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  • 1
    Publication Date: 1997-07-04
    Description: Angiogenesis is thought to depend on a precise balance of positive and negative regulation. Angiopoietin-1 (Ang1) is an angiogenic factor that signals through the endothelial cell-specific Tie2 receptor tyrosine kinase. Like vascular endothelial growth factor, Ang1 is essential for normal vascular development in the mouse. An Ang1 relative, termed angiopoietin-2 (Ang2), was identified by homology screening and shown to be a naturally occurring antagonist for Ang1 and Tie2. Transgenic overexpression of Ang2 disrupts blood vessel formation in the mouse embryo. In adult mice and humans, Ang2 is expressed only at sites of vascular remodeling. Natural antagonists for vertebrate receptor tyrosine kinases are atypical; thus, the discovery of a negative regulator acting on Tie2 emphasizes the need for exquisite regulation of this angiogenic receptor system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Maisonpierre, P C -- Suri, C -- Jones, P F -- Bartunkova, S -- Wiegand, S J -- Radziejewski, C -- Compton, D -- McClain, J -- Aldrich, T H -- Papadopoulos, N -- Daly, T J -- Davis, S -- Sato, T N -- Yancopoulos, G D -- New York, N.Y. -- Science. 1997 Jul 4;277(5322):55-60.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Regeneron Pharmaceuticals Inc., 777 Old Saw Mill River Road, Tarrytown, NY 10591, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9204896" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Angiopoietin-1 ; Angiopoietin-2 ; Animals ; Blood Vessels/embryology/*metabolism ; Cells, Cultured ; Cloning, Molecular ; Embryo, Mammalian/metabolism ; Endothelial Growth Factors/genetics/metabolism ; Endothelium, Vascular/*cytology/metabolism ; Female ; Humans ; Ligands ; Lymphokines/genetics/metabolism ; Membrane Glycoproteins/antagonists & inhibitors/metabolism ; Mice ; Mice, Transgenic ; Molecular Sequence Data ; *Neovascularization, Physiologic ; Phosphorylation ; Proteins/chemistry/*metabolism ; Rats ; Rats, Sprague-Dawley ; Receptor Protein-Tyrosine Kinases/*antagonists & inhibitors/metabolism ; Receptor, TIE-2 ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Vascular Endothelial Growth Factor A ; Vascular Endothelial Growth Factors
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  • 2
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-03-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thomas, K R -- Capecchi, M R -- New York, N.Y. -- Science. 1997 Mar 7;275(5305):1404-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9072801" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Anemia, Sickle Cell/*genetics ; B-Lymphocytes ; Cells, Cultured ; DNA, Recombinant ; *Gene Conversion ; Hemoglobin, Sickle/*genetics ; Humans ; Mutation ; Oligonucleotides/*genetics
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  • 3
    Publication Date: 1997-06-13
    Description: Two families of small peptides that bind to the human thrombopoietin receptor and compete with the binding of the natural ligand thrombopoietin (TPO) were identified from recombinant peptide libraries. The sequences of these peptides were not found in the primary sequence of TPO. Screening libraries of variants of one of these families under affinity-selective conditions yielded a 14-amino acid peptide (Ile-Glu-Gly-Pro-Thr-Leu-Arg-Gln-Trp-Leu-Ala-Ala-Arg-Ala) with high affinity (dissociation constant approximately 2 nanomolar) that stimulates the proliferation of a TPO-responsive Ba/F3 cell line with a median effective concentration (EC50) of 400 nanomolar. Dimerization of this peptide by a carboxyl-terminal linkage to a lysine branch produced a compound with an EC50 of 100 picomolar, which was equipotent to the 332-amino acid natural cytokine in cell-based assays. The peptide dimer also stimulated the in vitro proliferation and maturation of megakaryocytes from human bone marrow cells and promoted an increase in platelet count when administered to normal mice.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cwirla, S E -- Balasubramanian, P -- Duffin, D J -- Wagstrom, C R -- Gates, C M -- Singer, S C -- Davis, A M -- Tansik, R L -- Mattheakis, L C -- Boytos, C M -- Schatz, P J -- Baccanari, D P -- Wrighton, N C -- Barrett, R W -- Dower, W J -- New York, N.Y. -- Science. 1997 Jun 13;276(5319):1696-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Affymax Research Institute, 4001 Miranda Avenue, Palo Alto, CA 94304, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9180079" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Binding, Competitive ; Blood Platelets/cytology ; Cell Division ; Cell Line ; Cells, Cultured ; Consensus Sequence ; Dimerization ; Erythropoietin/pharmacology ; Hematopoiesis/drug effects ; Humans ; Megakaryocytes/cytology ; Mice ; Molecular Sequence Data ; *Neoplasm Proteins ; Oligopeptides/*metabolism/*pharmacology ; Peptide Library ; Peptides/metabolism/pharmacology ; Platelet Count ; Proto-Oncogene Proteins/*agonists/metabolism ; *Receptors, Cytokine ; Receptors, Thrombopoietin ; Recombinant Proteins/metabolism/pharmacology ; Thrombopoietin/*metabolism/pharmacology ; Transfection
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  • 4
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-08-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1997 Aug 22;277(5329):1037.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9289850" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Axonal Transport ; Axons/*metabolism ; Cell Nucleus/metabolism ; Cells, Cultured ; Cyclic AMP Response Element-Binding Protein/metabolism ; Gene Expression Regulation ; Nerve Growth Factors/*metabolism ; Neurons/*metabolism ; Proto-Oncogene Proteins/metabolism ; Rats ; Receptor Protein-Tyrosine Kinases/metabolism ; Receptor, trkA ; Receptors, Nerve Growth Factor/metabolism ; *Signal Transduction
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  • 5
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-05-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1997 May 2;276(5313):682.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9157547" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/diagnosis/enzymology/*genetics ; Brain/*enzymology ; Cells, Cultured ; Electron Transport Complex IV/*genetics/metabolism ; Energy Metabolism ; Humans ; Mitochondria/*genetics ; Mutation
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  • 6
    Publication Date: 1997-04-25
    Description: Spinal cord injuries result in paralysis, because when damaged neurons die they are not replaced. Neurogenesis of electrophysiologically functional neurons occurred in spinal cord cultured from postnatal rats. In these cultures, the numbers of immunocytochemically identified neurons increased over time. Additionally, neurons identified immunocytochemically or electrophysiologically incorporated bromodeoxyuridine, confirming they had differentiated from mitotic cells in vitro. These findings suggest that postnatal spinal cord retains the capacity to generate functional neurons. The presence of neuronal precursor cells in postnatal spinal cord may offer new therapeutic approaches for restoration of function to individuals with spinal cord injuries.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kehl, L J -- Fairbanks, C A -- Laughlin, T M -- Wilcox, G L -- DA07097/DA/NIDA NIH HHS/ -- DA07234/DA/NIDA NIH HHS/ -- DE00225/DE/NIDCR NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1997 Apr 25;276(5312):586-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Graduate Program in Neuroscience, University of Minnesota, Minneapolis, MN 55455, USA. 55455, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9110976" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Bromodeoxyuridine/metabolism ; Cell Differentiation ; Cells, Cultured ; Culture Media ; Glial Fibrillary Acidic Protein/analysis ; Immunohistochemistry ; Mitosis ; Neurons/chemistry/*cytology/metabolism ; Phosphopyruvate Hydratase/analysis ; Rats ; Spinal Cord/chemistry/*cytology ; Tubulin/analysis
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  • 7
    Publication Date: 1997-12-31
    Description: Natural killer T (NKT) lymphocytes express an invariant T cell antigen receptor (TCR) encoded by the Valpha14 and Jalpha281 gene segments. A glycosylceramide-containing alpha-anomeric sugar with a longer fatty acyl chain (C26) and sphingosine base (C18) was identified as a ligand for this TCR. Glycosylceramide-mediated proliferative responses of Valpha14 NKT cells were abrogated by treatment with chloroquine-concanamycin A or by monoclonal antibodies against CD1d/Vbeta8, CD40/CD40L, or B7/CTLA-4/CD28, but not by interference with the function of a transporter-associated protein. Thus, this lymphocyte shares distinct recognition systems with either T or NK cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kawano, T -- Cui, J -- Koezuka, Y -- Toura, I -- Kaneko, Y -- Motoki, K -- Ueno, H -- Nakagawa, R -- Sato, H -- Kondo, E -- Koseki, H -- Taniguchi, M -- New York, N.Y. -- Science. 1997 Nov 28;278(5343):1626-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉CREST (Core Research for Evolutional Science and Technology) Project, Japan Science and Technology Corporation (JST), 1-8-1 Inohana, Chuo, Chiba 260, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9374463" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD1/*immunology ; Carbohydrate Conformation ; Cells, Cultured ; Ceramides/chemistry/metabolism/*pharmacology ; Cerebrosides/chemistry/metabolism/*pharmacology ; Coculture Techniques ; Galactosylceramides/chemistry/metabolism/pharmacology ; Glucosylceramides/chemistry/metabolism/pharmacology ; Killer Cells, Natural/*immunology ; Ligands ; *Lymphocyte Activation ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Receptors, Antigen, T-Cell, alpha-beta/*immunology ; Structure-Activity Relationship ; T-Lymphocyte Subsets/*immunology
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  • 8
    Publication Date: 1997-01-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Keulen, W -- Nijhuis, M -- Schuurman, R -- Berkhout, B -- Boucher, C -- New York, N.Y. -- Science. 1997 Jan 10;275(5297):229; author reply 230-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8999550" target="_blank"〉PubMed〈/a〉
    Keywords: Anti-HIV Agents/*pharmacology ; Cells, Cultured ; Drug Resistance, Microbial ; Drug Therapy, Combination ; Genetic Variation ; HIV Infections/drug therapy/virology ; HIV Reverse Transcriptase/*genetics/metabolism ; HIV-1/drug effects/*enzymology/genetics ; Humans ; Lamivudine/*pharmacology/therapeutic use ; Mutation ; Reverse Transcriptase Inhibitors/*pharmacology ; Zidovudine/therapeutic use
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  • 9
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-02-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaiser, J -- New York, N.Y. -- Science. 1997 Feb 28;275(5304):1258.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9064779" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/*immunology/virology ; CD4-Positive T-Lymphocytes/immunology/*virology ; Cells, Cultured ; HIV/*physiology ; Humans ; Immunity, Innate ; Male ; Virus Replication
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  • 10
    Publication Date: 1997-05-30
    Description: Despite myriads of biological activities ascribed to uteroglobin (UG), a steroid-inducible secreted protein, its physiological functions are unknown. Mice in which the uteroglobin gene was disrupted had severe renal disease that was associated with massive glomerular deposition of predominantly multimeric fibronectin (Fn). The molecular mechanism that normally prevents Fn deposition appears to involve high-affinity binding of UG with Fn to form Fn-UG heteromers that counteract Fn self-aggregation, which is required for abnormal tissue deposition. Thus, UG is essential for maintaining normal renal function in mice, which raises the possibility that an analogous pathogenic mechanism may underlie genetic Fn-deposit human glomerular disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Z -- Kundu, G C -- Yuan, C J -- Ward, J M -- Lee, E J -- DeMayo, F -- Westphal, H -- Mukherjee, A B -- HL47620/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1997 May 30;276(5317):1408-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section on Developmental Genetics, Heritable Disorders Branch, National Institute of Child Health and Human Development (NICHD), National Insitutes of Health (NIH), Bethesda, MD 20892-1830, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9162006" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Crosses, Genetic ; Fibronectins/*metabolism ; Gene Targeting ; Humans ; Kidney Diseases/embryology/genetics/pathology ; *Kidney Glomerulus/embryology/metabolism/ultrastructure ; Mice ; Mice, Inbred C57BL ; Uteroglobin/deficiency/genetics/*physiology
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  • 11
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-05-02
    Description: Interest in bacterial pathogenesis has recently increased because of antibiotic resistance, the emergence of new pathogens and the resurgence of old ones, and the lack of effective therapeutics. The molecular and cellular mechanisms of microbial pathogenesis are currently being defined, with precise knowledge of both the common strategies used by multiple pathogenic bacteria and the unique tactics evolved by individual species to help establish infection. What is emerging is a new appreciation of how bacterial pathogens interact with host cells. Many host cell functions, including signal transduction pathways, cytoskeletal rearrangements, and vacuolar trafficking, are exploited, and these are the focus of this review. A bonus of this work is that bacterial virulence factors are providing new tools to study various aspects of mammalian cell functions, in addition to mechanisms of bacterial disease. Together these developments may lead to new therapeutic strategies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Finlay, B B -- Cossart, P -- New York, N.Y. -- Science. 1997 May 2;276(5313):718-25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Biotechnology Laboratory, University of British Columbia, Vancouver, B.C., Canada, V6T-1Z3. bfinlay@unixg.ubc.ca〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9115192" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Bacteria/genetics/*pathogenicity ; *Bacterial Adhesion ; Bacterial Infections/*microbiology ; Bacterial Physiological Phenomena ; Bacterial Toxins/toxicity ; Cells, Cultured ; Cytoskeleton/physiology ; Epithelial Cells ; Epithelium/microbiology ; Humans ; Phagocytosis ; Signal Transduction ; Vacuoles/microbiology ; Virulence/genetics
