamer (GGTTTTTGT) sequences were shown to be sufficient to cause the V-(D)-J joining, if the 12- and 23-base pair spacer rule is satisfied. A point mutation in the heptamer sequence, or a change in the combination of the two spacer lengths, drastically reduced the recombination.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Akira, S -- Okazaki, K -- Sakano, H -- AI-18790/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1987 Nov 20;238(4830):1134-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, University of California, Berkeley 94720.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3120312" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Chromosome Inversion ; *Genes, Immunoglobulin ; Genetic Vectors ; Humans ; Immunoglobulin Variable Region/*genetics ; Immunoglobulin kappa-Chains/genetics ; Mice ; Receptors, Antigen, T-Cell/genetics ; *Recombination, Genetic ; Retroviridae/genetics ; Sequence Homology, Nucleic Acid ; Structure-Activity Relationship
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    Three-dimensional structure of interleukin-2 (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-12-18
    Description: Interleukin-2 is an effector protein that participates in modulating the immune response; it has become a focal point for the study of lymphokine structure and function. The three-dimensional structure of the interleukin molecule has been solved to 3.0 angstrom resolution. Interleukin-2 has a novel alpha-helical tertiary structure that suggests one portion of the molecule forms a structural scaffold, which underlies the receptor binding facets of the molecule.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brandhuber, B J -- Boone, T -- Kenney, W C -- McKay, D B -- A1-00631/PHS HHS/ -- A1-19762/PHS HHS/ -- New York, N.Y. -- Science. 1987 Dec 18;238(4834):1707-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry and Biochemistry, University of Colorado, Boulder 80309.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3500515" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Interleukin-2/isolation & purification ; Mice ; Models, Molecular ; Protein Conformation ; Solvents ; X-Ray Diffraction
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    Genetic ablation: targeted expression of a toxin gene causes microphthalmia in transgenic mice (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-12-11
    Description: Lineage-specific regulatory elements can be used to direct expression of a variety of genes to specific tissues in transgenic mice. If the hybrid constructs contain a gene encoding a cytotoxic gene product, then genetic ablation of a specific cell lineage can be achieved. We have generated six transgenic mice by introducing into fertilized eggs the mouse gamma 2-crystallin promoter fused to the coding region of the diphtheria toxin A-chain gene. Three of these mice and all the transgenic offspring analyzed were microphthalmic. The lenses of these mice displayed considerable heterogeneity: some were almost normal morphologically but reduced in size, whereas others were grossly aberrant and deficient in nuclear fiber cells. These studies indicate that programmed ablation of specific cell types can be stably transmitted through the germ line.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Breitman, M L -- Clapoff, S -- Rossant, J -- Tsui, L C -- Glode, L M -- Maxwell, I H -- Bernstein, A -- CA 42354/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1987 Dec 11;238(4833):1563-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Mount Sinai Hospital Research Institute, Toronto, Ontario, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3685993" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Crystallins/*genetics ; Diphtheria Toxin/*genetics ; Eye/pathology ; *Genes ; Mice ; Mice, Transgenic ; Microphthalmos/*genetics/pathology ; Promoter Regions, Genetic
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    The relation between major histocompatibility complex (MHC) restriction and the capacity of Ia to bind immunogenic peptides (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-03-13
    Description: The capacity of purified I-Ad, I-Ed, I-Ak, and I-Ek to bind to protein derived peptides that have been previously reported to be T cell immunogens has been examined. For each of the 12 peptides studied strong binding to the relevant Ia restriction element was observed. All the peptides bound more than one Ia molecule; however, for 11 of 12 peptides, the dominant binding was to the restriction element, whereas in one instance the dominant binding was to a nonrestriction element. When the peptides were used to inhibit the presentation of antigen by prefixed accessory cells to T cells, an excellent correlation was found between the capacity of a peptide to inhibit the binding of an antigen to purified Ia and the capacity of the peptide to inhibit accessory cell presentation of the antigen. Thus, the binding of peptide to purified Ia is immunologically relevant, and Ia seems to be the only saturable molecule on the surface of the accessory cell involved in antigen presentation. Inhibition analysis also indicated that all peptides restricted to a particular Ia molecule competitively inhibited one another, suggesting that each Ia restriction element has a single binding site for antigen. Cross-linking of labeled peptides to Ia followed by electrophoretic analysis and autoradiography suggested that this single binding site is made up of portions of both alpha and beta chains of Ia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Buus, S -- Sette, A -- Colon, S M -- Miles, C -- Grey, H M -- AI 18634/AI/NIAID NIH HHS/ -- AI 22295/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1987 Mar 13;235(4794):1353-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2435001" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens/immunology ; Binding, Competitive ; Columbidae ; Cross-Linking Reagents ; Cytochrome c Group/immunology ; Epitopes/genetics/immunology ; Glutaral ; Histocompatibility Antigens Class II/*metabolism ; Hybridomas/immunology ; *Major Histocompatibility Complex ; Mice ; Moths ; Peptide Fragments/immunology ; Peptides/*immunology ; T-Lymphocytes/immunology
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    Efficacy of murine malaria sporozoite vaccines: implications for human vaccine development (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-04-24
    Description: As part of a study of potential vaccines against malaria, the protective efficacy of sporozoite subunit vaccines was determined by using the Plasmodium berghei murine malaria model. Mice were immunized with recombinant DNA-produced or synthetic peptide-carrier subunit vaccines derived from the repetitive epitopes of the Plasmodium berghei circumsporozoite gene, or with radiation-attenuated sporozoites. Immunization with subunit vaccines elicited humoral responses that were equivalent to or greater than those elicited by irradiated sporozoites, yet the protection against sporozoite challenge induced by either of the subunit vaccines was far less than that achieved by immunization with attenuated sporozoites. Passive and adoptive transfer studies demonstrated that subunit vaccines elicited predominantly antibody-mediated protection that was easily overcome whereas irradiated sporozoites induced potent cell-mediated immunity that protected against high challenge doses of sporozoites. These studies indicate that new strategies designed to induce cellular immunity will be required for efficacious sporozoite vaccines.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Egan, J E -- Weber, J L -- Ballou, W R -- Hollingdale, M R -- Majarian, W R -- Gordon, D M -- Maloy, W L -- Hoffman, S L -- Wirtz, R A -- Schneider, I -- New York, N.Y. -- Science. 1987 Apr 24;236(4800):453-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3551073" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antigens, Protozoan ; Antigens, Surface/*immunology ; Dose-Response Relationship, Immunologic ; Immunity, Cellular ; Immunization, Passive ; Malaria/*prevention & control ; Mice ; Oligopeptides/immunology ; Plasmodium berghei/*immunology ; *Protozoan Proteins ; Recombinant Fusion Proteins/immunology ; *Vaccines, Synthetic
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  • 39
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    Construction of synthetic immunogen: use of new T-helper epitope on malaria circumsporozoite protein (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-02-27
    Description: The circumsporozoite (CS) protein of Plasmodium falciparum is the focus of intense efforts to develop an antisporozoite malaria vaccine. Localization of sites for T-cell recognition on this molecule is critical for vaccine design. By using an algorithm designed to predict T-cell sites and a large panel of H-2 congenic mice, a major nonrepetitive T-cell site was located. When a synthetic peptide corresponding to this site was covalently linked to the major B-cell site on the molecule, an immunogen capable of eliciting a high-titer antibody response was formed. This peptide sequence could prime helper T cells for a secondary response to the intact CS protein. The new helper T-cell site is located outside the repetitive region of the CS protein and appears to be the immunodominant T site on the molecule. This approach should be useful in the rational design and construction of vaccines.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Good, M F -- Maloy, W L -- Lunde, M N -- Margalit, H -- Cornette, J L -- Smith, G L -- Moss, B -- Miller, L H -- Berzofsky, J A -- New York, N.Y. -- Science. 1987 Feb 27;235(4792):1059-62.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2434994" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antibody Formation ; Antigens, Protozoan/immunology ; Antigens, Surface/*immunology ; B-Lymphocytes/immunology ; Epitopes/*immunology ; Mice ; Peptide Fragments/chemical synthesis/*immunology ; Plasmodium falciparum/*immunology ; *Protozoan Proteins ; Receptors, Antigen, B-Cell/immunology ; Receptors, Antigen, T-Cell/immunology ; T-Lymphocytes/immunology ; T-Lymphocytes, Helper-Inducer/*immunology ; Vaccines/immunology
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    Clonal gene therapy: transplanted mouse fibroblast clones express human alpha 1-antitrypsin gene in vivo (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-08-14