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  • 12
    Publication Date: 1997-07-11
    Description: BOB.1/OBF.1 is a transcriptional coactivator that is constitutively expressed in B cells and interacts with the Oct1 and Oct2 transcription factors. Upon activation of Jurkat T cells and primary murine thymocytes with phorbol esters and ionomycin, BOB.1/OBF.1 expression and transactivation function were induced. BOB.1/OBF.1 was phosphorylated at Ser184 both in vivo and in vitro, and this modification was required for inducible activation. Mutation of Ser184 also diminished transactivation function in B cells, suggesting that the activating phosphorylation that is inducible in T cells is constitutively present in B cells. Thus, BOB.1/OBF.1 is a transcriptional coactivator that is critically regulated by posttranslational modifications to mediate cell type-specific gene expression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zwilling, S -- Dieckmann, A -- Pfisterer, P -- Angel, P -- Wirth, T -- New York, N.Y. -- Science. 1997 Jul 11;277(5323):221-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉MSZ, Institut fur Medizinische Strahlenkunde und Zellforschung, Universitat Wurzburg, Versbacher Strasse 5, 97078 Wurzburg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9211847" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; B-Lymphocytes/metabolism ; Cells, Cultured ; *DNA-Binding Proteins ; *Gene Expression Regulation ; HeLa Cells ; Homeodomain Proteins/metabolism ; Host Cell Factor C1 ; Humans ; Immunosuppressive Agents/pharmacology ; Ionomycin/pharmacology ; Jurkat Cells ; *Lymphocyte Activation ; Mice ; Molecular Sequence Data ; Octamer Transcription Factor-1 ; Phosphorylation ; Phosphoserine/metabolism ; Recombinant Fusion Proteins/metabolism ; T-Lymphocytes/immunology/*metabolism ; Tetradecanoylphorbol Acetate/pharmacology ; Trans-Activators/genetics/*metabolism ; Transcription Factors/metabolism ; *Transcriptional Activation
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  • 13
    Publication Date: 1997-10-10
    Description: The clonal selection theory states that B lymphocytes producing high-affinity immunoglobulins are selected from a pool of cells undergoing antibody gene mutation. Somatic hypermutation is a well-documented mechanism for achieving diversification of immune responses in mature B cells. Antibody genes were also found to be modified in such cells in germinal centers by recombination of the variable (V), diversity (D), and joining (J) segments. The ability to alter immunoglobulin expression by V(D)J recombination in the selective environment of the germinal center may be an additional mechanism for inactivation or diversification of immune responses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Papavasiliou, F -- Casellas, R -- Suh, H -- Qin, X F -- Besmer, E -- Pelanda, R -- Nemazee, D -- Rajewsky, K -- Nussenzweig, M C -- AI33890/AI/NIAID NIH HHS/ -- R01 AI033608/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1997 Oct 10;278(5336):298-301.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Immunology, Rockefeller University, New York, NY 10021, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9323210" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antibody Diversity ; B-Lymphocytes/*immunology ; Cells, Cultured ; DNA Nucleotidyltransferases/genetics/metabolism ; DNA-Binding Proteins/genetics ; Gene Expression ; *Gene Rearrangement, B-Lymphocyte ; Genes, Immunoglobulin ; Genes, RAG-1 ; Germinal Center/cytology/immunology ; Immunoglobulin Joining Region/*genetics ; Immunoglobulin M/biosynthesis/genetics ; Immunoglobulin Variable Region/*genetics ; Lymphocyte Activation ; Mice ; *Recombination, Genetic ; VDJ Recombinases
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  • 14
    Publication Date: 1997-03-28
    Description: Signal transmission by many cell surface receptors results in the activation of phosphoinositide (PI) 3-kinases that phosphorylate the 3' position of polyphosphoinositides. From a screen for mouse proteins that bind phosphoinositides, the protein GRP1was identified. GRP1 binds phosphatidylinositol-3,4,5-trisphosphate [PtdIns(3,4, 5)P3] through a pleckstrin homology (PH) domain and displays a region of high sequence similarity to the yeast Sec7 protein. The PH domain of the closely related protein cytohesin-1, which, through its Sec7 homology domain, regulates integrin beta2 and catalyzes guanine nucleotide exchange of the small guanine nucleotide-binding protein ARF1, was also found to specifically bind PtdIns(3,4,5)P3. GRP1 and cytohesin-1 appear to connect receptor-activated PI 3-kinase signaling pathways with proteins that mediate biological responses such as cell adhesion and membrane trafficking.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Klarlund, J K -- Guilherme, A -- Holik, J J -- Virbasius, J V -- Chawla, A -- Czech, M P -- DK30648/DK/NIDDK NIH HHS/ -- DK30898/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1997 Mar 28;275(5308):1927-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program in Molecular Medicine and Department of Biochemistry and Molecular Biology, University of Massachusetts Medical Center, 373 Plantation Street, Worcester, MA 01605, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9072969" target="_blank"〉PubMed〈/a〉
    Keywords: ADP-Ribosylation Factor 1 ; ADP-Ribosylation Factors ; Adipocytes/chemistry ; Amino Acid Sequence ; Animals ; Antigens, CD18/metabolism ; Blood Proteins/*chemistry ; Brain Chemistry ; Cell Adhesion Molecules/chemistry/*metabolism ; Cell Membrane/metabolism ; Cells, Cultured ; Cloning, Molecular ; DNA, Complementary ; Fungal Proteins/*chemistry ; GTP-Binding Proteins/metabolism ; *Guanine Nucleotide Exchange Factors ; Humans ; Mice ; Molecular Sequence Data ; Phosphatidylinositol 3-Kinases ; Phosphatidylinositol Phosphates/*metabolism ; *Phosphoproteins ; Phosphorylation ; Phosphotransferases (Alcohol Group Acceptor)/*metabolism ; Receptors, Cytoplasmic and Nuclear/metabolism ; Recombinant Fusion Proteins/chemistry/metabolism ; Sequence Homology, Amino Acid ; *Signal Transduction
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  • 15
    Publication Date: 1997-08-08
    Description: TRAIL (also called Apo2L) belongs to the tumor necrosis factor family, activates rapid apoptosis in tumor cells, and binds to the death-signaling receptor DR4. Two additional TRAIL receptors were identified. The receptor designated death receptor 5 (DR5) contained a cytoplasmic death domain and induced apoptosis much like DR4. The receptor designated decoy receptor 1 (DcR1) displayed properties of a glycophospholipid-anchored cell surface protein. DcR1 acted as a decoy receptor that inhibited TRAIL signaling. Thus, a cell surface mechanism exists for the regulation of cellular responsiveness to pro-apoptotic stimuli.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sheridan, J P -- Marsters, S A -- Pitti, R M -- Gurney, A -- Skubatch, M -- Baldwin, D -- Ramakrishnan, L -- Gray, C L -- Baker, K -- Wood, W I -- Goddard, A D -- Godowski, P -- Ashkenazi, A -- New York, N.Y. -- Science. 1997 Aug 8;277(5327):818-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Oncology, Genentech, South San Francisco, CA 94080-4918, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9242611" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; *Apoptosis ; Apoptosis Regulatory Proteins ; Cell Membrane/metabolism ; Cells, Cultured ; GPI-Linked Proteins ; Glycosylphosphatidylinositols/metabolism ; HeLa Cells ; Humans ; Ligands ; Membrane Glycoproteins/*metabolism ; Molecular Sequence Data ; NF-kappa B/metabolism ; Receptors, TNF-Related Apoptosis-Inducing Ligand ; Receptors, Tumor Necrosis Factor/chemistry/genetics/*metabolism ; Signal Transduction ; TNF-Related Apoptosis-Inducing Ligand ; Transfection ; Tumor Cells, Cultured ; Tumor Necrosis Factor Decoy Receptors ; Tumor Necrosis Factor-alpha/*metabolism
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  • 16
    Publication Date: 1997-01-31
    Description: The N-methyl-D-aspartate (NMDA) receptor mediates synaptic transmission and plasticity in the central nervous system (CNS) and is regulated by tyrosine phosphorylation. In membrane patches excised from mammalian central neurons, the endogenous tyrosine kinase Src was shown to regulate the activity of NMDA channels. The action of Src required a sequence [Src(40-58)] within the noncatalytic, unique domain of Src. In addition, Src coprecipitated with NMDA receptor proteins. Finally, endogenous Src regulated the function of NMDA receptors at synapses. Thus, NMDA receptor regulation by Src may be important in development, plasticity, and pathology in the CNS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yu, X M -- Askalan, R -- Keil, G J 2nd -- Salter, M W -- New York, N.Y. -- Science. 1997 Jan 31;275(5300):674-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Neuroscience, Hospital for Sick Children, Department of Physiology, University of Toronto, Toronto, Ontario, M5G 1X8 Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9005855" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cells, Cultured ; Ion Channel Gating ; Ion Channels/*metabolism ; Molecular Sequence Data ; N-Methylaspartate/metabolism ; Neurons/*metabolism ; Oligopeptides/pharmacology ; Patch-Clamp Techniques ; Phosphorylation ; Phosphotyrosine/metabolism ; Rats ; Rats, Wistar ; Receptors, N-Methyl-D-Aspartate/*metabolism ; Spinal Cord/cytology ; Synapses/*metabolism ; Synaptic Transmission ; src-Family Kinases/chemistry/*metabolism
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  • 17
    Publication Date: 1997-02-14
    Description: Posttetanic potentiation (PTP) is a common form of short-term synaptic plasticity that is generally thought to be entirely presynaptic. Consistent with that idea, PTP of evoked excitatory postsynaptic potentials at Aplysia sensory-motor neuron synapses in cell culture was reduced by presynaptic injection of a slow calcium chelator and was accompanied by an increase in the frequency but not the amplitude of spontaneous excitatory postsynaptic potentials. However, PTP was also reduced by postsynaptic injection of a rapid calcium chelator or postsynaptic hyperpolarization. Thus, PTP at these synapses is likely to involve a postsynaptic induction mechanism in addition to the known presynaptic mechanisms.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bao, J X -- Kandel, E R -- Hawkins, R D -- MH 26212/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1997 Feb 14;275(5302):969-73.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Neurobiology and Behavior, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9020078" target="_blank"〉PubMed〈/a〉
    Keywords: 1-Octanol ; Action Potentials ; Animals ; Aplysia ; Calcium/physiology ; Cells, Cultured ; Chelating Agents/pharmacology ; Egtazic Acid/analogs & derivatives/pharmacology ; Long-Term Potentiation ; Motor Neurons/*physiology ; *Neuronal Plasticity ; Neurons, Afferent/*physiology ; Octanols/pharmacology ; Serotonin/pharmacology ; Synapses/*physiology ; *Synaptic Transmission
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  • 18
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-01-10
    Description: In vivo, cytoplasmic microtubules are nucleated and anchored by their minus ends at the centrosome and are believed to turn over by a mechanism termed dynamic instability: depolymerization and repolymerization at their plus ends. In cytoplasmic fragments of fish melanophores, microtubules were shown to detach from their nucleation site and depolymerize from their minus ends. Free microtubules moved toward the periphery by treadmilling-growth at one end and shortening from the opposite end. Frequent release from nucleation sites may be a general property of centrosomes and permit a minus-end mechanism of microtubule turnover and treadmilling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rodionov, V I -- Borisy, G G -- GM25062/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1997 Jan 10;275(5297):215-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Biology, University of Wisconsin, Madison, WI 53706, USA. ggborisy@facstaf.wisc.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8985015" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Membrane/metabolism ; Cells, Cultured ; Centrosome/metabolism ; Cytoplasm/metabolism/ultrastructure ; Fishes ; Kinetics ; Melanophores/ultrastructure ; Microtubules/metabolism/*physiology/ultrastructure ; Movement ; Pigments, Biological/metabolism ; Polymers
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  • 19
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-04-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kelner, K L -- New York, N.Y. -- Science. 1997 Apr 25;276(5312):547.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9148416" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Calcium-Binding Proteins ; Cells, Cultured ; Electric Stimulation ; Hippocampus ; Membrane Glycoproteins/metabolism ; Membrane Proteins/metabolism ; Nerve Tissue Proteins/metabolism ; Neurons/metabolism ; Neurotransmitter Agents/*metabolism ; R-SNARE Proteins ; Rats ; Recombinant Fusion Proteins/metabolism ; Synapses/*metabolism ; Synaptic Transmission ; Synaptotagmins
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  • 20
    Publication Date: 1997-01-31
    Description: The relation between an antigenic peptide that can stimulate a mature T cell and the natural peptide that promoted selection of this cell in the thymus is still unknown. An experimental system was devised to address this issue in vivo-mice expressing neopeptides in thymic stromal cells after adenovirus-mediated delivery of invariant chain-peptide fusion proteins. In this system, selection of T cells capable of responding to a given antigenic peptide could be promoted by the peptide itself, by closely related analogs lacking agonist and antagonist activity, or by ostensibly unrelated peptides. However, the precise repertoire of T cells selected was dictated by the particular neopeptide expressed.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nakano, N -- Rooke, R -- Benoist, C -- Mathis, D -- New York, N.Y. -- Science. 1997 Jan 31;275(5300):678-83.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut de Genetique et de Biologie Moleculaire et Cellulaire (INSERM, CNRS, Universite Louis Pasteur), 1 rue Laurent Fries, 67404 Illkirch, C.U. de Strasbourg, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9005856" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoviridae/genetics ; Amino Acid Sequence ; Animals ; Antigen-Presenting Cells/immunology ; Antigens, Differentiation, B-Lymphocyte/genetics ; Cells, Cultured ; Cloning, Molecular ; Cross Reactions ; Cytochrome c Group/immunology ; DNA, Complementary/genetics ; Genetic Vectors ; Histocompatibility Antigens Class II/genetics ; Hybridomas ; Interleukin-2/biosynthesis ; *Lymphocyte Activation ; Mice ; Molecular Sequence Data ; Peptides/chemistry/*immunology ; Receptors, Antigen, T-Cell/*immunology ; Recombinant Fusion Proteins ; T-Lymphocytes/*immunology ; Thymus Gland/cytology/*immunology
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  • 21
    Publication Date: 1997-04-11
    Description: Osteoclasts are multinucleated cells responsible for bone resorption. During the resorption cycle, osteoclasts undergo dramatic changes in their polarity, and resorbing cells reveal four functionally and structurally different membrane domains. Bone degradation products, both organic and inorganic, were endocytosed from the ruffled border membrane. They were then found to be transported in vesicles through the cell to the plasma membrane domain, located in the middle of the basal membrane, where they were liberated into the extracellular space. These results explain how resorbing osteoclasts can simultaneously remove large amounts of matrix degradation products and penetrate into bone.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Salo, J -- Lehenkari, P -- Mulari, M -- Metsikko, K -- Vaananen, H K -- New York, N.Y. -- Science. 1997 Apr 11;276(5310):270-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy and Biocenter, University of Oulu, Kajaanintie 52 A, 90220 Oulu, Finland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9092479" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/metabolism ; Animals ; Biological Transport ; Biotin/metabolism ; Bone Matrix/*metabolism ; *Bone Resorption ; Cattle ; Cell Membrane/metabolism/ultrastructure ; Cell Polarity ; Cells, Cultured ; Endocytosis ; Extracellular Space/metabolism ; Microscopy, Confocal ; Microscopy, Electron ; Minerals/metabolism ; Organelles/metabolism ; Osteocalcin/metabolism ; Osteoclasts/*metabolism/ultrastructure ; Rats ; Tetracycline/metabolism
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  • 22
    Publication Date: 1997-10-23
    Description: A mechanism by which members of the ciliary neurotrophic factor (CNTF)-leukemia inhibitory factor cytokine family regulate gliogenesis in the developing mammalian central nervous system was characterized. Activation of the CNTF receptor promoted differentiation of cerebral cortical precursor cells into astrocytes and inhibited differentiation of cortical precursors along a neuronal lineage. Although CNTF stimulated both the Janus kinase-signal transducer and activator of transcription (JAK-STAT) and Ras-mitogen-activated protein kinase signaling pathways in cortical precursor cells, the JAK-STAT signaling pathway selectively enhanced differentiation of these precursors along a glial lineage. These findings suggest that cytokine activation of the JAK-STAT signaling pathway may be a mechanism by which cell fate is controlled during mammalian development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bonni, A -- Sun, Y -- Nadal-Vicens, M -- Bhatt, A -- Frank, D A -- Rozovsky, I -- Stahl, N -- Yancopoulos, G D -- Greenberg, M E -- NIHP30-HD 18655/HD/NICHD NIH HHS/ -- R01 CA43855/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1997 Oct 17;278(5337):477-83.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Neuroscience, Children's Hospital, and Department of Neurobiology, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9334309" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD/metabolism ; Astrocytes/*cytology/drug effects/metabolism ; Cell Differentiation ; Cell Division ; Cell Lineage ; Cells, Cultured ; Cerebral Cortex/*cytology/embryology ; Ciliary Neurotrophic Factor ; Cytokine Receptor gp130 ; DNA-Binding Proteins/*metabolism ; Dimerization ; Glial Fibrillary Acidic Protein/biosynthesis ; Growth Inhibitors/metabolism/pharmacology ; *Interleukin-6 ; Janus Kinase 1 ; Leukemia Inhibitory Factor ; Leukemia Inhibitory Factor Receptor alpha Subunit ; Lymphokines/metabolism/pharmacology ; Membrane Glycoproteins/metabolism ; Nerve Growth Factors/pharmacology ; Nerve Tissue Proteins/metabolism/pharmacology ; Platelet-Derived Growth Factor/pharmacology ; Protein-Tyrosine Kinases/*metabolism ; Rats ; Receptor Protein-Tyrosine Kinases/metabolism ; Receptor, Ciliary Neurotrophic Factor ; Receptors, Cytokine/metabolism ; Receptors, Nerve Growth Factor/metabolism ; Receptors, OSM-LIF ; STAT1 Transcription Factor ; STAT3 Transcription Factor ; *Signal Transduction ; Stem Cells/cytology ; Trans-Activators/*metabolism
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  • 23
    Publication Date: 1997-10-24
    Description: CD8(+) T lymphocytes from individuals infected with human immunodeficiency virus-type 1 (HIV-1) secrete a soluble activity that suppresses infection by HIV-1. A protein associated with this activity was purified from the culture supernatant of an immortalized CD8(+) T cell clone and identified as the beta-chemokine macrophage-derived chemokine (MDC). MDC suppressed infection of CD8(+) cell-depleted peripheral blood mononuclear cells by primary non-syncytium-inducing and syncytium-inducing isolates of HIV-1 and the T cell line-adapted isolate HIV-1IIIB. MDC was expressed in activated, but not resting, peripheral blood mononuclear cells and binds a receptor on activated primary T cells. These observations indicate that beta-chemokines are responsible for a major proportion of HIV-1-specific suppressor activity produced by primary T cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pal, R -- Garzino-Demo, A -- Markham, P D -- Burns, J -- Brown, M -- Gallo, R C -- DeVico, A L -- N01-AI-55279/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1997 Oct 24;278(5338):695-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Advanced BioScience Laboratories, 5510 Nicholson Lane, Kensington, MD 20895, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9381181" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Antiviral Agents/*immunology ; Blotting, Northern ; CD8-Positive T-Lymphocytes/*immunology ; Calcium/blood ; Cell Line ; Cell Line, Transformed ; Cells, Cultured ; Chemokine CCL22 ; Chemokines, CC/chemistry/*immunology/isolation & purification/metabolism ; HIV Core Protein p24/biosynthesis ; HIV Infections/immunology ; HIV-1/*immunology/physiology ; Humans ; Leukocytes, Mononuclear/immunology/metabolism/*virology ; Lymphocyte Activation ; Receptors, Chemokine/metabolism ; Receptors, HIV/metabolism ; T-Lymphocytes/immunology
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  • 24
    Publication Date: 1997-04-11
    Description: The chemokine receptors CXCR4 and CCR5 have recently been shown to act as coreceptors, in concert with CD4, for human immunodeficiency virus-type 1 (HIV-1) infection. RANTES and other chemokines that interact with CCR5 and block infection of peripheral blood mononuclear cell cultures inhibit infection of primary macrophages inefficiently at best. If used to treat HIV-1-infected individuals, these chemokines could fail to influence HIV replication in nonlymphocyte compartments while promoting unwanted inflammatory side effects. A derivative of RANTES that was created by chemical modification of the amino terminus, aminooxypentane (AOP)-RANTES, did not induce chemotaxis and was a subnanomolar antagonist of CCR5 function in monocytes. It potently inhibited infection of diverse cell types (including macrophages and lymphocytes) by nonsyncytium-inducing, macrophage-tropic HIV-1 strains. Thus, activation of cells by chemokines is not a prerequisite for the inhibition of viral uptake and replication. Chemokine receptor antagonists like AOP-RANTES that achieve full receptor occupancy at nanomolar concentrations are strong candidates for the therapy of HIV-1-infected individuals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Simmons, G -- Clapham, P R -- Picard, L -- Offord, R E -- Rosenkilde, M M -- Schwartz, T W -- Buser, R -- Wells, T N -- Proudfoot, A E -- New York, N.Y. -- Science. 1997 Apr 11;276(5310):276-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Virology Group, Chester Beatty Laboratories, Institute of Cancer Research, 237 Fulham Road, London SW3 6JB, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9092481" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD4/metabolism ; Binding, Competitive ; Cats ; Cell Line ; Cells, Cultured ; Chemokine CCL4 ; Chemokine CCL5/metabolism/pharmacology ; Chemotaxis, Leukocyte ; HIV-1/*drug effects/physiology ; HeLa Cells ; Humans ; Macrophage Inflammatory Proteins/metabolism ; Macrophages/drug effects/*virology ; Receptors, CCR5 ; *Receptors, Chemokine ; Receptors, Cytokine/*antagonists & inhibitors/metabolism ; Receptors, HIV/*antagonists & inhibitors/metabolism ; T-Lymphocytes/drug effects/*virology ; Virus Replication/drug effects
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  • 25
    Publication Date: 1997-02-14
    Description: A lymphocyte population that expresses surface markers found on T cells and natural killer (NK) cells secretes large amounts of interleukin-4 (IL-4) immediately after T cell receptor ligation. These NK-like T cells are thus thought to be important for the initiation of type 2 T helper cell (TH2) responses. CD1-deficient mice were found to lack this lymphocyte subset, but they could nevertheless mount a protypical TH2 response; after immunization with antibody to immunoglobulin D (IgD), CD1-deficient mice produced IgE. Thus, although dependent on CD1 for their development, IL-4-secreting NK-like T cells are not required for TH2 responses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Smiley, S T -- Kaplan, M H -- Grusby, M J -- R01 A140171/PHS HHS/ -- New York, N.Y. -- Science. 1997 Feb 14;275(5302):977-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cancer Biology, Harvard School of Public Health (HSPH), Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9020080" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies/immunology ; Antibodies, Anti-Idiotypic/immunology ; Antigens, CD1/genetics/*physiology ; Antigens, CD3/immunology ; Cells, Cultured ; Gene Targeting ; Immunoglobulin D/immunology ; Immunoglobulin E/*biosynthesis ; Immunophenotyping ; Interferon-gamma/genetics/secretion ; Interleukin-4/biosynthesis/genetics/*secretion ; Killer Cells, Natural/immunology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; RNA, Messenger/genetics/metabolism ; Receptors, Antigen, T-Cell/immunology ; T-Lymphocyte Subsets/*immunology ; Th2 Cells/immunology ; beta 2-Microglobulin/genetics/physiology
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  • 26
    Publication Date: 1997-02-14
    Description: The mechanisms responsible for thyrocyte destruction in Hashimoto's thyroiditis (HT) are poorly understood. Thyrocytes from HT glands, but not from nonautoimmune thyroids, expressed Fas. Interleukin-1beta (IL-1beta), abundantly produced in HT glands, induced Fas expression in normal thyrocytes, and cross-linking of Fas resulted in massive thyrocyte apoptosis. The ligand for Fas (FasL) was shown to be constitutively expressed both in normal and HT thyrocytes and was able to kill Fas-sensitive targets. Exposure to IL-1beta induced thyrocyte apoptosis, which was prevented by antibodies that block Fas, suggesting that IL-1beta-induced Fas expression serves as a limiting factor for thyrocyte destruction. Thus, Fas-FasL interactions among HT thyrocytes may contribute to clinical hypothyroidism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Giordano, C -- Stassi, G -- De Maria, R -- Todaro, M -- Richiusa, P -- Papoff, G -- Ruberti, G -- Bagnasco, M -- Testi, R -- Galluzzo, A -- A.066/Telethon/Italy -- New York, N.Y. -- Science. 1997 Feb 14;275(5302):960-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Immunology, Endocrinology Section, Institute of Clinica Medica, University of Palermo, Palermo, Italy.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9020075" target="_blank"〉PubMed〈/a〉
    Keywords: Antibodies, Monoclonal/immunology ; Antigens, CD95/biosynthesis/immunology/*metabolism ; *Apoptosis ; Cells, Cultured ; Cytokines/pharmacology ; Fas Ligand Protein ; Humans ; Immunoenzyme Techniques ; Interleukin-1/pharmacology ; Membrane Glycoproteins/biosynthesis/*metabolism ; Nucleic Acid Synthesis Inhibitors/pharmacology ; Polymerase Chain Reaction ; Protein Synthesis Inhibitors/pharmacology ; RNA, Messenger/genetics/metabolism ; Recombinant Proteins/pharmacology ; Thyroid Gland/*metabolism/pathology ; Thyroiditis, Autoimmune/*etiology/metabolism/pathology ; Tumor Cells, Cultured
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  • 27
    Publication Date: 1997-03-14
    Description: The organization of calcium (Ca2+) stores in the sarcoplasmic and endoplasmic reticulum (S-ER) is poorly understood. The dynamics of the storage and release of calcium in the S-ER of intact, cultured astrocytes and arterial myocytes were studied with high-resolution imaging methods. The S-ER appeared to be a continuous tubular network; nevertheless, calcium stores in the S-ER were organized into small, spatially distinct compartments that functioned as discrete units. Cyclopiazonic acid (an inhibitor of the calcium pump in the S-ER membrane) and caffeine or ryanodine unloaded different, spatially separate compartments. Heterogeneity of calcium stores was also revealed in cells activated by physiological agonists. These results suggest that cells can generate spatially and temporally distinct calcium signals to control individual calcium-dependent processes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Golovina, V A -- Blaustein, M P -- HL-32276/HL/NHLBI NIH HHS/ -- NS-16106/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1997 Mar 14;275(5306):1643-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology and Center for Vascular Biology and Hypertension, University of Maryland School of Medicine, Baltimore, MD 21201, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9054358" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Astrocytes/*metabolism/ultrastructure ; Caffeine/pharmacology ; Calcium/*metabolism ; Calcium-Transporting ATPases/antagonists & inhibitors ; Cells, Cultured ; Endoplasmic Reticulum, Smooth/*metabolism/ultrastructure ; Fluorescent Dyes/metabolism ; Fura-2/analogs & derivatives/metabolism ; Glutamic Acid/pharmacology ; Indoles/pharmacology ; Mice ; Mitochondria/metabolism ; Mitochondria, Muscle/metabolism ; Muscle, Smooth, Vascular/cytology/*metabolism/ultrastructure ; Rats ; Ryanodine/pharmacology ; Sarcoplasmic Reticulum/*metabolism/ultrastructure ; Serotonin/pharmacology