    Description: A retroviral vector was used to insert human alpha 1-antitrypsin (alpha 1AT) complementary DNA into the genome of mouse fibroblasts to create a clonal population of mouse fibroblasts secreting human alpha 1AT. After demonstrating that this clone of fibroblasts produced alpha 1AT after more than 100 population doublings in the absence of selection pressure, the clone was transplanted into the peritoneal cavities of nude mice. When the animals were evaluated 4 weeks later, human alpha 1AT was detected in both sera and the epithelial surface of the lungs. The transplanted clone of fibroblasts could be recovered from the peritoneal cavities of those mice and demonstrated to still be producing human alpha 1AT. Thus, even after removal of selective pressure, a single clone of retroviral vector-infected cells that expressed an exogenous gene in vitro, continued to do so in vivo, and when recovered, continued to produce the product of the exogenous gene.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Garver, R I Jr -- Chytil, A -- Courtney, M -- Crystal, R G -- New York, N.Y. -- Science. 1987 Aug 14;237(4816):762-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3497452" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Clone Cells/metabolism ; DNA/*genetics ; DNA, Recombinant ; Fibroblasts/metabolism/*transplantation ; Humans ; Lung/metabolism ; Mice ; Mice, Nude ; Peritoneal Cavity ; Retroviridae/genetics ; *Transformation, Genetic ; alpha 1-Antitrypsin/biosynthesis/*genetics
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    Beta 1-6 branching of Asn-linked oligosaccharides is directly associated with metastasis (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-05-01
    Description: Neoplastic transformation has been associated with a variety of structural changes in cell surface carbohydrates, most notably increased sialylation and beta 1-6-linked branching of complex-type asparagine (Asn)-linked oligosaccharides (that is, -GlcNAc beta 1-6Man alpha 1-6Man beta 1-). However, little is known about the relevant glycoproteins or how these transformation-related changes in oligosaccharide biosynthesis may affect the malignant phenotype. Here it is reported that a cell surface glycoprotein, gp 130, is a major target of increased beta 1-6-linked branching and that the expression of these oligosaccharide structures is directly related to the metastatic potential of the cells. Glycosylation mutants of a metastatic tumor cell line were selected that are deficient in both beta 1-6 GlcNAc transferase V activity and metastatic potential in situ. Moreover, induction of increased beta 1-6 branching in clones of a nonmetastatic murine mammary carcinoma correlated strongly with acquisition of metastatic potential. The results indicate that increased beta 1-6-linked branching of complex-type oligosaccharides on gp 130 may be an important feature of tumor progression related to increased metastatic potential.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dennis, J W -- Laferte, S -- Waghorne, C -- Breitman, M L -- Kerbel, R S -- R0I-CA41233/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1987 May 1;236(4801):582-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2953071" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Asparagine ; Carbohydrate Conformation ; Cell Line ; Cell Transformation, Neoplastic ; Glucosyltransferases/metabolism ; Glycosylation ; Lysosome-Associated Membrane Glycoproteins ; *Membrane Glycoproteins ; Membrane Proteins/metabolism ; Mice ; Mutation ; *N-Acetylglucosaminyltransferases ; *Neoplasm Metastasis ; Neoplasms, Experimental/genetics/metabolism ; *Oligosaccharides/biosynthesis ; Structure-Activity Relationship
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    Severely impaired adipsin expression in genetic and acquired obesity (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-07-24
    Description: Adipsin, a serine protease homolog, is synthesized and secreted by adipose cells and is found in the bloodstream. The expression of adipsin messenger RNA (mRNA) and protein was analyzed in rodents during metabolic perturbations and in several experimental models of obesity. Adipsin mRNA abundance is increased in adipose tissue during fasting in normal rats and in diabetes due to streptozotocin-induced insulin deficiency. Adipsin mRNA abundance decreased during the continuous infusion of glucose, which induces a hyperglycemic, hyperinsulinemic state that is accompanied by an increased adipose mass; it is suppressed (greater than 100-fold) in two strains of genetically obese mice (db/db and ob/ob), compared to their congenic counterparts, and is also reduced when obesity is induced chemically by injection of monosodium glutamate into newborn mice. Circulating adipsin protein is decreased in these animal models of obesity, as determined by immunoblotting with antisera to adipsin. Little change in adipsin expression is observed in a model of obesity obtained by pure overfeeding of normal rats (cafeteria model). These data suggest a possible role for adipsin in the above-mentioned disordered metabolic states, and raise the possibility that adipsin expression may be used to distinguish obesities that arise from certain genetic or metabolic defects from those that result from pure overfeeding.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Flier, J S -- Cook, K S -- Usher, P -- Spiegelman, B M -- AM28082/AM/NIADDK NIH HHS/ -- AM31405/AM/NIADDK NIH HHS/ -- DK34605/DK/NIDDK NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1987 Jul 24;237(4813):405-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3299706" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue/enzymology ; Animals ; Antigen-Antibody Complex ; Complement Factor D ; Endopeptidases/*genetics/metabolism ; Immune Sera ; Mice ; Mice, Obese ; Obesity/*enzymology/genetics ; RNA, Messenger/genetics ; Reference Values ; *Serine Endopeptidases ; *Transcription, Genetic
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    Modulation of memory processing by cholecystokinin: dependence on the vagus nerve (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-05-15
    Description: Allowing mice access to food immediately after an aversive training session enhances memory retention. Cholecystokinin-octapeptide (CCK-8), which is a gastrointestinal hormone released during feeding, also enhances memory retention when administered intraperitoneally. This memory-enhancing effect of CCK-8 is blocked when the vagus nerve is cut, indicating that CCK-8 may produce its effect on memory retention by activating ascending fibers in the vagus nerve. Thus, CCK-8, a peripherally acting peptide, may mediate the memory-enhancing effects of feeding.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Flood, J F -- Smith, G E -- Morley, J E -- New York, N.Y. -- Science. 1987 May 15;236(4803):832-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3576201" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Avoidance Learning/drug effects ; Electroshock ; Male ; Memory/*drug effects ; Mice ; Mice, Inbred Strains ; Sincalide/*pharmacology ; Vagotomy ; Vagus Nerve/drug effects/*physiology
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    Encystation and expression of cyst antigens by Giardia lamblia in vitro (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-02-27
    Description: The cyst form of Giardia lamblia is responsible for transmission of giardiasis, a common waterborne intestinal disease. In these studies, encystation of Giardia lamblia in vitro was demonstrated by morphologic, immunologic, and biochemical criteria. In the suckling mouse model, the jejunum was shown to be a major site of encystation of the parasite. Small intestinal factors were therefore tested as stimuli of encystation. An antiserum that reacted with cysts, but not with cultured trophozoites was raised in rabbits and used as a sensitive probe for differentiation in vitro. Cultured trophozoites that were exposed to bile salts showed a more than 20-fold increase in the number of oval, refractile cells that reacted strongly with anticyst antibodies, and in the expression of major cyst antigens. Exposure to primary bile salts resulted in higher levels of encystation than exposure to secondary bile salts. These studies will aid in understanding the differentiation of an important protozoan pathogen.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gillin, F D -- Reiner, D S -- Gault, M J -- Douglas, H -- Das, S -- Wunderlich, A -- Sauch, J F -- AI 19863/AI/NIAID NIH HHS/ -- AM 35108/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1987 Feb 27;235(4792):1040-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3547646" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Protozoan/*analysis ; Bile Acids and Salts/pharmacology ; Enzyme-Linked Immunosorbent Assay ; Fluorescent Antibody Technique ; Giardia/drug effects/immunology/*physiology ; Giardiasis/parasitology ; Intestines/parasitology ; Mice
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    Tumor necrosis factor (cachectin) as an essential mediator in murine cerebral malaria (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-09-04
    Description: Tumor necrosis factor, or cachectin (TNF-alpha), a protein with a wide range of biological activities, is produced mainly by macrophages and may be important in inflammatory processes. The role of TNF-alpha in the pathogenesis of cerebral malaria was investigated in a murine model. Most CBA mice infected with Plasmodium berghei anka die between days 6 and 14 with acute neurological manifestations unrelated to the level of parasitemia, whereas mice of some other strains have malaria of the same severity that ends in death after 3 to 4 weeks without neurological manifestations. The activity of serum TNF-alpha was considerably increased in CBA/Ca mice with cerebral malaria but not in Plasmodium berghei-infected mice that did not develop this complication. One injection of rabbit antibody to TNF-alpha on day 4 or 7 fully protected infected mice from cerebral malaria without modifying the parasitemia, whereas immunoglobulins from normal rabbit had no effect. In mice with cerebral malaria, the cerebral vessels showed focal accumulations of packed macrophages often containing infected erythrocytes; this lesion was not seen in mice treated with antibody to TNF-alpha or in untreated mice without cerebral malaria. These findings indicate that TNF-alpha has an important role in the pathogenesis of cerebral malaria in this murine model and suggest that local accumulation and activation of macrophages may lead to the predominance of lesions in the central nervous system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grau, G E -- Fajardo, L F -- Piguet, P F -- Allet, B -- Lambert, P H -- Vassalli, P -- New York, N.Y. -- Science. 1987 Sep 4;237(4819):1210-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3306918" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain Diseases/etiology/pathology/*physiopathology ; Cerebral Cortex/pathology ; Glycoproteins/*physiology ; *Macrophage Activation ; Macrophages/cytology ; Malaria/complications/pathology/*physiopathology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred CBA ; Plasmodium berghei ; Tumor Necrosis Factor-alpha
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    Immunological self, nonself discrimination (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-02-20