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  • 28
    Publication Date: 1997-08-08
    Description: Most somatic cells die after a finite number of cell divisions, a phenomenon described as senescence. The p21(CIP1/WAF1) gene encodes an inhibitor of cyclin-dependent kinases. Inactivation of p21 by two sequential rounds of targeted homologous recombination was sufficient to bypass senescence in normal diploid human fibroblasts. At the checkpoint between the prereplicative phase of growth and the phase of chromosome replication, cells lacking p21 failed to arrest the cell cycle in response to DNA damage, but their apoptotic response and genomic stability were unaltered. These results establish the feasibility of using gene targeting for genetic studies of normal human cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brown, J P -- Wei, W -- Sedivy, J M -- GM41690/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1997 Aug 8;277(5327):831-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Cell Biology, and Biochemistry, Brown University, Providence, RI 02912, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9242615" target="_blank"〉PubMed〈/a〉
    Keywords: Apoptosis ; Aspartate Carbamoyltransferase/genetics ; Carbamoyl-Phosphate Synthase (Glutamine-Hydrolyzing)/genetics ; Cell Aging/*genetics ; Cell Division ; Cells, Cultured ; Cyclin-Dependent Kinase Inhibitor p21 ; Cyclins/*genetics/physiology ; DNA Damage ; Dihydroorotase/genetics ; Electroporation ; Fibroblasts ; G1 Phase ; *Gene Deletion ; Gene Targeting ; Genetic Vectors ; Humans ; Multienzyme Complexes/genetics ; Telomere/physiology
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  • 29
    Publication Date: 1997-04-11
    Description: Activation of CD4(+) T lymphocytes from human immunodeficiency virus-type 1 (HIV-1)-infected donors with immobilized antibodies to CD3 and CD28 induces a virus-resistant state. This effect is specific for macrophage-tropic HIV-1. Transcripts encoding CXCR4/Fusin, the fusion cofactor used by T cell line-tropic isolates, were abundant in CD3/CD28-stimulated cells, but transcripts encoding CCR5, the fusion cofactor used by macrophage-tropic viruses, were not detectable. Thus, CD3/CD28 costimulation induces an HIV-1-resistant phenotype similar to that seen in some highly exposed and HIV-uninfected individuals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Carroll, R G -- Riley, J L -- Levine, B L -- Feng, Y -- Kaushal, S -- Ritchey, D W -- Bernstein, W -- Weislow, O S -- Brown, C R -- Berger, E A -- June, C H -- St Louis, D C -- New York, N.Y. -- Science. 1997 Apr 11;276(5310):273-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Henry M. Jackson Foundation for the Advancement of Military Medicine, Rockville, MD 20850, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9092480" target="_blank"〉PubMed〈/a〉
    Keywords: Antibodies, Monoclonal/immunology ; Antigens, CD28/*immunology ; Antigens, CD3/immunology ; CD4-Positive T-Lymphocytes/*immunology/metabolism/*virology ; Cells, Cultured ; Gene Expression Regulation ; HIV-1/*physiology ; Humans ; Interleukin-2/immunology ; *Lymphocyte Activation ; Membrane Fusion ; Membrane Proteins/*genetics ; Muromonab-CD3/immunology ; Phytohemagglutinins/pharmacology ; RNA, Messenger/genetics/metabolism ; Receptors, CCR5 ; Receptors, CXCR4 ; Receptors, Cytokine/genetics ; Receptors, HIV/*genetics ; Up-Regulation ; Virus Replication
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  • 30
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-09-26
    Description: The upper cervical corticospinal tract was transected on one side in adult rats. A suspension of ensheathing cells cultured from adult rat olfactory bulb was injected into the lesion site. This induced unbranched, elongative growth of the cut corticospinal axons. The axons grew through the transplant and continued to regenerate into the denervated caudal host tract. Rats with complete transections and no transplanted cells did not use the forepaw on the lesioned side for directed reaching. Rats in which the transplanted cells had formed a continuous bridge across the lesion exhibited directed forepaw reaching on the lesioned side.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Y -- Field, P M -- Raisman, G -- New York, N.Y. -- Science. 1997 Sep 26;277(5334):2000-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Norman and Sadie Lee Research Centre, Division of Neurobiology, National Institute for Medical Research, Medical Research Council, London NW7 1AA, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9302296" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/*physiology/ultrastructure ; Brain Tissue Transplantation ; Cell Transplantation ; Cells, Cultured ; Denervation ; Female ; Microscopy, Electron ; Myelin Sheath/physiology ; *Nerve Regeneration ; Neuroglia/physiology/*transplantation/ultrastructure ; Olfactory Bulb/*cytology ; Olfactory Nerve/*cytology ; Rats ; Spinal Cord/*physiology ; Spinal Cord Injuries/*surgery
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 31
    Publication Date: 1997-06-27
    Description: Parsley cells recognize the fungal plant pathogen Phytophthora sojae through a plasma membrane receptor. A pathogen-derived oligopeptide elicitor binds to this receptor and thereby stimulates a multicomponent defense response through sequential activation of ion channels and an oxidative burst. An elicitor-responsive mitogen-activated protein (MAP) kinase was identified that acts downstream of the ion channels but independently or upstream of the oxidative burst. Upon receptor-mediated activation, the MAP kinase is translocated to the nucleus where it might interact with transcription factors that induce expression of defense genes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ligterink, W -- Kroj, T -- zur Nieden, U -- Hirt, H -- Scheel, D -- New York, N.Y. -- Science. 1997 Jun 27;276(5321):2054-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Microbiology and Genetics, Vienna Biocenter, Dr.-Bohr-Gasse 9, A-1030 Vienna, Austria.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9197271" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Amphotericin B/pharmacology ; Anthracenes/pharmacology ; Calcium-Calmodulin-Dependent Protein Kinases/chemistry/genetics/*metabolism ; Cell Nucleus/enzymology ; Cells, Cultured ; Enzyme Activation ; Fungal Proteins/*pharmacology ; Ion Channels/drug effects/metabolism ; Membrane Glycoproteins/*pharmacology ; Molecular Sequence Data ; Onium Compounds/pharmacology ; Peptide Fragments/pharmacology ; Phosphorylation ; Phytophthora/metabolism ; Plants/*enzymology/genetics/microbiology ; Respiratory Burst/drug effects
    Print ISSN: 0036-8075
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  • 32
    Publication Date: 1997-04-25
    Description: It is unclear whether organ-specific autoantigens are critical for the development of primary Sjogren's syndrome (SS). A 120-kilodalton organ-specific autoantigen was purified from salivary gland tissues of an NFS/sld mouse model of human SS. The amino-terminal residues were identical to those of the human cytoskeletal protein alpha-fodrin. The purified antigen induced proliferative T cell responses and production of interleukin-2 and interferon-gamma in vitro. Neonatal immunization with the 120-kilodalton antigen prevented the disease in mice. Sera from patients with SS reacted positively with purified antigen and recombinant human alpha-fodrin protein, whereas those from patients with systemic lupus erythematosus and rheumatoid arthritis did not. Thus, the immune response to 120-kilodalton alpha-fodrin could be important in the initial development of primary SS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Haneji, N -- Nakamura, T -- Takio, K -- Yanagi, K -- Higashiyama, H -- Saito, I -- Noji, S -- Sugino, H -- Hayashi, Y -- New York, N.Y. -- Science. 1997 Apr 25;276(5312):604-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Tokushima University School of Dentistry, 3 Kuramotocho, Tokushima 770, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9110981" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Arthritis, Rheumatoid/immunology ; Autoantibodies/biosynthesis/immunology ; Autoantigens/*immunology/isolation & purification ; Carrier Proteins/*immunology/isolation & purification ; Cells, Cultured ; Disease Models, Animal ; Humans ; Immunization ; Immunoblotting ; Interferon-gamma/biosynthesis ; Interleukin-2/biosynthesis ; Lupus Erythematosus, Systemic/immunology ; Lymphocyte Activation ; Mice ; Mice, Inbred Strains ; Microfilament Proteins/*immunology/isolation & purification ; Molecular Sequence Data ; Organ Specificity ; Recombinant Fusion Proteins/immunology ; Salivary Glands/immunology ; Sjogren's Syndrome/*immunology/prevention & control ; T-Lymphocytes/immunology
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  • 33
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-04-04
    Description: Marrow stromal cells can be isolated from other cells in marrow by their tendency to adhere to tissue culture plastic. The cells have many of the characteristics of stem cells for tissues that can roughly be defined as mesenchymal, because they can be differentiated in culture into osteoblasts, chondrocytes, adipocytes, and even myoblasts. Therefore, marrow stromal cells present an intriguing model for examining the differentiation of stem cells. Also, they have several characteristics that make them potentially useful for cell and gene therapy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Prockop, D J -- New York, N.Y. -- Science. 1997 Apr 4;276(5309):71-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Gene Therapy, Allegheny University of the Health Sciences, MCP-Hahnemann School of Medicine, 245 North 15 Street, Mail Stop 421, Philadelphia, PA 19102, USA. prockop@allegheny.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9082988" target="_blank"〉PubMed〈/a〉
    Keywords: Adipocytes/cytology ; Animals ; *Bone Marrow Cells ; Bone Marrow Transplantation ; Cartilage/cytology ; Cell Differentiation ; Cells, Cultured ; Cytokines/metabolism ; Genetic Therapy ; Humans ; Muscle Fibers, Skeletal/cytology ; Osteoblasts/cytology ; Stem Cells/*cytology/physiology ; Stromal Cells/*cytology/physiology
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  • 34
    Publication Date: 1997-08-22
    Description: Nerve growth factor (NGF) is a neurotrophic factor secreted by cells that are the targets of innervation of sympathetic and some sensory neurons. However, the mechanism by which the NGF signal is propagated from the axon terminal to the cell body, which can be more than 1 meter away, to influence biochemical events critical for growth and survival of neurons has remained unclear. An NGF-mediated signal transmitted from the terminals and distal axons of cultured rat sympathetic neurons to their nuclei regulated phosphorylation of the transcription factor CREB (cyclic adenosine monophosphate response element-binding protein). Internalization of NGF and its receptor tyrosine kinase TrkA, and their transport to the cell body, were required for transmission of this signal. The tyrosine kinase activity of TrkA was required to maintain it in an autophosphorylated state upon its arrival in the cell body and for propagation of the signal to CREB within neuronal nuclei. Thus, an NGF-TrkA complex is a messenger that delivers the NGF signal from axon terminals to cell bodies of sympathetic neurons.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Riccio, A -- Pierchala, B A -- Ciarallo, C L -- Ginty, D D -- New York, N.Y. -- Science. 1997 Aug 22;277(5329):1097-100.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, Johns Hopkins University School of Medicine, 725 North Wolfe Street, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9262478" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; *Axonal Transport ; Axons/*metabolism ; Carbazoles/pharmacology ; Cell Membrane/metabolism ; Cells, Cultured ; Cyclic AMP Response Element-Binding Protein/*metabolism ; Indole Alkaloids ; Microspheres ; Nerve Growth Factors/*metabolism/pharmacology ; Neurons/*metabolism ; Phosphorylation ; Proto-Oncogene Proteins/antagonists & inhibitors/*metabolism ; Rats ; Receptor Protein-Tyrosine Kinases/antagonists & inhibitors/*metabolism ; Receptor, trkA ; Receptors, Nerve Growth Factor/antagonists & inhibitors/*metabolism ; Signal Transduction ; Superior Cervical Ganglion/cytology
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  • 35
    Publication Date: 1997-11-21
    Description: Induction of apoptosis by oncogenes like c-myc may be important in restraining the emergence of neoplasia. However, the mechanism by which c-myc induces apoptosis is unknown. CD95 (also termed Fas or APO-1) is a cell surface transmembrane receptor of the tumor necrosis factor receptor family that activates an intrinsic apoptotic suicide program in cells upon binding either its ligand CD95L or antibody. c-myc-induced apoptosis was shown to require interaction on the cell surface between CD95 and its ligand. c-Myc acts downstream of the CD95 receptor by sensitizing cells to the CD95 death signal. Moreover, IGF-I signaling and Bcl-2 suppress c-myc-induced apoptosis by also acting downstream of CD95. These findings link two apoptotic pathways previously thought to be independent and establish the dependency of Myc on CD95 signaling for its killing activity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hueber, A O -- Zornig, M -- Lyon, D -- Suda, T -- Nagata, S -- Evan, G I -- New York, N.Y. -- Science. 1997 Nov 14;278(5341):1305-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Imperial Cancer Research Fund (ICRF) Laboratories, 44 Lincoln's Inn Fields, London WC2A 3PX, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9360929" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; *Adaptor Proteins, Signal Transducing ; Animals ; Antigens, CD95/*metabolism ; *Apoptosis ; Autocrine Communication ; Carrier Proteins/metabolism ; Cell Line ; Cell Membrane/metabolism ; Cells, Cultured ; Fas Ligand Protein ; Fas-Associated Death Domain Protein ; Gene Expression Regulation ; Genes, myc ; Insulin-Like Growth Factor I/pharmacology/physiology ; Membrane Glycoproteins/*metabolism ; Mice ; Proto-Oncogene Proteins c-bcl-2/pharmacology/physiology ; Proto-Oncogene Proteins c-myc/*metabolism ; Rats