    Description: The ability of immunodominant peptides derived from several antigen systems to compete with each other for T cell activation was studied. Only peptides restricted by a given transplantation antigen are mutually competitive. There is a correlation between haplotype restriction, ability to bind to the appropriate transplantation antigen, and ability to inhibit activation of other T cells restricted by the same transplantation antigen. An exception was noted in that a peptide derived from an antigen, bacteriophage lambda cI repressor, binds to the I-Ed molecule in a specific way, yet is not I-Ed-restricted. Comparison of the sequence of the repressor peptide with that of other peptides able to bind to (and be restricted by) I-Ed and a polymorphic region of the I-Ed molecule itself revealed a significant degree of homology. Thus, peptides restricted by a given class II molecule appear to be homologous to a portion of the class II molecule itself. The repressor-derived peptide is identical at several polymorphic residues at this site, and this may account for the failure of I-Ed to act as a restriction element. Comparison of antigenic peptide sequences with transplantation antigen sequences suggests a model that provides a basis for explaining self, nonself discrimination as well as alloreactivity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Guillet, J G -- Lai, M Z -- Briner, T J -- Buus, S -- Sette, A -- Grey, H M -- Smith, J A -- Gefter, M L -- AI13357/AI/NIAID NIH HHS/ -- AI18634/AI/NIAID NIH HHS/ -- CA28900/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1987 Feb 20;235(4791):865-70.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2433769" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens/*immunology ; Autoantigens/immunology ; *DNA-Binding Proteins ; Epitopes ; Histocompatibility Antigens Class II/*immunology ; Hybridomas ; Isoantigens/immunology ; Lymphocyte Activation ; Mice ; Micrococcal Nuclease/immunology ; Ovalbumin/immunology ; Protein Binding ; Receptors, Immunologic/*immunology ; Repressor Proteins/immunology ; T-Lymphocytes/*immunology ; T-Lymphocytes, Helper-Inducer/immunology ; Viral Proteins ; Viral Regulatory and Accessory Proteins
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    Recombinant interferon enhances monoclonal antibody-targeting of carcinoma lesions in vivo (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-02-20
    Description: Heterogeneity in the expression of tumor-associated antigens, as defined by the binding of monoclonal antibodies, is a characteristic common to most, if not all, human carcinoma cell populations. Antigen-negative cells within the population can escape detection and therapy by their failure to bind the appropriate antibody. Therefore, the extent of antigenic heterogeneity is an important consideration when designing protocols for the management of cancer by administration of monoclonal antibodies. One approach to counteracting the effect of antigenic heterogeneity is the use of clone A of recombinant human leukocyte interferon (Hu-IFN-alpha A). Administration of Hu-IFN-alpha A in vivo effectively increased the amount of tumor antigen expressed by a human colon xenograft in situ and augmented the localization of a radiolabeled monoclonal antibody to the tumor site. Concomitant administration of Hu-IFN-alpha A and monoclonal antibody may thus be effective in overcoming the antigenic heterogeneity of carcinoma cell populations and in enhancing the efficacy of monoclonal antibodies in the detection and treatment of carcinoma lesions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Greiner, J W -- Guadagni, F -- Noguchi, P -- Pestka, S -- Colcher, D -- Fisher, P B -- Schlom, J -- New York, N.Y. -- Science. 1987 Feb 20;235(4791):895-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3580039" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/*administration & dosage ; Antigens, Neoplasm/*immunology ; Antigens, Surface/immunology ; Carcinoma/*immunology ; Colonic Neoplasms/*immunology ; HLA Antigens/immunology ; Humans ; Interferon Type I/*administration & dosage ; Mice ; Mice, Nude ; Neoplasm Transplantation
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    Forskolin and phorbol esters reduce the same potassium conductance of mouse neurons in culture (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-01-16
    Description: Second messenger systems may modulate neuronal activity through protein phosphorylation. However, interactions between two major second messenger pathways, the cyclic AMP and phosphatidylinositol systems, are not well understood. The effects of activators of cyclic AMP-dependent protein kinase and protein kinase C on resting membrane properties, action potentials, and currents recorded from mouse dorsal root ganglion neurons and cerebral hemisphere neurons grown in primary dissociated cell culture were investigated. Neither forskolin (FOR) nor phorbol 12,13-dibutyrate (PDBu) altered resting membrane properties but both increased the duration of calcium-dependent action potentials in both central and peripheral neurons. By means of the single-electrode voltage clamp technique, FOR and PDBu were shown to decrease the same voltage-dependent potassium conductance. This suggests that two independent second messenger systems may affect the same potassium conductance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grega, D S -- Werz, M A -- Macdonald, R L -- NS 07231/NS/NINDS NIH HHS/ -- NS 19613/NS/NINDS NIH HHS/ -- NS 19692/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1987 Jan 16;235(4786):345-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2432663" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials/*drug effects ; Animals ; Brain/cytology ; Calcium/physiology ; Cells, Cultured ; Colforsin/*pharmacology ; Electric Conductivity ; Ganglia, Spinal/cytology ; Ion Channels/physiology ; Membrane Potentials ; Mice ; Neurons/drug effects/*physiology ; Phorbol Esters/*pharmacology ; Potassium/*physiology
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    Diversity of alpha-fetoprotein gene expression in mice is generated by a combination of separate enhancer elements (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-01-02
    Description: The 5' flanking region of the mouse alpha-fetoprotein (AFP) gene contains a tissue-specific promoter and three upstream regulatory elements that behave as classical enhancers. At least one of these enhancers is now shown to be required for the tissue-specific expression of the AFP gene when it is introduced into the mouse genome by microinjection of cloned DNA fragments into fertilized eggs. Each enhancer can direct expression in the appropriate tissues, the visceral endoderm of the yolk sac, the fetal liver, and the gastrointestinal tract, but each exerts different influence in these three tissues. These differences may explain the tissue-specific diversity in the levels of expression characteristic of the AFP gene. The postnatal repression of transcription of the AFP gene in both liver and gut, as well as the reinitiation of its transcription during liver regeneration, is mimicked by the introduced gene when it is linked to the enhancer domains together or singly. Thus, the DNA sequence elements responsible for directing the activation of AFP transcription, its repression, and reinduction are contained in a limited segment of DNA within or 5' to the gene (or both) and are operative in the absence of the closely linked albumin gene.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hammer, R E -- Krumlauf, R -- Camper, S A -- Brinster, R L -- Tilghman, S M -- CA06927/CA/NCI NIH HHS/ -- CA28050/CA/NCI NIH HHS/ -- HD17321/HD/NICHD NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1987 Jan 2;235(4784):53-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2432657" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cloning, Molecular ; *Enhancer Elements, Genetic ; Gene Expression Regulation ; Genes ; *Genes, Regulator ; Intestines/physiology ; Liver/physiology ; Mice ; Promoter Regions, Genetic ; RNA, Messenger/genetics ; Tissue Distribution ; Transcription, Genetic ; Transfection ; Yolk Sac/physiology ; alpha-Fetoproteins/*genetics
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    A transgenic mouse model for human neurofibromatosis (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-09-11
    Description: Human T-lymphotropic virus type 1 (HTLV-1) has been associated with the neurologic disorder tropical spastic paraparesis and possibly with multiple sclerosis. The tat gene of HTLV-1 under control of its own long terminal repeat is capable of inducing tumors in transgenic mice. The morphologic and biologic properties of these tumors indicate their close resemblance to human neurofibromatosis (von Recklinghausen's disease), the most common single gene disorder to affect the nervous system. The high spontaneous incidence of this disease, together with the diverse clinical and pathologic features associated with it, suggests that environmental factors may account for some of the observed cases. Multiple tumors developed simultaneously in the transgenic tat mice at approximately 3 months of age, and the phenotype was successfully passed through three generations. The tumors arise from the nerve sheaths of peripheral nerves and are composed of perineural cells and fibroblasts. Tumor cells from these mice adapt easily to propagation in culture and continue to express the tat protein in significant amounts. When transplanted into nude mice, these cultured cells efficiently induce tumors. Evidence of HTLV-1 infection in patients with neural and other soft tissue tumors is needed in order to establish a link between infection by this human retrovirus and von Recklinghausen's disease and other nonlymphoid tumors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hinrichs, S H -- Nerenberg, M -- Reynolds, R K -- Khoury, G -- Jay, G -- New York, N.Y. -- Science. 1987 Sep 11;237(4820):1340-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2888191" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Deltaretrovirus Infections/*genetics/pathology ; Disease Models, Animal ; Fluorescent Antibody Technique ; Genetic Engineering ; Humans ; Mice ; Mice, Nude ; Neurofibromatosis 1/*genetics/microbiology/pathology ; Viral Fusion Proteins/analysis
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    Antibody research garners Nobel Prize (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-10-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J L -- New York, N.Y. -- Science. 1987 Oct 23;238(4826):484-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3310235" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies/genetics ; *Antibody Diversity ; History, 20th Century ; Humans ; Japan/ethnology ; Mice ; *Nobel Prize ; United States
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    The molecular control of blood cell development (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-12-04
    Description: The establishment of a cell culture system for the clonal development of blood cells has made it possible to identify the proteins that regulate the growth and differentiation of different blood cell lineages and to discover the molecular basis of normal and abnormal cell development in blood forming tissues. A model system with myeloid blood cells has shown that (i) normal blood cells require different proteins to induce cell multiplication (growth inducers) and cell differentiation (differentiation inducers), (ii) there is a hierarchy of growth inducers as cells become more restricted in their developmental program, and (iii) a cascade of interactions between proteins determines the correct balance between immature and mature cells in normal blood cell development. Gene cloning has shown that there is a family of different genes for these proteins. Normal protein regulators of blood cell development can control the abnormal growth of certain types of leukemic cells and suppress malignancy by inducing differentiation to mature nondividing cells. Chromosome abnormalities that give rise to malignancy in these leukemic cells can be bypassed and their effects nullified by inducing differentiation, which stops cells from multiplying. These blood cell regulatory proteins are active in culture and in the body, and they can be used clinically to correct defects in blood cell development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sachs, L -- New York, N.Y. -- Science. 1987 Dec 4;238(4832):1374-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Weizmann Institute of Science, Rehovot, Israel.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3317831" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bone Marrow Cells ; Cell Differentiation/drug effects ; Cells, Cultured ; Clone Cells/cytology ; Colony-Stimulating Factors/physiology/therapeutic use ; *Hematopoiesis/drug effects ; Hematopoietic Stem Cells/cytology ; Humans ; Interleukin-3/physiology/therapeutic use ; Leukemia, Myeloid/drug therapy/physiopathology ; Mice ; Neoplastic Stem Cells/drug effects/pathology
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    The biology and chemistry of fertilization (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-01-30
    Description: Fertilization of eggs by sperm, the means by which sexual reproduction takes place in nearly all multicellular organisms, is fundamental to the maintenance of life. In both mammals and nonmammals, the pathway that leads to fusion of an egg with a single sperm consists of many steps that occur in a compulsory order. These steps include species-specific cellular recognition, intracellular and intercellular membrane fusions, and enzyme-catalyzed modifications of cellular investments. In several instances, the molecular mechanisms that underlie these events during mammalian fertilization are beginning to be revealed.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wassarman, P M -- New York, N.Y. -- Science. 1987 Jan 30;235(4788):553-60.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3027891" target="_blank"〉PubMed〈/a〉
    Keywords: Acrosome/physiology ; Animals ; *Fertilization ; Glycoproteins/physiology ; Humans ; Male ; Membrane Fusion ; Mice ; Ovum/*physiology ; Receptors, Cell Surface/physiology ; Sea Urchins ; Spermatozoa/*physiology
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    Early restriction of the human antibody repertoire (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-11-06
    Description: Diversification of the antibody repertoire in mammals results from a series of apparently random somatically propagated gene rearrangement and mutational events. Nevertheless, it is well known that the adult repertoire of antibody specificities is acquired in a developmentally programmed fashion. As previously shown, rearrangement of the gene segments encoding the heavy-chain variable regions (VH) of mouse antibodies is also developmentally ordered: the number of VH gene segments rearranged in B lymphocytes of fetal mice is small but increased progressively after birth. In this report, human fetal B-lineage cells were also shown to rearrange a highly restricted set of VH gene segments. In a sample of heavy-chain transcripts from a 130-day human fetus the most frequently expressed human VH element proved to be closely related to the VH element most frequently expressed in murine fetal B-lineage cells. These observations are important in understanding the development of immunocompetence.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schroeder, H W Jr -- Hillson, J L -- Perlmutter, R M -- AI07470/AI/NIAID NIH HHS/ -- GM07454/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1987 Nov 6;238(4828):791-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, University of Washington, Seattle 98195.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3118465" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Amino Acid Sequence ; Animals ; B-Lymphocytes/immunology ; Base Sequence ; Fetus ; *Genes, Immunoglobulin ; Humans ; Immunoglobulin Heavy Chains/genetics ; Immunoglobulin Variable Region/genetics ; Mice ; Molecular Sequence Data ; Mutation ; Sequence Homology, Nucleic Acid
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    Implantation of genetically engineered fibroblasts into mice: implications for gene therapy (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-05-08
    Description: In a variety of human genetic diseases, replacement of the absent or defective protein provides significant therapeutic benefits. As a model for a somatic cell gene therapy system, cultured murine fibroblasts were transfected with a human growth hormone (hGH) fusion gene and cells from one of the resulting clonal lines were subsequently implanted into various locations in mice. Such implants synthesized and secreted hGH, which was detectable in the serum. The function of the implants depended on their location and size, and on the histocompatibility of the donor cells with their recipients. The expression of hGH could be modified by addition of regulatory effectors, and, with appropriate immunosuppression, the implants survived for more than 3 months. This approach to gene therapy, here termed "transkaryotic implantation," is potentially applicable to many genetic diseases in that the transfected cell line can be extensively characterized prior to implantation, several anatomical sites are suitable for implantation, and regulated expression of the gene of therapeutic interest can be obtained.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Selden, R F -- Skoskiewicz, M J -- Howie, K B -- Russell, P S -- Goodman, H M -- AM-07055/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1987 May 8;236(4802):714-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3472348" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; DNA, Recombinant ; Fibroblasts/immunology/*transplantation ; *Genetic Engineering ; Graft Survival ; Growth Hormone/biosynthesis/*genetics ; Humans ; Immunosuppression ; Kidney ; Kinetics ; Mice ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Plasmids ; Therapeutics ; Transfection
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    The glucocorticoid receptor protein binds to transfer RNA (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-01-23
    Description: The glucocorticoid receptor from mouse AtT-20 cells exists in three forms: the untransformed receptor (9.1S; Mr of 319,000), a large oligomeric molecule that does not bind to DNA; the transformed receptor (4S; Mr of 96,000), which is formed by dissociation of untransformed receptor after steroid binding and which binds to DNA to modulate gene expression; and an intermediate size receptor (6S; Mr of 132,000), which also binds to DNA and contains a bound small RNA molecule. This RNA species has now been purified and identified as transfer RNA (tRNA). The three tRNA's for the basic amino acids accounted for about 78% of the total amino acid-accepting activity [arginine (52%), lysine (17%), and histidine (9%)], while the remaining 22% was represented by six other tRNA species. This tRNA-binding activity of the glucocorticoid receptor may reflect post-transcriptional mechanisms of regulating gene expression, such as alterations in the translational efficiency of or the modulation of the stability of hormone-induced proteins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ali, M -- Vedeckis, W V -- AM-36086/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1987 Jan 23;235(4787):467-70.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3798121" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; DNA-Binding Proteins/metabolism ; Gene Expression Regulation ; Mice ; Molecular Weight ; RNA, Transfer/classification/*metabolism ; Receptors, Glucocorticoid/*metabolism
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    Adrenal medulla grafts enhance recovery of striatal dopaminergic fibers (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-08-21
    Description: The drug, 1-methyl-4-phenyl-1,2,5,6-tetrahydropyridine (MPTP), depletes striatal dopamine levels in primates and certain rodents, including mice, and produces parkinsonian-like symptoms in humans and nonhuman primates. To investigate the consequences of grafting adrenal medullary tissue into the brain of a rodent model of Parkinson's disease, a piece of adult mouse adrenal medulla was grafted unilaterally into mouse striatum 1 week after MPTP treatment. This MPTP treatment resulted in the virtual disappearance of tyrosine hydroxylase-immunoreactive fibers and severely depleted striatal dopamine levels. At 2, 4, and 6 weeks after grafting, dense tyrosine hydroxylase-immunoreactive fibers were observed in the grafted striatum, while only sparse fibers were seen in the contralateral striatum. In all cases, tyrosine hydroxylase-immunoreactive fibers appeared to be from the host rather than from the grafts, which survived poorly. These observations suggest that, in mice, adrenal medullary grafts exert a neurotrophic action in the host brain to enhance recovery of dopaminergic neurons. This effect may be relevant to the symptomatic recovery in Parkinson's disease patients who have received adrenal medullary grafts.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bohn, M C -- Cupit, L -- Marciano, F -- Gash, D M -- NS00910/NS/NINDS NIH HHS/ -- NS15109/NS/NINDS NIH HHS/ -- NS20832/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1987 Aug 21;237(4817):913-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2887034" target="_blank"〉PubMed〈/a〉
    Keywords: 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine ; Adrenal Medulla/*transplantation ; Animals ; Corpus Striatum/*physiology ; Dopamine/*physiology ; Fluorescent Antibody Technique ; Mice ; Neurons/drug effects ; Phenylethanolamine N-Methyltransferase/metabolism ; Pyridines/pharmacology ; Substantia Nigra/physiology ; Tyrosine 3-Monooxygenase/metabolism
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    Solo actions of AIDS virus coat (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-08-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barnes, D M -- New York, N.Y. -- Science. 1987 Aug 28;237(4818):971-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3039663" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/microbiology ; Animals ; Chick Embryo ; HIV/*physiology ; HIV Envelope Protein gp120 ; Humans ; Mice ; Neurons/microbiology ; Retroviridae Proteins/physiology ; Viral Envelope Proteins/physiology