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  • 36
    Publication Date: 1997-02-07
    Description: Generally, impulse propagation in cardiac tissue is assumed to be impaired by a reduction of intercellular electrical coupling or by the presence of structural discontinuities. Contrary to this notion, the spatially uniform reduction of electrical coupling induced successful conduction in discontinuous cardiac tissue structures exhibiting unidirectional conduction block. This seemingly paradoxical finding can be explained by a nonsymmetric effect of uncoupling on the current source and the current sink in the preparations used. It suggests that partial cellular uncoupling might prevent the initiation of cardiac arrhythmias that are dependent on the presence of unidirectional conduction block.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rohr, S -- Kucera, J P -- Fast, V G -- Kleber, A G -- New York, N.Y. -- Science. 1997 Feb 7;275(5301):841-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, University of Bern, Buhlplatz 5, CH-3012 Bern, Switzerland. rohr@pyl.unibe.ch〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9012353" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Arrhythmias, Cardiac/physiopathology ; Cells, Cultured ; Diffusion ; Fatty Acids, Monounsaturated/pharmacology ; Gap Junctions/physiology ; Heart/*physiology ; Heart Conduction System/*physiology ; Microscopy, Video ; Rats
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  • 37
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-01-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vogel, G -- New York, N.Y. -- Science. 1997 Jan 31;275(5300):621.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9019818" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Chromosome Mapping ; *Chromosomes, Human, Pair 1 ; Chromosomes, Human, Pair 3 ; Cytoskeletal Proteins ; Eye Proteins/*genetics ; Genetic Linkage ; Genetic Markers ; Glaucoma, Open-Angle/*genetics ; *Glycoproteins ; Humans ; Mice ; Mutation ; Proteins/secretion ; Steroids/pharmacology ; Trabecular Meshwork/cytology/drug effects/secretion
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  • 38
    Publication Date: 1997-10-10
    Description: Substance P is released in the spinal cord in response to painful stimuli, but its role in nociceptive signaling remains unclear. When a conjugate of substance P and the ribosome-inactivating protein saporin was infused into the spinal cord, it was internalized and cytotoxic to lamina I spinal cord neurons that express the substance P receptor. This treatment left responses to mild noxious stimuli unchanged, but markedly attenuated responses to highly noxious stimuli and mechanical and thermal hyperalgesia. Thus, lamina I spinal cord neurons that express the substance P receptor play a pivotal role in the transmission of highly noxious stimuli and the maintenance of hyperalgesia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mantyh, P W -- Rogers, S D -- Honore, P -- Allen, B J -- Ghilardi, J R -- Li, J -- Daughters, R S -- Lappi, D A -- Wiley, R G -- Simone, D A -- MH56368/MH/NIMH NIH HHS/ -- NS23970/NS/NINDS NIH HHS/ -- NS31223/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1997 Oct 10;278(5336):275-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Neurobiology Laboratory (151), Veterans Administration Medical Center, Minneapolis, MN 55417, USA. manty001@maroon.tc.umn.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9323204" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Capsaicin ; Cell Membrane/metabolism ; Cells, Cultured ; Fluorescent Antibody Technique ; Hyperalgesia/physiopathology/*therapy ; *Immunotoxins ; Injections, Spinal ; *N-Glycosyl Hydrolases ; Neurons/cytology/*metabolism ; Pain/physiopathology ; *Pain Management ; Pain Measurement ; Plant Proteins/metabolism/pharmacology ; Rats ; Rats, Sprague-Dawley ; Receptors, Neurokinin-1/biosynthesis/*metabolism ; Ribosome Inactivating Proteins, Type 1 ; Signal Transduction ; Spinal Cord/*cytology/metabolism ; Substance P/*metabolism/pharmacology
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  • 39
    Publication Date: 1997-04-25
    Description: The gene encoding the BCL-6 transcriptional repressor is frequently translocated and mutated in diffuse large cell lymphoma. Mice with a disrupted BCL-6 gene developed myocarditis and pulmonary vasculitis, had no germinal centers, and had increased expression of T helper cell type 2 cytokines. The BCL-6 DNA recognition motif resembled sites bound by the STAT (signal transducers and activators of transcription) transcription factors, which mediate cytokine signaling. BCL-6 could repress interleukin-4 (IL-4)-induced transcription when bound to a site recognized by the IL-4-responsive transcription factor Stat6. Thus, dysregulation of STAT-responsive genes may underlie the inflammatory disease in BCL-6-deficient mice and participate in lymphoid malignancies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dent, A L -- Shaffer, A L -- Yu, X -- Allman, D -- Staudt, L M -- New York, N.Y. -- Science. 1997 Apr 25;276(5312):589-92.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Metabolism Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9110977" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/immunology ; Cells, Cultured ; Cytokines/*biosynthesis ; DNA-Binding Proteins/genetics/*physiology ; Ficoll/analogs & derivatives/immunology ; Germinal Center/*immunology ; Hemocyanin/immunology ; Immunoglobulins/biosynthesis ; Inflammation/*immunology/pathology ; Interferon-gamma/biosynthesis ; Interleukin-4/metabolism ; Interleukins/biosynthesis/metabolism ; Lymphocyte Activation ; Mice ; Myocarditis/immunology/pathology ; Proto-Oncogene Proteins/genetics/*physiology ; Proto-Oncogene Proteins c-bcl-6 ; Receptors, IgE/genetics ; STAT6 Transcription Factor ; Signal Transduction ; Spleen/immunology ; T-Lymphocytes/immunology ; Th2 Cells/immunology ; Trans-Activators/metabolism ; Transcription Factors/genetics/*physiology ; Transcription, Genetic ; Trinitrobenzenes/immunology ; Vasculitis/immunology/pathology
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  • 40
    Publication Date: 1997-07-18
    Description: Proteins of the Bcl-2 family are intracellular membrane-associated proteins that regulate programmed cell death (apoptosis) either positively or negatively by as yet unknown mechanisms. Bax, a pro-apoptotic member of the Bcl-2 family, was shown to form channels in lipid membranes. Bax triggered the release of liposome-encapsulated carboxyfluorescein at both neutral and acidic pH. At physiological pH, release could be blocked by Bcl-2. Bcl-2, in contrast, triggered carboxyfluorescein release at acidic pH only. In planar lipid bilayers, Bax formed pH- and voltage-dependent ion-conducting channels. Thus, the pro-apoptotic effects of Bax may be elicited through an intrinsic pore-forming activity that can be antagonized by Bcl-2.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Antonsson, B -- Conti, F -- Ciavatta, A -- Montessuit, S -- Lewis, S -- Martinou, I -- Bernasconi, L -- Bernard, A -- Mermod, J J -- Mazzei, G -- Maundrell, K -- Gambale, F -- Sadoul, R -- Martinou, J C -- New York, N.Y. -- Science. 1997 Jul 18;277(5324):370-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Geneva Biomedical Research Institute, Glaxo Wellcome R&D S. A., 1288 Plan les Ouates, Geneva, Switzerland. beau6063@ggr.co.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9219694" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Cell Membrane Permeability ; Cells, Cultured ; Erythrocytes/cytology ; Fluoresceins/metabolism ; Hemolysis ; Humans ; Hydrogen-Ion Concentration ; Ion Channels/*physiology ; Lipid Bilayers ; Liposomes ; Membrane Potentials ; Neurons/cytology ; Patch-Clamp Techniques ; Proto-Oncogene Proteins/pharmacology/*physiology ; Proto-Oncogene Proteins c-bcl-2/antagonists & inhibitors/pharmacology/*physiology ; Sheep ; Sympathetic Nervous System/cytology ; bcl-2-Associated X Protein
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  • 41
    Publication Date: 1997-08-01
    Description: The c-Jun amino-terminal kinase (JNK) is a member of the stress-activated group of mitogen-activated protein (MAP) kinases that are implicated in the control of cell growth. A murine cytoplasmic protein that binds specifically to JNK [the JNK interacting protein-1 (JIP-1)] was characterized and cloned. JIP-1 caused cytoplasmic retention of JNK and inhibition of JNK-regulated gene expression. In addition, JIP-1 suppressed the effects of the JNK signaling pathway on cellular proliferation, including transformation by the Bcr-Abl oncogene. This analysis identifies JIP-1 as a specific inhibitor of the JNK signal transduction pathway and establishes protein targeting as a mechanism that regulates signaling by stress-activated MAP kinases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dickens, M -- Rogers, J S -- Cavanagh, J -- Raitano, A -- Xia, Z -- Halpern, J R -- Greenberg, M E -- Sawyers, C L -- Davis, R J -- CA43855/CA/NCI NIH HHS/ -- CA65861/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1997 Aug 1;277(5326):693-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Program in Molecular Medicine, Department of Biochemistry and Molecular Biology, University of Massachusetts Medical School, 373 Plantation Street, Worcester, MA 01605, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9235893" target="_blank"〉PubMed〈/a〉
    Keywords: Activating Transcription Factor 2 ; Animals ; COS Cells ; Calcium-Calmodulin-Dependent Protein Kinases/*metabolism ; Carrier Proteins/chemistry/*metabolism ; Cell Nucleus/metabolism ; Cell Transformation, Neoplastic ; Cells, Cultured ; Cloning, Molecular ; Cyclic AMP Response Element-Binding Protein/metabolism ; Cytoplasm/metabolism ; Fusion Proteins, bcr-abl/metabolism ; Gene Expression Regulation ; JNK Mitogen-Activated Protein Kinases ; Mitogen-Activated Protein Kinase 9 ; *Mitogen-Activated Protein Kinases ; Molecular Sequence Data ; Phosphorylation ; Protein Kinases/metabolism ; Proto-Oncogene Proteins c-jun/metabolism ; Recombinant Fusion Proteins/metabolism ; *Signal Transduction ; Transcription Factors/metabolism ; Transcriptional Activation ; Transfection
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  • 42
    Publication Date: 1997-02-14
    Description: Putative endothelial cell (EC) progenitors or angioblasts were isolated from human peripheral blood by magnetic bead selection on the basis of cell surface antigen expression. In vitro, these cells differentiated into ECs. In animal models of ischemia, heterologous, homologous, and autologous EC progenitors incorporated into sites of active angiogenesis. These findings suggest that EC progenitors may be useful for augmenting collateral vessel growth to ischemic tissues (therapeutic angiogenesis) and for delivering anti- or pro-angiogenic agents, respectively, to sites of pathologic or utilitarian angiogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Asahara, T -- Murohara, T -- Sullivan, A -- Silver, M -- van der Zee, R -- Li, T -- Witzenbichler, B -- Schatteman, G -- Isner, J M -- 2824/PHS HHS/ -- 53354/PHS HHS/ -- 57516/PHS HHS/ -- New York, N.Y. -- Science. 1997 Feb 14;275(5302):964-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine (Cardiology), St. Elizabeth's Medical Center, Tufts University School of Medicine, 736 Cambridge Street, Boston, MA 02135, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9020076" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD34/analysis ; Biomarkers/analysis ; Cell Differentiation ; Cell Separation ; Cells, Cultured ; Endothelium, Vascular/chemistry/*cytology ; Flow Cytometry ; Hindlimb/blood supply ; Humans ; Ischemia/physiopathology ; Mice ; Mice, Inbred C57BL ; Mice, Nude ; Mice, Transgenic ; *Neovascularization, Physiologic ; Nitric Oxide Synthase/analysis ; Rabbits ; Receptor Protein-Tyrosine Kinases/analysis ; Receptors, Growth Factor/analysis ; Receptors, Vascular Endothelial Growth Factor ; Stem Cells/chemistry/*cytology
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  • 43
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-04-04
    Description: In the vertebrate central nervous system, multipotential cells have been identified in vitro and in vivo. Defined mitogens cause the proliferation of multipotential cells in vitro, the magnitude of which is sufficient to account for the number of cells in the brain. Factors that control the differentiation of fetal stem cells to neurons and glia have been defined in vitro, and multipotential cells with similar signaling logic can be cultured from the adult central nervous system. Transplanting cells to new sites emphasizes that neuroepithelial cells have the potential to integrate into many brain regions. These results focus attention on how information in external stimuli is translated into the number and types of differentiated cells in the brain. The development of therapies for the reconstruction of the diseased or injured brain will be guided by our understanding of the origin and stability of cell type in the central nervous system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McKay, R -- New York, N.Y. -- Science. 1997 Apr 4;276(5309):66-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Biology, National Institute of Neurological Disorders and Stroke, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9082987" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/cytology/embryology ; Brain Tissue Transplantation ; Cell Differentiation ; Cell Line ; Cell Lineage ; Cell Movement ; Cell Transplantation ; Cells, Cultured ; Central Nervous System/*cytology/embryology ; Central Nervous System Diseases/therapy ; Humans ; Neuroglia/*cytology ; Neurons/*cytology ; Spinal Cord/cytology/embryology ; Stem Cells/*cytology/physiology
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  • 44
    Publication Date: 1997-01-31