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    Genetic reconstitution of functional acetylcholine receptor channels in mouse fibroblasts (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-12-18
    Description: Foreign genes can be stably integrated into the genome of a cell by means of DNA-mediated gene transfer techniques, and large quantities of homogenous cells that continuously express these gene products can then be isolated. Such an expression system can be used to study the functional consequences of introducing specific mutations into genes and to study the expressed protein in the absence of cellular components with which it is normally in contact. All four Torpedo acetylcholine receptor (AChR) subunit complementary DNA's were introduced into the genome of a mouse fibroblast cell by DNA-mediated gene transfer. A clonal cell line that stably produced high concentrations of correctly assembled cell surface AChR's and formed proper ligand-gated ion channels was isolated. With this new expression system, recombinant DNA, biochemical, pharmacological, and electrophysiological techniques were combined to study Torpedo AChR's in a single intact system. The physiological and pharmacological profiles of Torpedo AChR's expressed in mouse fibroblast cells differ in some details from those described earlier, and may provide a more accurate reflection of the properties of this receptor in its natural environment.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Claudio, T -- Green, W N -- Hartman, D S -- Hayden, D -- Paulson, H L -- Sigworth, F J -- Sine, S M -- Swedlund, A -- NS 07102/NS/NINDS NIH HHS/ -- NS 21501/NS/NINDS NIH HHS/ -- NS 21714/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1987 Dec 18;238(4834):1688-94.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, CT 06510.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3686008" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cell Membrane/physiology ; Fibroblasts/metabolism ; *Genes ; Kinetics ; Mice ; Receptors, Cholinergic/*genetics/metabolism ; Torpedo ; *Transfection
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    Glucocorticoid receptor-like antigen in lymphoma cell membranes: correlation to cell lysis (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-04-24
    Description: S-49 mouse lymphoma cells undergo lysis when treated with glucocorticoids; the mechanism of this effect is not understood. A protein was detected in the plasma membrane of these cells by means of direct immunofluorescent labeling with a monoclonal antibody to the soluble glucocorticoid receptor. Cellular heterogeneity in the content of this glucocorticoid receptor-like molecule was evident. By immunoadsorption to antibody-coated tissue culture plates, the cells were separated into populations positive (100%) and depleted (38%) for this membrane antigen. Gel electrophoresis, specific immunoblot, and autoradiographic (binding of [3H]dexamethasone mesylate) analysis of the membrane proteins from the membrane antigen-positive group revealed multiple protein bands ranging in size from 85 to 145 kilodaltons. Furthermore, comparison of the glucocorticoid sensitivity of these groups of cells showed complete lysis of the membrane antigen-positive cells and only partial lysis of the antigen-deficient group, which suggests that the lysis response of cells to glucocorticoids is mediated by a glucocorticoid receptor-like molecule located in the plasma membrane.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gametchu, B -- CA17701/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1987 Apr 24;236(4800):456-61.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3563523" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Neoplasm/*analysis ; Antigens, Surface/*analysis ; Cell Line ; Cell Membrane/immunology/metabolism ; Cell Nucleus/metabolism ; Cell Survival/drug effects ; Cytoplasm/metabolism ; Dexamethasone/metabolism/pharmacology ; Lymphoma/*immunology ; Mice ; Molecular Weight ; Receptors, Glucocorticoid/*immunology/metabolism
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    A chicken transferrin gene in transgenic mice escapes X-chromosome inactivation (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-05-01
    Description: Mammalian X-chromosome inactivation involves a coordinate shutting down of physically linked genes. Several proposed models require the presence of specific sequences near genes to permit the spread of inactivation into these regions. If such models are correct, one might predict that heterologous genes transferred onto the X chromosome might lack the appropriate signal sequences and therefore escape inactivation. To determine whether a foreign gene inserted into the X chromosome is subject to inactivation, transgenic mice harboring 11 copies of the complete, 17-kilobase chicken transferrin gene on the X chromosome were used. Male mice hemizygous for this insert were bred with females bearing Searle's translocation, an X-chromosome rearrangement that is always active in heterozygous females (the unrearranged X chromosome is inactive). Female offspring bearing the Searle's translocation and the chicken transferrin gene had the same amount of chicken transferrin messenger RNA in liver as did transgenic male mice or transgenic female mice lacking the Searle's chromosome. This result shows that the inserted gene is not subject to X-chromosome inactivation and suggests that the inactivation process cannot spread over 187 kilobases of DNA in the absence of specific signal sequences required for inactivation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Goldman, M A -- Stokes, K R -- Idzerda, R L -- McKnight, G S -- Hammer, R E -- Brinster, R L -- Gartler, S M -- HD14412/HD/NICHD NIH HHS/ -- HD16659/HD/NICHD NIH HHS/ -- HD17321/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1987 May 1;236(4801):593-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2437652" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chickens ; DNA/metabolism ; *Dosage Compensation, Genetic ; Female ; Male ; Methylation ; Mice ; Transferrin/*genetics ; *Transformation, Genetic ; Translocation, Genetic ; X Chromosome ; Y Chromosome ; alpha-Fetoproteins/genetics
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    In situ detection of beta-galactosidase in lenses of transgenic mice with a gamma-crystallin/lacZ gene (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-01-23
    Description: Transgenic mice carrying the gamma 2-crystallin promoter fused to the coding region of the bacterial lacZ gene were generated. The offspring of three founder mice expressed high levels of the enzyme solely in the central nuclear fiber cells of the lens as measured by an in situ assay for the detection of beta-galactosidase activity. These results suggest that gamma 2-crystallin sequences between -759 to +45 contain essential information required for appropriate tissue-specific and temporal regulation of the mouse gamma 2-crystallin gene. In a broader context, this study also demonstrates the utility of beta-galactosidase hybrid gene constructs for monitoring the activity of gene regulatory elements in transgenic mice.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Goring, D R -- Rossant, J -- Clapoff, S -- Breitman, M L -- Tsui, L C -- New York, N.Y. -- Science. 1987 Jan 23;235(4787):456-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3099390" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cataract/enzymology ; Crystallins/*genetics ; Galactosidases/*genetics ; Gene Expression Regulation ; *Lac Operon ; Lens, Crystalline/*physiology ; Mice ; Promoter Regions, Genetic ; Recombinant Fusion Proteins/*genetics ; Recombinant Proteins/*genetics ; Tissue Distribution ; Transfection ; beta-Galactosidase/*genetics/metabolism
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    YIGSR, a synthetic laminin pentapeptide, inhibits experimental metastasis formation (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-11-20
    Description: The invasion of tumor cells through basement membranes is a critical step in the formation of metastases. The binding of the malignant cells to laminin in the basement membranes allows their attachment and activates their invasiveness. Recently a synthetic nonapeptide from the B1 chain sequence of laminin was identified as a major site for cell binding. A pentapeptide within the nonapeptide sequence was found to reduce the formation of lung colonies in mice injected with melanoma cells and also to inhibit the invasiveness of the cells in vitro.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Iwamoto, Y -- Robey, F A -- Graf, J -- Sasaki, M -- Kleinman, H K -- Yamada, Y -- Martin, G R -- New York, N.Y. -- Science. 1987 Nov 20;238(4830):1132-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Developmental Biology and Anomalies, National Institute of Drug Research, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2961059" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Basement Membrane/physiopathology ; Binding Sites ; Cell Adhesion/*drug effects ; *Laminin ; Lung Neoplasms/secondary ; Melanoma, Experimental/pathology/physiopathology ; Mice ; Neoplasm Metastasis/*prevention & control ; Oligopeptides/*chemical synthesis/pharmacology ; Receptors, Immunologic/*drug effects ; Receptors, Laminin ; Structure-Activity Relationship
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    Macrophage cytotoxicity: role for L-arginine deiminase and imino nitrogen oxidation to nitrite (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-01-23
    Description: Previous studies have shown that cytotoxic activated macrophages cause inhibition of DNA synthesis, of mitochondrial respiration, and of aconitase activity in tumor target cells. An L-arginine-dependent biochemical pathway synthesizing L-citrulline and nitrite, coupled to an effector mechanism, is now shown to cause this pattern of metabolic inhibition. Murine cytotoxic activated macrophages synthesize L-citrulline and nitrite in the presence of L-arginine but not D-arginine. L-Citrulline and nitrite biosynthesis by cytotoxic activated macrophages is inhibited by NG-monomethyl-L-arginine, which also inhibits this cytotoxic effector mechanism. This activated macrophage cytotoxic effector system is associated with L-arginine deiminase activity, and the imino nitrogen removed from the guanido group of L-arginine by the deiminase reaction subsequently undergoes oxidation to nitrite. L-Homoarginine, an alternative substrate for this deiminase, is converted to L-homocitrulline with concurrent nitrite synthesis and similar biologic effects.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hibbs, J B Jr -- Taintor, R R -- Vavrin, Z -- New York, N.Y. -- Science. 1987 Jan 23;235(4787):473-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2432665" target="_blank"〉PubMed〈/a〉
    Keywords: Ammonia/biosynthesis ; Animals ; Cells, Cultured ; Citrulline/biosynthesis ; Cytotoxicity, Immunologic ; Homoarginine/metabolism ; Hydrolases/metabolism ; *Macrophage Activation ; Macrophages/*physiology ; Mice ; Nitrates/metabolism ; Nitrites/metabolism