    Description: A signaling pathway was delineated by which insulin-like growth factor 1 (IGF-1) promotes the survival of cerebellar neurons. IGF-1 activation of phosphoinositide 3-kinase (PI3-K) triggered the activation of two protein kinases, the serine-threonine kinase Akt and the p70 ribosomal protein S6 kinase (p70(S6K)). Experiments with pharmacological inhibitors, as well as expression of wild-type and dominant-inhibitory forms of Akt, demonstrated that Akt but not p70(S6K) mediates PI3-K-dependent survival. These findings suggest that in the developing nervous system, Akt is a critical mediator of growth factor-induced neuronal survival.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dudek, H -- Datta, S R -- Franke, T F -- Birnbaum, M J -- Yao, R -- Cooper, G M -- Segal, R A -- Kaplan, D R -- Greenberg, M E -- DK39519/DK/NIDDK NIH HHS/ -- R01 CA18689/CA/NCI NIH HHS/ -- R01 CA43855/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1997 Jan 31;275(5300):661-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, Children's Hospital, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9005851" target="_blank"〉PubMed〈/a〉
    Keywords: Androstadienes/pharmacology ; Animals ; *Apoptosis/drug effects ; Calcium-Calmodulin-Dependent Protein Kinases/metabolism ; Cell Survival/drug effects ; Cells, Cultured ; Cerebellum/cytology ; Chromones/pharmacology ; Enzyme Activation ; Enzyme Inhibitors/pharmacology ; Insulin/pharmacology ; Insulin-Like Growth Factor I/*pharmacology ; Morpholines/pharmacology ; Neurons/*cytology/drug effects/enzymology ; Phosphatidylinositol 3-Kinases ; Phosphotransferases (Alcohol Group Acceptor)/metabolism ; Protein-Serine-Threonine Kinases/*metabolism ; Proto-Oncogene Proteins/chemistry/genetics/*metabolism ; Proto-Oncogene Proteins c-akt ; Rats ; Ribosomal Protein S6 Kinases ; *Signal Transduction ; Transfection
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  • 45
    Publication Date: 1997-08-22
    Description: Anandamide, an endogenous ligand for central cannabinoid receptors, is released from neurons on depolarization and rapidly inactivated. Anandamide inactivation is not completely understood, but it may occur by transport into cells or by enzymatic hydrolysis. The compound N-(4-hydroxyphenyl)arachidonylamide (AM404) was shown to inhibit high-affinity anandamide accumulation in rat neurons and astrocytes in vitro, an indication that this accumulation resulted from carrier-mediated transport. Although AM404 did not activate cannabinoid receptors or inhibit anandamide hydrolysis, it enhanced receptor-mediated anandamide responses in vitro and in vivo. The data indicate that carrier-mediated transport may be essential for termination of the biological effects of anandamide, and may represent a potential drug target.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Beltramo, M -- Stella, N -- Calignano, A -- Lin, S Y -- Makriyannis, A -- Piomelli, D -- New York, N.Y. -- Science. 1997 Aug 22;277(5329):1094-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Neurosciences Institute, 10640 J. J. Hopkins Drive, San Diego, CA 92121, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9262477" target="_blank"〉PubMed〈/a〉
    Keywords: Analgesics/pharmacology ; Animals ; Arachidonic Acids/antagonists & inhibitors/*metabolism/pharmacology ; Astrocytes/drug effects/*metabolism ; Benzoxazines ; Biological Transport/drug effects ; Bromcresol Green/pharmacology ; Cannabinoids/antagonists & inhibitors/*metabolism/pharmacology ; Cells, Cultured ; Colforsin/pharmacology ; Cyclic AMP/metabolism ; Endocannabinoids ; Male ; Mice ; Morpholines/pharmacology ; Naphthalenes/pharmacology ; Neurons/drug effects/*metabolism ; Piperidines/pharmacology ; Polyunsaturated Alkamides ; Pyrazoles/pharmacology ; Rats ; Receptors, Cannabinoid ; Receptors, Drug/agonists/metabolism
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  • 46
    Publication Date: 1997-01-24
    Description: Heterotrimeric GTP-binding proteins (G proteins) participate in cellular signaling and regulate a variety of physiological processes. Disruption of the gene encoding the G protein subunit alpha13 (Galpha13) in mice impaired the ability of endothelial cells to develop into an organized vascular system, resulting in intrauterine death. In addition, Galpha13 (-/-) embryonic fibroblasts showed greatly impaired migratory responses to thrombin. These results demonstrate that Galpha13 participates in the regulation of cell movement in response to specific ligands, as well as in developmental angiogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Offermanns, S -- Mancino, V -- Revel, J P -- Simon, M I -- AG 12288/AG/NIA NIH HHS/ -- GM 34236/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1997 Jan 24;275(5299):533-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biology 147-75, California Institute of Technology, Pasadena, CA 91125, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8999798" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood ; Bradykinin/pharmacology ; Cell Differentiation ; *Cell Movement/drug effects ; Cells, Cultured ; Embryo, Mammalian/metabolism ; Embryonic and Fetal Development ; Endothelium, Vascular/*cytology/embryology ; Female ; Fibronectins/pharmacology ; GTP-Binding Proteins/genetics/*physiology ; Gene Expression ; Gene Targeting ; Heterozygote ; Homozygote ; Lysophospholipids/pharmacology ; Male ; Mice ; Mice, Inbred C57BL ; *Neovascularization, Physiologic ; Signal Transduction ; Thrombin/pharmacology
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  • 47
    Publication Date: 1997-06-20
    Description: The avian sarcoma virus 16 (ASV 16) is a retrovirus that induces hemangiosarcomas in chickens. Analysis of the ASV 16 genome revealed that it encodes an oncogene that is derived from the cellular gene for the catalytic subunit of phosphoinositide 3-kinase (PI 3-kinase). The gene is referred to as v-p3k, and like its cellular counterpart c-p3k, it is a potent transforming gene in cultured chicken embryo fibroblasts (CEFs). The products of the viral and cellular p3k genes have PI 3-kinase activity. CEFs transformed with either gene showed elevated levels of phosphatidylinositol 3,4-bisphosphate and phosphatidylinositol 3,4,5-trisphosphate and activation of Akt kinase.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chang, H W -- Aoki, M -- Fruman, D -- Auger, K R -- Bellacosa, A -- Tsichlis, P N -- Cantley, L C -- Roberts, T M -- Vogt, P K -- CA 42564/CA/NCI NIH HHS/ -- GM 41890/GM/NIGMS NIH HHS/ -- R01 GM041890/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1997 Jun 20;276(5320):1848-50.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Experimental Medicine, Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9188528" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Avian Sarcoma Viruses/*genetics/physiology ; *Cell Transformation, Neoplastic ; *Cell Transformation, Viral ; Cells, Cultured ; Chick Embryo ; Chickens ; Cloning, Molecular ; Enzyme Activation ; Genes, Viral ; Hemangiosarcoma/genetics/virology ; Molecular Sequence Data ; *Oncogenes ; Phosphatidylinositol 3-Kinases ; Phosphatidylinositol Phosphates/metabolism ; Phosphotransferases (Alcohol Group Acceptor)/*genetics/metabolism ; Platelet-Derived Growth Factor/pharmacology ; Protein-Serine-Threonine Kinases/metabolism ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins c-akt ; Signal Transduction ; Transfection
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  • 48
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-05-30
    Description: Human and bovine capillary endothelial cells were switched from growth to apoptosis by using micropatterned substrates that contained extracellular matrix-coated adhesive islands of decreasing size to progressively restrict cell extension. Cell spreading also was varied while maintaining the total cell-matrix contact area constant by changing the spacing between multiple focal adhesion-sized islands. Cell shape was found to govern whether individual cells grow or die, regardless of the type of matrix protein or antibody to integrin used to mediate adhesion. Local geometric control of cell growth and viability may therefore represent a fundamental mechanism for developmental regulation within the tissue microenvironment.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, C S -- Mrksich, M -- Huang, S -- Whitesides, G M -- Ingber, D E -- CA55833/CA/NCI NIH HHS/ -- GM30367/GM/NIGMS NIH HHS/ -- HL47699/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1997 May 30;276(5317):1425-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Surgery, Children's Hospital-Harvard Medical School, Enders 1007, 300 Longwood Avenue, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9162012" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD29/physiology ; Apoptosis/*physiology ; Cattle ; Cell Adhesion/physiology ; Cell Division/*physiology ; Cell Size/*physiology ; Cells, Cultured ; Endothelium, Vascular/*cytology/physiology ; Extracellular Matrix/physiology ; Fibronectins/physiology ; Humans ; Integrins/physiology ; Ligands ; Vitronectin/physiology
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  • 49
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-06-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gura, T -- New York, N.Y. -- Science. 1997 Jun 20;276(5320):1788-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9206838" target="_blank"〉PubMed〈/a〉
    Keywords: Bone Marrow/pathology/virology ; Cells, Cultured ; Dendritic Cells/*virology ; Herpesvirus 8, Human/metabolism/*pathogenicity ; Humans ; Interleukin-6/*biosynthesis/genetics ; Multiple Myeloma/pathology/*virology ; Paraproteinemias/pathology ; Polymerase Chain Reaction ; RNA, Messenger/analysis/genetics ; Sarcoma, Kaposi/virology ; Stromal Cells/metabolism/virology
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  • 50
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-09-12
    Description: In the developing nervous system, glial cells guide axons to their target areas, but it is unknown whether they help neurons to establish functional synaptic connections. The role of glial cells in synapse formation and function was studied in cultures of purified neurons from the rat central nervous system. In glia-free cultures, retinal ganglion cells formed synapses with normal ultrastructure but displayed little spontaneous synaptic activity and high failure rates in evoked synaptic transmission. In cocultures with neuroglia, the frequency and amplitude of spontaneous postsynaptic currents were potentiated by 70-fold and 5-fold, respectively, and fewer transmission failures occurred. Glial cells increased the action potential-independent quantal release by 12-fold without affecting neuronal survival. Thus, developing neurons in culture form inefficient synapses that require glial signals to become fully functional.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pfrieger, F W -- Barres, B A -- New York, N.Y. -- Science. 1997 Sep 12;277(5332):1684-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Stanford University, School of Medicine, Sherman Fairchild Science Building, 299 Campus Drive, Stanford, CA 94305-5125, USA. fpfrieg@mdc-berlin.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9287225" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Astrocytes/physiology ; Cell Survival ; Cells, Cultured ; Coculture Techniques ; Microglia/physiology ; Neuroglia/*physiology ; Oligodendroglia/physiology ; Rats ; Rats, Sprague-Dawley ; Retinal Ganglion Cells/cytology/*physiology/ultrastructure ; Synapses/*physiology/ultrastructure ; *Synaptic Transmission
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  • 51
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1978-03-10
    Description: Several strains of attenuated rabies virus lacking the capacity to kill adult mice acquired a high lethal potential for mice after one to five serial passages in murine or human neuroblastoma cells. The virulence acquired after passage in neuroblastoma cells is a stable genetic trait retained during subsequent passage of viruses in nonneuroblastoma cell systems.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Clark, H F -- New York, N.Y. -- Science. 1978 Mar 10;199(4333):1072-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/628831" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cells, Cultured ; Mice ; Neuroblastoma/*microbiology ; Neurons/microbiology ; Rabies Vaccines/toxicity ; Rabies virus/genetics/*pathogenicity ; Vaccines, Attenuated/toxicity ; Virus Replication
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  • 52
    Publication Date: 1978-04-07
    Description: The FBL-3 lymphoma cell line caused impaired antibody formation in vivo when injected into mice intraperitoneally, and in vitro when added to normal syngeneic spleen cells immunized in vitro with sheep erythrocytes. Immunosuppression occurred only when intact viable tumor cells were cocultivated with the normal spleen cells. As few as 10(5) FBL-3 cells, when added to 5 X 10(6) normal cells, impaired antibody formation. However, cell-free extracts of filtrates from even much larger numbers of tumor cells did not affect antibody formation, either in vitro or in vivo. Heating the tumor cells at 56 degrees C or irradiation with as little as 1000 rads completely abolished immunosuppressive activity, both in vitro and in vivo. Separation of viable tumor cells from target antibody-forming cells by cell-impermeable membranes prevented immunosuppression, showing that direct cell-to-cell contact is required for immunosuppression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cimprich, R S -- Specter, S -- Friedman, H -- New York, N.Y. -- Science. 1978 Apr 7;200(4337):60-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/635572" target="_blank"〉PubMed〈/a〉
    Keywords: *Antibody Formation ; Cell Communication ; Cells, Cultured ; *Immunosuppression ; Lymphoma/*immunology ; Neoplasms, Experimental/immunology
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  • 53
    Publication Date: 1978-05-05
    Description: The presence of diazepam in culutres of chicken embryo myoblasts arrests normal muscle cell differentiation. High concentrations of the drug reversibly prevent myoblasts from fusing to form multinucleated myotubes. Lower concentrations of diazepam allow cell fusion to occur, but inhibit the synthesis and accumulation of myosin heavy chain, implying that cell fusion does not obligate myoblasts to synthesize and accumulate large quantities of muscle specific protein. The effect of diazepam on muscle cells in culture is direct and specific.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bandman, E -- Walker, C R -- Strohman, R C -- New York, N.Y. -- Science. 1978 May 5;200(4341):559-61.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/565534" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation/drug effects ; Cell Fusion/drug effects ; Cells, Cultured ; Chick Embryo ; Diazepam/*pharmacology ; Dose-Response Relationship, Drug ; Macromolecular Substances ; Muscles/cytology/*drug effects ; Myosins/*biosynthesis