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    Molecular cloning of complementary DNA encoding the avian receptor for vitamin D (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-03-06
    Description: Vitamin D3 receptors are intracellular proteins that mediate the nuclear action of the active metabolite 1,25-dihydroxyvitamin D3 [1,25(OH)2D3]. Two receptor-specific monoclonal antibodies were used to recover the complementary DNA (cDNA) of this regulatory protein from a chicken intestinal lambda gt11 cDNA expression library. The amino acid sequences that were deduced from this cDNA revealed a highly conserved cysteine-rich region that displayed homology with a domain characteristic of other steroid receptors and with the gag-erbA oncogene product of avian erythroblastosis virus. RNA selected via hybridization with this DNA sequence directed the cell-free synthesis of immunoprecipitable vitamin D3 receptor. Northern blot analysis of polyadenylated RNA with these cDNA probes revealed two vitamin D receptor messenger RNAs (mRNAs) of 2.6 and 3.2 kilobases in receptor-containing chicken tissues and a major cross-hybridizing receptor mRNA species of 4.2 kilobases in mouse 3T6 fibroblasts. The 4.2-kilobase species was substantially increased by prior exposure of 3T6 cells to 1,25(OH)2D3. This cDNA represents perhaps the rarest mRNA cloned to date in eukaryotes, as well as the first receptor sequence described for an authentic vitamin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McDonnell, D P -- Mangelsdorf, D J -- Pike, J W -- Haussler, M R -- O'Malley, B W -- New York, N.Y. -- Science. 1987 Mar 6;235(4793):1214-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3029866" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Calcitriol/metabolism ; Chickens/*metabolism ; Cholecalciferol/*metabolism ; Cloning, Molecular ; DNA/*genetics ; Genetic Code ; Mice ; Molecular Conformation ; RNA, Messenger/metabolism ; Receptors, Steroid/*genetics/metabolism
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    Making contacts in the developing embryo (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-04-03
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J L -- New York, N.Y. -- Science. 1987 Apr 3;236(4797):30-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3563488" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Surface/*physiology ; *Cell Adhesion ; Cell Adhesion Molecules ; Chick Embryo ; Embryo, Mammalian/*cytology ; Mice
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    The tat gene of human T-lymphotropic virus type 1 induces mesenchymal tumors in transgenic mice (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-09-11
    Description: Human T-lymphotropic virus type 1 (HTLV-1) is a suspected causative agent of adult T-cell leukemia. One of the viral genes encodes a protein (tat) that not only results in transactivation of viral gene expression but may also regulate the expression of certain cellular genes that are important for cell growth. Transgenic mice that expressed the authentic tat protein under the control of the HTLV-1 long terminal repeat were generated, and cell types that are permissive for the viral promoter and the effects of the tat gene on these cells were studied. Three of eight founder mice with high levels of expression of the transgene in muscle were bred and then analyzed. All developed soft tissue tumors at multiple sites between 13 to 17 weeks of age. This phenotype was transmitted to nine of nine offspring that inherited the tat gene and were available for analysis. The remaining five founders expressed the transgene in the thymus, as well as in muscle. This second group of mice all exhibited extensive thymic depletion and growth retardation; in all of these mice, death occurred between 3 to 6 weeks of age before tumors became macroscopically visible. The tat gene under the control of the HTLV-1 regulatory region showed tissue-specific expression and the tat protein efficiently induced mesenchymal tumors. The data establish tat as an oncogenic protein and HTLV-1 as a transforming virus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nerenberg, M -- Hinrichs, S H -- Reynolds, R K -- Khoury, G -- Jay, G -- New York, N.Y. -- Science. 1987 Sep 11;237(4820):1324-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2888190" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Deltaretrovirus/*genetics ; Deltaretrovirus Infections/*genetics ; Female ; *Genes, Viral ; Genetic Engineering ; Genetic Vectors ; Male ; Mesenchymoma/genetics/*microbiology ; Mice ; Pedigree ; Plasmids ; Protein Biosynthesis ; Transcription, Genetic
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    Region-specific expression of two mouse homeo box genes (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-03-13
    Description: Mammalian homeo box genes have been identified on the basis of sequence homology to Drosophila homeotic and segmentation genes. These studies examine the distribution of transcripts from two mouse homeo box genes, Hox-2.1 and Hox-3.1, throughout the latter third of prenatal development. Transcripts from these genes are regionally localized along the rostro-caudal axis of the developing central nervous system, yielding expression patterns very similar to patterns of Drosophila homeotic gene expression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Utset, M F -- Awgulewitsch, A -- Ruddle, F H -- McGinnis, W -- GM09966/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1987 Mar 13;235(4794):1379-82.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2881353" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn/genetics ; Base Sequence ; Brain/metabolism ; Cell Differentiation ; Drosophila melanogaster/genetics ; Fetus/metabolism ; *Gene Expression Regulation ; *Genes, Homeobox ; Mice ; Morphogenesis ; Nucleic Acid Hybridization ; Spinal Cord/metabolism ; Transcription, Genetic
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    Construction of a novel oncogene based on synthetic sequences encoding epidermal growth factor (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-01-16
    Description: The autocrine model postulates that constitutive release of a mitogenic growth factor can lead to uncontrolled proliferation and cell transformation. A synthetic polynucleotide encoding epidermal growth factor conferred a tumorigenic phenotype on cells. These cells were transformed through the action of an autocrine circuit having an extracellular component.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stern, D F -- Hare, D L -- Cecchini, M A -- Weinberg, R A -- CA07285-03/CA/NCI NIH HHS/ -- R01CA39964/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1987 Jan 16;235(4786):321-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3492043" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal ; Cell Division ; *Cell Transformation, Neoplastic/pathology ; DNA, Recombinant ; Epidermal Growth Factor/antagonists & inhibitors/*genetics/immunology ; Gene Expression Regulation ; Mice ; Neoplasms, Experimental/genetics/pathology ; *Oncogenes ; Rats ; Transfection
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    T-cell tumor elimination as a result of T-cell receptor-mediated activation (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-07-03
    Description: It has recently been shown that activation of murine T-cell hybridomas with antigen inhibits their growth in vitro. The "suicide" of these neoplastic T cells upon stimulation with antigen suggested the possibility that activation via the antigen-specific receptor could also inhibit the growth of neoplastic T cells in vivo. To test this, mice were subcutaneously inoculated with antigen-specific T-cell hybridomas and then treated intraperitoneally with antigen. Administration of the appropriate antigen immediately after inoculation with the T-cell hybridoma abrogated tumor formation; antigen administered after tumors had become established decreased the tumor burden and, in a substantial fraction of animals, led to long-term survival. The efficacy of antigen therapy was due to both a direct inhibitory effect on tumor growth and the induction of host immunity. These studies demonstrate the utility of cellular activation as a means of inhibiting neoplastic T-cell growth in vivo and provide a rationale for studying the use of less selective reagents that can mimic the activating properties of antigen, such as monoclonal antibodies, in the treatment of T-cell neoplasms of unknown antigen specificity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ashwell, J D -- Longo, D L -- Bridges, S H -- New York, N.Y. -- Science. 1987 Jul 3;237(4810):61-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3037698" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Cycle ; Cytochrome c Group/immunology ; Hybridomas/*immunology ; *Lymphocyte Activation ; Mice ; Muramidase/immunology ; Neoplasms, Experimental/*immunology/pathology ; Receptors, Antigen, T-Cell/*physiology ; T-Lymphocytes/*immunology/pathology
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    Germline organization of the murine T cell receptor beta-chain genes (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-10-23
    Description: The complete germline organization of the beta-chain genes of the murine T cell receptor was elucidated in order to obtain the structural basis for understanding the mechanisms of somatic DNA rearrangements. Twenty of the 22 known variable (V beta) genes are clustered within 250 kilobases of DNA 5' to the constant region (C beta) genes. These V beta genes share the same transcriptional orientation as the diversity (D beta), joining (J beta), and C beta genes, which implies that chromosomal deletion is the mechanism for most V beta to D beta-J beta rearrangements. Within this V beta cluster, the distance between the most proximal V beta gene and the D beta-J beta-C beta cluster is 320 kilobases, as determined by field-inversion gel electrophoresis. The large distance between V beta and D beta, relative to that between D beta and J beta, may have significant implications for the ordered rearrangement of the T cell receptor beta-chain genes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chou, H S -- Nelson, C A -- Godambe, S A -- Chaplin, D D -- Loh, D Y -- GM07067/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1987 Oct 23;238(4826):545-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2821625" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromosome Deletion ; Chromosome Mapping ; DNA/genetics ; DNA Restriction Enzymes ; Electrophoresis ; Macromolecular Substances ; Mice ; Mice, Inbred BALB C ; Mice, Mutant Strains ; Nucleic Acid Hybridization ; Receptors, Antigen, T-Cell/*genetics ; Transcription, Genetic
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    Cyclic AMP-modulated potassium channels in murine B cells and their precursors (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-03-06
    Description: A voltage-dependent potassium current (the delayed rectifier) has been found in murine B cells and their precursors with the whole-cell patch-clamp technique. The type of channel involved in the generation of this current appears to be present throughout all stages of pre-B-cell differentiation, since it is detected in pre-B cell lines infected with Abelson murine leukemia virus; these cell lines represent various phases of B-cell development. Thus, the presence of this channel is not obviously correlated with B-cell differentiation. Although blocked by Co2+, the channel, or channels, does not appear to be activated by Ca2+ entry. It is, however, inactivated by high intracellular Ca2+ concentrations. In addition, elevation of intracellular adenosine 3', 5'-monophosphate induces at all potentials a rapid decrease in the peak potassium conductance and increased rates of activation and inactivation. Therefore, potassium channels can be physiologically modulated by second messengers in lymphocytes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Choquet, D -- Sarthou, P -- Primi, D -- Cazenave, P A -- Korn, H -- New York, N.Y. -- Science. 1987 Mar 6;235(4793):1211-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2434998" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/*metabolism/physiology ; Calcium/pharmacology ; Cell Differentiation ; Colforsin/pharmacology ; Cyclic AMP/*physiology ; Guanosine Triphosphate/pharmacology ; Immunocompetence ; Ion Channels/*drug effects/metabolism ; Lipopolysaccharides/pharmacology ; Mice ; Potassium/*metabolism
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    Adipsin: a circulating serine protease homolog secreted by adipose tissue and sciatic nerve (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-07-24
    Description: Adipsin is a serine protease homolog whose primary structure was predicted from the nucleotide sequence of a differentiation-dependent adipocyte messenger RNA. Immunoblots probed with antisera to synthetic peptides identify two forms of adipsin that are synthesized and secreted by 3T3 adipocytes. These proteins of 44 and 37 kilodaltons are converted to 25.5 kilodaltons by enzymatic deglycosylation. Although adipsin is principally synthesized in adipose tissue, it is also produced by sciatic nerve and is found in the bloodstream. Because of the apparent restriction of adipsin synthesis to tissues highly active in lipid metabolism, its presence in serum, and its modulation in altered metabolic states, this molecule may play a previously unrecognized role in systemic lipid metabolism or energy balance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cook, K S -- Min, H Y -- Johnson, D -- Chaplinsky, R J -- Flier, J S -- Hunt, C R -- Spiegelman, B M -- AM07230/AM/NIADDK NIH HHS/ -- AM31405/AM/NIADDK NIH HHS/ -- DK34605/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1987 Jul 24;237(4813):402-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3299705" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue/*enzymology ; Animals ; Cells, Cultured ; Complement Factor D ; Endopeptidases/blood/genetics/*secretion ; Male ; Mice ; Molecular Weight ; Organ Culture Techniques ; RNA, Messenger/genetics ; Sciatic Nerve/*enzymology ; *Serine Endopeptidases ; Transcription, Genetic
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  • 74
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    Phagocytosis of Candida albicans enhances malignant behavior of murine tumor cells (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-12-11
    Description: Murine tumor cells were induced to phagocytize either Candida albicans or group A streptococcal cells. The presence of microbial particles within the tumor cell cytoplasm had no effect on in vitro tumor cell growth. However, when Candida albicans-infected tumor cells were injected into syngeneic mice, they formed tumors that grew faster, invaded the surrounding normal tissue more rapidly and metastasized more rapidly than control tumor cells. Tumor cells infected with group A streptococcal particles did not grow faster or show increased malignant behavior. These data indicate that the in vivo behavior of malignant tumor cells can be modulated by microbial particles, which are often present in the microenvironment of the growing tumor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ginsburg, I -- Fligiel, S E -- Kunkel, R G -- Riser, B L -- Varani, J -- New York, N.Y. -- Science. 1987 Dec 11;238(4833):1573-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Oral Biology, Hebrew University--Hadassah School of Dental Medicine, Jerusalem, Israel.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3317835" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Candida albicans ; Cell Line ; Fibrosarcoma/pathology/*physiopathology ; Mice ; Mice, Inbred C57BL ; *Phagocytosis ; Streptococcus pyogenes
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    Identification of a T3-associated gamma delta T cell receptor on Thy-1+ dendritic epidermal Cell lines (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-05-15
    Description: The murine epidermis contains a subpopulation of bone marrow-derived lymphocytes that have a dendritic morphology and that express Thy-1 and T3 cell-surface antigens but not other markers (L3T4 or Lyt-2) characteristic of mature peripheral T lymphocytes. An alternative type of T cell receptor was earlier identified on a subpopulation of murine thymocytes with a similar phenotype (T3+, L3T4-, Lyt-2-), but not on peripheral murine T lymphocytes. Two independently derived Thy-1+, L3T4-, and Lyt-2- dendritic cell lines of epidermal origin that express a T3-associated disulfide-linked heterodimer composed of a 34-kilodalton gamma-chain and 46-kilodalton partner (the delta chain) have now been identified. Analysis of N-linked glycosylation revealed that this receptor is similar to that detected on thymocytes. These results demonstrate that Thy-1+ dendritic epidermal cell lines can express gamma delta T cell receptors in vitro and suggest that Thy-1+ dendritic epidermal cells express such receptors in vivo. The localization of these gamma delta T cell receptor-expressing cells in the epidermis may be of importance for understanding the function of these receptors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koning, F -- Stingl, G -- Yokoyama, W M -- Yamada, H -- Maloy, W L -- Tschachler, E -- Shevach, E M -- Coligan, J E -- F32AM07219-03/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1987 May 15;236(4803):834-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2883729" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Surface/*analysis ; Antigens, Thy-1 ; Bone Marrow/immunology ; Cell Line ; Mice ; Molecular Weight ; Receptors, Antigen, T-Cell/*analysis ; T-Lymphocytes/*immunology
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    A sea urchin gene encodes a polypeptide homologous to epidermal growth factor (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-09-18
    Description: A sea urchin DNA clone complementary to an embryonic messenger RNA whose protein product bears striking homology to the epidermal growth factor family of proteins has been identified and characterized. The structure of the protein is similar to that of previously identified regulatory genes in Drosophila and Caenorhabditis. RNA gel blot hybridization showed a unique temporal pattern of expression of this gene during embryogenesis and transcript enrichment in the embryonic ectoderm. These results suggest that this member of the epidermal growth factor gene family plays a role in early development decisions in sea urchin embryos.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hursh, D A -- Andrews, M E -- Raff, R A -- R01 HD21986/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1987 Sep 18;237(4821):1487-90.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3498216" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cysteine/analysis ; DNA/analysis ; Epidermal Growth Factor/*genetics ; Gene Expression Regulation ; Humans ; Mice ; Nucleic Acid Hybridization ; Peptides/*genetics ; RNA, Messenger/metabolism ; Repetitive Sequences, Nucleic Acid ; Sea Urchins/genetics
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    Megabase-scale mapping of the HLA gene complex by pulsed field gel electrophoresis (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-03-13
    Description: In the study of the genetic structure of mammalian chromosomes, there exists a "resolution gap" between molecular cloning experiments and meiotic linkage analyses. This gap has discouraged attempts to construct full-scale genetic maps of mammalian chromosomes. The organization of the human major histocompatibility complex was examined within this range by pulsed field gel electrophoresis. The data obtained indicate that the complex spans over 3000 kilobases and enable the construction of a megabase-scale molecular map. These results indicate that the techniques employed in DNA extraction, enzymatic digestion, electrophoresis, and hybridization are suitable for the efficient analysis of megabase regions of mammalian chromosomes and effectively bridge the resolution gap between molecular cloning and classical genetics.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lawrance, S K -- Smith, C L -- Srivastava, R -- Cantor, C R -- Weissman, S M -- 5-T35-CA-39782/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1987 Mar 13;235(4794):1387-90.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3029868" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Composition ; DNA/genetics ; DNA Restriction Enzymes ; Electrophoresis ; HLA Antigens/*genetics ; HLA-D Antigens/genetics ; Humans ; *Major Histocompatibility Complex ; Mice ; Nucleic Acid Hybridization
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    Protein-binding sites in Ig gene enhancers determine transcriptional activity and inducibility (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-06-19
    Description: Individual protein-binding sites within the mouse immunoglobulin heavy chain and kappa light chain gene enhancers were altered, making it possible to examine the functional role of the sites during transcription. The E motifs, which bind factors that are present in many if not all cells, mostly behave as transcriptional activating sites. The only known heavy chain enhancer site that binds a lymphocyte-specific factor, the "octamer" site, plays a critical role in transcription but only in a truncated form of the enhancer. In the full enhancer, no one site is crucial because of an apparent functional redundancy. The site in the kappa enhancer that binds a factor specific to mature B cells, kappa B, was crucial to the constitutive activity of the enhancer in B cells. This factor is also inducible in pre-B cells, and the site was necessary for inducibility of the kappa enhancer. Thus, the sites defined by protein binding are important for the functional activity of immunoglobulin enhancers, with the sites that bind proteins restricted in their cellular distribution playing the most important roles.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lenardo, M -- Pierce, J W -- Baltimore, D -- New York, N.Y. -- Science. 1987 Jun 19;236(4808):1573-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3109035" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites ; *Enhancer Elements, Genetic ; *Genes, Regulator ; Immunoglobulin Heavy Chains/*genetics ; Immunoglobulin kappa-Chains/*genetics ; Lymphocytes/immunology ; Mice ; Mice, Inbred BALB C ; Multiple Myeloma/metabolism ; Mutation ; *Transcription, Genetic