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  • 54
    Publication Date: 1978-03-31
    Description: Mouse spinal neurons grown in tissue culture were used to study the electrophysiological pharmacology of the opiate peptide leucine-enkephalin. Enkephalin depressed glutamate-evoked responses in a noncompetitive manner independent of any other effects on membrane properties. The results demonstrate a neuromodulatory action of opiate peptide functionally distinct from the conventional neurotransmitter class of operation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barker, J L -- Neale, J H -- Smith, T G Jr -- Macdonald, R L -- New York, N.Y. -- Science. 1978 Mar 31;199(4336):1451-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/204016" target="_blank"〉PubMed〈/a〉
    Keywords: Cells, Cultured ; Endorphins/*pharmacology ; Enkephalins/antagonists & inhibitors/*pharmacology ; Excitatory Amino Acid Antagonists ; Glutamates/*pharmacology ; Iontophoresis ; Naloxone/pharmacology ; Neurons/*drug effects ; Spinal Cord ; Synapses/*drug effects ; Synaptic Transmission/*drug effects
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  • 55
    Publication Date: 1978-12-15
    Description: We have examined the hypothesis that diploid cells grown in vitro age, and propose that only proliferative potential and not life-span is telescoped. We suggest that explanted or transplanted diploid cells are driven to divide by the process of subculturing in vitro or in vivo and, in response to this pressure, also complete their differentiation and become refractory to further mitotic stimulation. We conclude that differentiation rather than "mortality" distinguishes diploid from transformed cells and that the former may not age in vitro, but are lost because culture methods are selective for cycling cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bell, E -- Marek, L F -- Levinstone, D S -- Merrill, C -- Sher, S -- Young, I T -- Eden, M -- New York, N.Y. -- Science. 1978 Dec 15;202(4373):1158-63.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/725592" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Cycle ; *Cell Differentiation ; *Cell Division ; *Cell Survival ; Cells, Cultured ; Fibroblasts
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  • 56
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1978-04-21
    Description: Skeletal muscles lose acetylcholinesterase in culture as a result of denervation. A protein fraction isolated from peripheral nerves maintained the level of acetylcholinesterase in cultures of aneural embryonic muscle or denervated adult chicken muscle. These results indicate that trophic regulation of muscle acetylcholinesterase might be mediated by a protein produced by nerves.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Oh, T H -- Markelonis, G J -- New York, N.Y. -- Science. 1978 Apr 21;200(4339):337-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/635593" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcholinesterase/biosynthesis/*metabolism ; Cells, Cultured ; Enzyme Induction/drug effects ; Muscle Denervation ; Muscles/*enzymology ; Nerve Tissue Proteins/*pharmacology ; Peripheral Nerves/*physiology
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  • 57
    Publication Date: 1978-05-19
    Description: Barbiturate anesthetics, but not anticonvulsants, abolish the spontaneous activity of cultured spinal cord neurons; directly increase membrane conductance, an effect which is suppressed by the gamma-aminobutyric acid (GABA) antagonists picrotoxin and penicillin; and are more potent than anticonvulsants in augmenting GABA and depressing glutamate responses. Barbiturate anticonvulsants abolish picrotoxin-induced convulsive activity. These results indicate qualitative and quantitative differences between anesthetic and anticonvulsant barbiturates, which may explain their different clinical effects.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Macdonald, R L -- Barker, J L -- New York, N.Y. -- Science. 1978 May 19;200(4343):775-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/205953" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials/drug effects ; Cells, Cultured ; Electric Conductivity ; Glutamates/pharmacology ; Membrane Potentials/drug effects ; Neurons/*drug effects ; Pentobarbital/*pharmacology ; Phenobarbital/*pharmacology ; Picrotoxin/pharmacology ; Receptors, Neurotransmitter/drug effects ; gamma-Aminobutyric Acid/pharmacology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 58
    Publication Date: 1978-03-31
    Description: The opiate etorphine depresses monosynaptic excitatory postsynaptic potentials (EPSP's) elicited in spinal cord cells by activation of dorsal root ganglion cells in murine neuronal cell culture. The depression is reversed by naloxone. Statistical analysis of the synaptic responses reveals that the opiate reduces EPSP quantal content at this synapse without altering quantal size. Therefore, the opiate action is presynaptic and affects transmitter release rather than postsynaptic responsiveness.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Macdonald, R L -- Nelson, P G -- New York, N.Y. -- Science. 1978 Mar 31;199(4336):1449-51.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/204015" target="_blank"〉PubMed〈/a〉
    Keywords: Cells, Cultured ; Depression, Chemical ; Dose-Response Relationship, Drug ; Etorphine/*pharmacology ; Ganglia, Spinal/*drug effects ; Membrane Potentials/drug effects ; Morphinans/*pharmacology ; Naloxone/pharmacology ; Nerve Endings/drug effects ; Spinal Cord/drug effects ; Synapses/drug effects ; Synaptic Transmission/*drug effects
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  • 59
    Publication Date: 1978-06-09
    Description: Prior incubation of rat anterior pituitary cells with 17beta-estradiol led to an almost complete reversal of the inhibitory effect of two dopamine agonists, dihydroergocornine and RU 24213, on both basal prolactin release and thyrotropin releasing hormone-induced prolactin release. These experiments thus demonstrate a direct interference of dopamine action by a peripheral hormone. Prolactin secretion by pituitary cells in primary culture could possibly serve as an easily accessible model of a system under dopaminergic control.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Raymond, V -- Beaulieu, M -- Labrie, F -- Boissier, J -- New York, N.Y. -- Science. 1978 Jun 9;200(4346):1173-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/418505" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Dihydroergotoxine/antagonists & inhibitors ; *Dopamine Antagonists ; Estradiol/*pharmacology ; Female ; Phenethylamines/antagonists & inhibitors ; Pituitary Gland, Anterior/*drug effects/secretion ; Prolactin/*secretion ; Rats ; Thyrotropin-Releasing Hormone/pharmacology
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  • 60
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1978-03-31
    Description: Arguments are presented for the hypothesis that during an early stage of development the cells which become principal neurons of the autonomic nervous system possess information regarding the positions they will occupy within the body. A second stage of development, during which a decision is made regarding which neurotransmitter to employ, is delayed until each neuron has assumed its permanent position in the body and has sampled, presumably via its growing axons, the peripheral field which it will innervate. The development of cholinergic mechanisms takes precedence; adrenergic neurons may develop only when cholinergic sites have been occupied. An extended period during which the differentiation of transmitter mechanisms may be modulated permits the neuron to adequately sample the periphery prior to commitment to a specific transmitter economy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bunge, R -- Johnson, M -- Ross, C D -- New York, N.Y. -- Science. 1978 Mar 31;199(4336):1409-16.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24273" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenergic Fibers/cytology ; Animals ; Autonomic Nervous System/*embryology/growth & development ; Cell Differentiation ; Cells, Cultured ; Chimera ; Cholinergic Fibers/cytology ; Embryonic Induction ; Ganglia, Autonomic/cytology ; Heart/innervation ; Intestines/innervation ; Nerve Endings/ultrastructure ; Neurotransmitter Agents/metabolism ; Phylogeny ; Synaptic Vesicles/ultrastructure
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  • 61
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1983-11-11
    Description: When injected into mice, the synthetic double-stranded polynucleotide poly(inosinic) X poly(cytidylic) acid induces high natural killer (NK) cell activity within 4 to 12 hours. Induction of NK activity in mice immunized 2 or 3 days previously, or the addition of NK cells to cultures immunized in vitro 2 or 3 days previously, promotes early termination of the ongoing primary immunoglobulin M antibody response. A target for NK cells is a population of accessory cells that has interacted with antigen and is necessary for sustaining the antibody response. The inference is strong that NK cells induced normally by immunization also terminate the usual antibody response in vivo by elimination of antigen-exposed accessory cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Abruzzo, L V -- Rowley, D A -- 5-T32-CA-09267/CA/NCI NIH HHS/ -- R01-10242/PHS HHS/ -- New York, N.Y. -- Science. 1983 Nov 11;222(4624):581-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6685343" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antibody Formation ; Antibody-Producing Cells/immunology ; Cells, Cultured ; Homeostasis ; Killer Cells, Natural/*immunology/radiation effects ; Lymphocyte Cooperation ; Lymphocytes/*immunology ; Mice ; Poly I-C/immunology ; Spleen/immunology
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  • 62
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1983-04-22
    Description: The human parasite Trypanosoma brucei gambiense grew continuously at 37 degrees C in primary cultures of murine bone marrow. Cultured parasites remained virulent for mice. Rapid parasite growth coincided with the appearance of adherent adipocyte-epitheloid cell aggregates that also promoted hematopoiesis. This culture system should permit studies of host cell control of trypanosome proliferation, pathogenic effects of trypanosomes on blood cell development, and the relative trypanocidal and marrow suppressive activities of drugs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Balber, A E -- CA 14049/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1983 Apr 22;220(4595):421-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6836284" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Bone Marrow ; Cells, Cultured ; Culture Media ; Humans ; Mice ; Mice, Inbred BALB C ; Trypanosoma brucei brucei/growth & development ; Trypanosoma brucei gambiense/*growth & development ; Trypanosomiasis, African/parasitology
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  • 63
    Publication Date: 1983-03-18
    Description: Immunohistochemical techniques were used to confirm biochemical evidence that parenchymal cells isolated from adult rat liver and maintained in nonreplicating monolayer culture for 2 days synthesized type IV basement membrane collagen. On continued incubation in serum-free medium, the hepatocytes also synthesized the interstitial collagens, types I and III. Consistent with these results in culture, type IV collagen was localized to the hepatocytes in slices of pathologic rat liver. Hence collagen formation is a previously unrecognized function of the hepatocyte that may be important in the pathogenesis of liver fibrosis or cirrhosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Diegelmann, R F -- Guzelian, P S -- Gay, R -- Gay, S -- AM18976/AM/NIADDK NIH HHS/ -- DE02570/DE/NIDCR NIH HHS/ -- HL11310/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1983 Mar 18;219(4590):1343-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6828863" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Basement Membrane/metabolism ; Cells, Cultured ; Collagen/*biosynthesis/immunology ; Liver/cytology/*metabolism ; Molecular Weight ; Rats
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  • 64
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1983-12-09
    Description: Nonmalignant diploid human fibroblast cells (GM3498B) derived from a skin biopsy of a patient with Bloom's syndrome have been transformed by transfection with DNA from a tumorigenic mouse cell line (Ha-8) carrying a single copy of the Harvey murine sarcoma virus (Ha-MuSV) genome. The transformed cell lines have an extended life-span, form colonies in agarose, and proliferate in nude mice--characteristics of neoplastic transformation. Like the parental cells, they also exhibit a high spontaneous level of sister chromatid exchanges. Finally, the transformed cells contain most, if not all, of the Ha-MuSV genome as well as the human rasH sequence. These experiments show that these diploid nonmalignant human cells can be used as recipients in transfection experiments for studying the genetic control of neoplastic transformation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Doniger, J -- Di Paolo, J A -- Popescu, N C -- New York, N.Y. -- Science. 1983 Dec 9;222(4628):1144-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6648529" target="_blank"〉PubMed〈/a〉
    Keywords: Bloom Syndrome/*genetics ; Cell Adhesion ; *Cell Transformation, Neoplastic ; Cells, Cultured ; DNA, Neoplasm/*genetics ; Humans ; Oncogenes ; Transfection
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  • 65
    Publication Date: 1983-04-08