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    The T cell receptor (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-11-20
    Description: The primary structure of T cell receptor proteins and genes is well understood. Immunologists are now trying to understand the properties of these interesting molecules. Evidence suggests that T cell alpha beta receptors recognize a complex of an antigen-derived peptide bound to one of the cell-surface products of the major histocompatibility complex (MHC) genes. It is likely that alpha beta receptors and MHC proteins have coevolved to have some affinity for each other. During T cell development in the thymus, cells bearing self-reactive receptors are deleted by the mechanisms of tolerance, and cells are preferentially allowed to mature if they bear receptors that will be able to recognize antigen plus self-MHC after they have become full-fledged T cells. Some explanations for these phenomena have been tested, but no satisfactory theory can yet be proposed to account for them.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marrack, P -- Kappler, J -- AI17134/AI/NIAID NIH HHS/ -- AI18785/AI/NIAID NIH HHS/ -- AI22295/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1987 Nov 20;238(4830):1073-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Medicine, 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/3317824" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Genes ; Histocompatibility Antigens Class II/*physiology ; Humans ; Immune Tolerance ; Macromolecular Substances ; Major Histocompatibility Complex ; Mice ; Receptors, Antigen, T-Cell/*physiology ; T-Lymphocytes/*physiology ; Thymus Gland/physiology
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    Epidermal-growth-factor-dependent transformation by a human EGF receptor proto-oncogene (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-12-04
    Description: The epidermal growth factor (EGF) receptor gene EGFR has been placed in a retrovirus vector to examine the growth properties of cells that experimentally overproduce a full-length EGF receptor. NIH 3T3 cells transfected with the viral DNA or infected with the corresponding rescued retrovirus developed a fully transformed phenotype in vitro that required both functional EGFR expression and the presence of EGF in the growth medium. Cells expressing 4 x 10(5) EGF receptors formed tumors in nude mice, while control cells did not. Therefore, the EGFR retrovirus, which had a titer on NIH 3T3 cells that was greater than 10(7) focus-forming units per milliliter, can efficiently transfer and express this gene, and increased numbers of EGF receptors can contribute to the transformed phenotype.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Velu, T J -- Beguinot, L -- Vass, W C -- Willingham, M C -- Merlino, G T -- Pastan, I -- Lowy, D R -- New York, N.Y. -- Science. 1987 Dec 4;238(4832):1408-10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Cellular Oncology, National Cancer Institute, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3500513" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Transformation, Neoplastic/chemically induced/*genetics ; Cells, Cultured ; DNA, Recombinant ; Epidermal Growth Factor/*pharmacology ; Fibroblasts/pathology ; Genetic Vectors ; Harvey murine sarcoma virus/genetics ; Humans ; Male ; Mice ; Mice, Nude ; Neoplasms, Experimental/etiology ; *Proto-Oncogenes ; Receptor, Epidermal Growth Factor/drug effects/*genetics ; Recombinant Proteins/genetics
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    Raf, a trans-acting locus, regulates the alpha-fetoprotein gene in a cell-autonomous manner (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-04-17
    Description: Genetic analysis provides an approach for identifying regulatory loci that govern the expression of specific genes within the context of the entire organism. Such analyses have defined two unlinked regulatory loci, termed raf and Rif, that modulate the levels of alpha-fetoprotein in liver. Of primary importance for the isolation and characterization of the raf product is to determine whether it is produced by the hepatocyte or whether it is produced by a different cell type. By means of analysis of alpha-fetoprotein expression in livers of embryo aggregation chimeras derived from mice of different raf genotypes it was possible to conclude that the product of the raf locus is expressed as a hepatocyte autonomous function that acts in trans to regulate the level of alpha-fetoprotein messenger RNA.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vogt, T F -- Solter, D -- Tilghman, S M -- CA06927/CA/NCI NIH HHS/ -- CA28050/CA/NCI NIH HHS/ -- HD17720/HD/NICHD NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1987 Apr 17;236(4799):301-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2436297" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chimera ; Crosses, Genetic ; Gene Expression Regulation ; *Genes ; *Genes, Regulator ; Genotype ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mosaicism ; Polymorphism, Restriction Fragment Length ; RNA, Messenger/genetics ; Species Specificity ; alpha-Fetoproteins/*genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 82
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    Introduction of a normal human chromosome 11 into a Wilms' tumor cell line controls its tumorigenic expression (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-04-10
    Description: The development of Wilms' tumor, a pediatric nephroblastoma, has been associated with a deletion in the p13 region of chromosome 11. The structure and function or functions of this deleted genetic material are unknown. The role of this deletion in the process of malignant transformation was investigated by introducing a normal human chromosome 11 into a Wilms' tumor cell line by means of the microcell transfer technique. These variant cells, derived by microcell hybridization, expressed similar transformed traits in culture as the parental cell line. Furthermore, expression of several proto-oncogenes by the parental cells was unaffected by the introduction of this chromosome. However, the ability of these cells to form tumors in nude mice was completely suppressed. Transfer of other chromosomes, namely X and 13, had no effect on the tumorigenicity of the Wilms' tumor cells. These studies provide support for the existence of genetic information on chromosome 11 which can control the malignant expression of Wilms' tumor cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weissman, B E -- Saxon, P J -- Pasquale, S R -- Jones, G R -- Geiser, A G -- Stanbridge, E J -- CA 19401/CA/NCI NIH HHS/ -- SO7RR05469-23/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1987 Apr 10;236(4798):175-80.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3031816" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Transformation, Neoplastic/genetics ; Cells, Cultured ; *Chromosomes, Human, Pair 11 ; Gene Expression Regulation ; Humans ; Hybrid Cells ; Karyotyping ; Mice ; Mice, Nude ; Oncogenes ; Suppression, Genetic ; Wilms Tumor/*genetics/pathology
    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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  • 83
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    Regulation in vitro of metallothionein gene binding factors (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-03-13
    Description: Mouse nuclear factors that bind to an upstream metal regulatory element of the mouse metallothionein-I gene have been identified by DNA footprinting and oligonucleotide band shift assays. The formation of complexes at this site can be activated 20- to 40-fold by the vitro addition of ionic cadmium. The activation reaction is rapid, reversible by a metal chelator, and may involve multiple proteins. These results suggest that the initial step in cadmium detoxification is an interaction between the metal and nuclear DNA-binding factors leading to an increase in metallothionein gene transcription. The ability to observe metal activation in vitro makes this a powerful system to study the biochemistry of eukaryotic gene regulation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Seguin, C -- Hamer, D H -- New York, N.Y. -- Science. 1987 Mar 13;235(4794):1383-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3103216" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cadmium/pharmacology ; Cell Nucleus/analysis ; DNA/genetics/metabolism ; DNA-Binding Proteins/metabolism ; Deoxyribonuclease I ; Edetic Acid/pharmacology ; Exodeoxyribonucleases ; *Genes, Regulator ; Metallothionein/*genetics ; Mice ; Oligonucleotides/genetics ; Transcription Factors/metabolism ; *Transcription, Genetic
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 84
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    RNA complementary to a herpesvirus alpha gene mRNA is prominent in latently infected neurons (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-02-27
    Description: In initial attempts to define the molecular events responsible for the latent state of herpes simplex virus, in situ hybridization was utilized to search for virally encoded RNA transcripts in latently infected sensory neurons. The use of cloned probes representing the entire viral genome indicated that transcripts encoded within terminal repeats were present. When the alpha genes encoding ICP-0, ICP-4, and ICP-27 and the gamma 1 gene encoding VP-5 were employed, only RNA transcripts hybridizing to the ICP-0 probe were detected. In latently infected cells, the ICP-0--related transcripts were localized principally in the nucleus; this was not the case in acutely (productively) infected neurons or in neurons probed for RNA transcripts coding for actin. In Northern blotting experiments, an RNA of 2.6 kilobases was detected with the ICP-0 probe. When single-stranded DNAs from the ICP-0 region were used as probes, RNA from the strand complementary to that encoding ICP-0 messenger RNA (mRNA) was the major species detected. This RNA species may play a significant role in maintaining the latent infection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stevens, J G -- Wagner, E K -- Devi-Rao, G B -- Cook, M L -- Feldman, L T -- AI-06246/AI/NIAID NIH HHS/ -- CA 11861/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1987 Feb 27;235(4792):1056-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2434993" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Ganglia, Spinal/microbiology ; *Genes, Viral ; Herpes Simplex/microbiology ; Mice ; Neurons/*microbiology ; Nucleic Acid Hybridization ; RNA/*genetics ; RNA, Complementary ; RNA, Messenger/genetics ; RNA, Viral/*genetics ; Simplexvirus/*genetics ; Transcription, Genetic ; Viral Proteins/genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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