    Description: Cultured bronchial epithelial and fibroblastic cells from humans were used to study DNA damage and toxicity caused by formaldehyde. Formaldehyde caused the formation of cross-links between DNA and proteins, caused single-strand breaks in DNA, and inhibited the resealing of single-strand breaks produced by ionizing radiation. Formaldehyde also inhibited the unscheduled DNA synthesis that occurs after exposure of cells to ultraviolet irradiation or to benzo[a]pyrene diolexpoxide but at doses substantially higher than those required to inhibit the resealing of x-ray-induced single-strand breaks. Therefore, formaldehyde could exert its mutagenic and carcinogenic effects by both damaging DNA and inhibiting DNA repair.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grafstrom, R C -- Fornace, A J Jr -- Autrup, H -- Lechner, J F -- Harris, C C -- New York, N.Y. -- Science. 1983 Apr 8;220(4593):216-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6828890" target="_blank"〉PubMed〈/a〉
    Keywords: Bronchi/*cytology/drug effects ; Cells, Cultured ; *DNA/biosynthesis ; DNA Repair/*drug effects ; Epithelium/drug effects ; Fibroblasts/drug effects ; Formaldehyde/*pharmacology ; Humans
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  • 66
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1983-10-07
    Description: Suspensions of embryonic chick neuronal cells adhered to monolayers of glial cells, but few neurons bound to control monolayers of fibroblastic cells from meninges or skin. Neuronal cell-glial cell adhesion was inhibited by prior incubation of the neurons with Fab' fragments of antibodies to neuronal membranes. In contrast, antibodies to the neural cell adhesion molecule (N-CAM) did not inhibit the binding. These results suggest that a specific adhesive mechanism between neurons and glial cells exists and that it is mediated by CAM's that differ from those so far identified.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grumet, M -- Rutishauser, U -- Edelman, G M -- AI-11378/AI/NIAID NIH HHS/ -- HD-09635/HD/NICHD NIH HHS/ -- HD-16550/HD/NICHD NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1983 Oct 7;222(4619):60-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6194561" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal ; Antigen-Antibody Complex ; *Cell Adhesion ; Cell Membrane/immunology ; Cells, Cultured ; Chick Embryo ; Epitopes ; Immunoglobulin Fab Fragments ; Neuroglia/*physiology ; Neurons/immunology/*physiology
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  • 67
    Publication Date: 1983-09-23
    Description: Evidence is presented that a tumor-derived transforming growth factor is responsible for stimulating bone resorption and causing hypercalcemia in an animal tumor model of the hypercalcemia of malignancy. Both conditioned medium harvested from cultured tumor cells and tumor extracts of the transplantable rat Leydig cell tumor associated with hypercalcemia contained a macromolecular bone resorbing factor with the chemical characteristics of a tumor-derived transforming growth factor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ibbotson, K J -- D'Souza, S M -- Ng, K W -- Osborne, C K -- Niall, M -- Martin, T J -- Mundy, G R -- AM-28149/AM/NIADDK NIH HHS/ -- CA-29537/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1983 Sep 23;221(4617):1292-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6577602" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Bone Resorption ; Calcium ; Cells, Cultured ; Culture Media ; Growth Substances/*physiology ; Hypercalcemia/*etiology ; Leydig Cell Tumor/complications/*physiopathology ; Male ; Neoplasm Proteins/*physiology ; Neoplasms, Experimental/complications/physiopathology ; Peptides/*physiology ; Rats ; Transforming Growth Factors
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  • 68
    Publication Date: 1983-04-01
    Description: The tissue culture condition that is required for the type of chromosome breakage seen at most fragile sites, namely, the absence of folic acid and thymidine in the medium, greatly enhanced micronucleus formation in proliferating lymphocyte cultures from normal individuals. This suggests that chromosome breakage at fragile sites and the apparently spontaneous damage that gives rise to micronuclei are controlled by the same mechanism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jacky, P B -- Beek, B -- Sutherland, G R -- New York, N.Y. -- Science. 1983 Apr 1;220(4592):69-70.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6828880" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Cell Nucleus/drug effects/ultrastructure ; Cells, Cultured ; Child ; *Chromosome Aberrations ; Chromosome Fragile Sites ; *Chromosome Fragility ; Culture Media ; Dose-Response Relationship, Drug ; Female ; Folic Acid/pharmacology ; Humans ; Lymphocytes/ultrastructure ; Male ; Middle Aged ; Thymidine/pharmacology
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  • 69
    Publication Date: 1983-09-23
    Description: When cultured in a hypoxic environment similar to that found in the center of a wound, macrophages secreted active angiogenesis factor into the medium. Under conditions similar to those of well-oxygenated tissue, macrophages did not secrete active angiogenesis factor. Macrophages that secreted the factor at hypoxic conditions stopped secreting it when returned to room air. Thus the control of angiogenesis in wound healing may be the result of macrophages responding to tissue oxygen tension without the necessity of interacting with other cell types or biochemical signals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Knighton, D R -- Hunt, T K -- Scheuenstuhl, H -- Halliday, B J -- Werb, Z -- Banda, M J -- GM27345/GM/NIGMS NIH HHS/ -- HL26323/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1983 Sep 23;221(4617):1283-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6612342" target="_blank"〉PubMed〈/a〉
    Keywords: Angiogenesis Inducing Agents/*biosynthesis ; Animals ; Anoxia/physiopathology ; Cells, Cultured ; Cornea ; Growth Substances/*biosynthesis ; Macrophages/*physiology ; Models, Biological ; Oxygen/*physiology ; Rabbits ; *Wound Healing
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  • 70
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1983-02-04
    Description: The distribution of keratin intermediate filaments, previously considered static in organization and imperturbable by conventional drugs used to alter the structure and organization of the cytoskeleton, can be altered significantly by treatment with colchicine and cytochalasin D. The loss of microfilaments and microtubules converts the keratin cytoskeleton from a branching, even distribution to a series of starlike structures whose filaments are maintained by multiple membrane attachment sites. These findings provide a means for manipulating cytokeratin organization to investigate the role of keratins in cytoskeletal structure and function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Knapp, L W -- O'Guin, W M -- Sawyer, R H -- New York, N.Y. -- Science. 1983 Feb 4;219(4584):501-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6186022" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Colchicine/*pharmacology ; Cytochalasin D ; Cytochalasins/*pharmacology ; Cytoskeleton/*drug effects ; Epithelium ; *Keratins ; Mice ; Microtubules/drug effects
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  • 71
    Publication Date: 1983-11-11
    Description: Endothelial cells from human blood vessels were cultured in vitro, with doubling times of 17 to 21 hours for 42 to 79 population doublings. Cloned human endothelial cell strains were established for the first time and had similar proliferative capacities. This vigorous cell growth was achieved by addition of heparin to culture medium containing reduced concentrations of endothelial cell growth factor. The routine cloning and long-term culture of human endothelial cells will facilitate studying the human endothelium in vitro.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thornton, S C -- Mueller, S N -- Levine, E M -- AG-00839/AG/NIA NIH HHS/ -- T32-CA-09171/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1983 Nov 11;222(4624):623-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6635659" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Division/drug effects ; Cells, Cultured ; Clone Cells/enzymology ; Endothelium/*cytology ; Growth Substances/pharmacology ; Heparin/*pharmacology ; Humans ; Time Factors
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  • 72
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1983-05-27
    Description: Parasympathetic neurons, when cultured alone, lose sensitivity to acetylcholine, but if striated muscle is included in the culture, neuronal chemosensitivity is maintained. The membrane remnants of myotubes ruptured by osmotic shock also supported the responsiveness of the cultured neurons to transmitter, whereas muscle-conditioned medium or membrane remnants of nonmuscle embryonic skin cells did not support this responsiveness. The regulation of chemosensitivity by contact of neurons with the target cell membrane may be important in the formation and maintenance of neuronal circuitry.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tuttle, J B -- NS-10338/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1983 May 27;220(4600):977-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6133352" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcholine/physiology ; Animals ; Cell Membrane/physiology ; Cells, Cultured ; Chick Embryo ; Fibroblasts/physiology ; Muscles/*physiology ; Nervous System/growth & development ; Neurons/*physiology ; Neurotransmitter Agents/*physiology ; Synapses/physiology
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  • 73
    Publication Date: 1983-10-28
    Description: A protoplast fusion method was developed to stably transfect human cells with pSV2-derived plasmids at frequencies greater than 10(-3). This procedure made it possible to test the biological effect of a hepatitis B virus (HBV) gene independent of the viral structures required for infection. A pSV2gpt+ plasmid constructed to carry a subgenomic fragment of HBV that contained the core antigen gene (HBc gene) was transfected into human cells. A human epithelial cell line was stably transfected with the HBc+ gene by selecting recipient cells for expression of guanine phosphoribosyl transferase expression. With this gpt+/HBc+ cell line it was shown that growth in serum-free medium or treatment with 5'-azacytidine stimulates the production of the HBV core antigen. A hepatocellular carcinoma carrying the entire HBV genome was stimulated to produce the HBc gene product in response to the same factors that stimulated HBcAg production in the gpt+/HBc+ cell line constructed by transfection. The temporal relation between the cytopathologic response and HBc gene expression was similar for both cell types, indicating a primary role for HBc gene expression in the cytopathology of HBV-infected human liver.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yoakum, G H -- Korba, B E -- Lechner, J F -- Tokiwa, T -- Gazdar, A F -- Seeley, T -- Siegel, M -- Leeman, L -- Autrup, H -- Harris, C C -- New York, N.Y. -- Science. 1983 Oct 28;222(4622):385-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6194563" target="_blank"〉PubMed〈/a〉
    Keywords: Azacitidine/pharmacology ; Cell Fusion ; *Cell Transformation, Viral ; Cells, Cultured ; Cytopathogenic Effect, Viral ; Gene Expression Regulation/drug effects ; Genes, Viral ; Hepatitis B Core Antigens/*genetics ; Humans ; Transfection
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  • 74
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1983-01-21
    Description: Highly purified preparations of insulin receptor catalyzed the phosphorylation of the 95,000-dalton subunit of the insulin receptor. This subunit of the insulin receptor was also labeled with [alpha-32P]8-azidoadenosine 5'-triphosphate, a photoaffinity label for adenosine triphosphate binding sites. The identity of the 95,000-dalton band was confirmed in both cases by precipitation with a monoclonal antibody to the insulin receptor. These results suggest that the insulin receptor is itself a protein kinase.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roth, R A -- Cassell, D J -- New York, N.Y. -- Science. 1983 Jan 21;219(4582):299-301.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6849137" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Cell Line ; Cells, Cultured ; Lymphocytes ; Molecular Weight ; Phosphoproteins/physiology ; Protein Kinases/*physiology ; Receptor, Insulin/*physiology
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  • 75
    Publication Date: 1984-01-13
    Description: Cultures of human diploid fibroblasts contain cells that respond to exposure to the first component of complement (C1) by initiating DNA synthesis and growth. The plasma membranes of these cells have specific binding sites for the C1q subcomponent of C1. A fluorescence-activated cell sorter was used to isolate a subset of cells with a high affinity for C1q, and the growth and synthesis activities of these high-affinity cells were studied after numerous replications in vitro. These cells synthesize DNA and grow faster than the parent cultures and low-affinity cells, and they produce two to three times as much protein. About 40 percent of their total protein synthesis activity is directed to collagen production, unusually high proportions of collagen types III and V being produced. These properties and the high affinity of the cells for C1q are retained for at least six cell transfers. This phenotype has the properties expected of fibroblasts in healing wounds and inflamed tissues.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bordin, S -- Page, R C -- Narayanan, A S -- DE-02600/DE/NIDCR NIH HHS/ -- DE-03301/DE/NIDCR NIH HHS/ -- New York, N.Y. -- Science. 1984 Jan 13;223(4632):171-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6691142" target="_blank"〉PubMed〈/a〉
    Keywords: *Antigens, CD44 ; Carrier Proteins ; Cell Division ; Cell Separation ; Cells, Cultured ; Collagen/*biosynthesis/classification ; DNA/*biosynthesis ; Fibroblasts/analysis/cytology/*physiology ; Flow Cytometry ; Gingiva ; Humans ; *Membrane Glycoproteins ; Mitochondrial Proteins ; Phenotype ; *Protein Biosynthesis ; Receptors, Complement/*analysis
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  • 76
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1983-01-14
    Description: Two plasmids containing nonoverlapping deletions of the herpes simplex virus thymidine kinase gene were introduced into thymidine kinase-deficient mouse L cells by DNA-mediated gene transfer. Thymidine kinase-producing transformants were generated by a mixture of the two plasmids at a frequency significantly greater than that generated by either plasmid alone. Southern blot analyses demonstrated that functional thymidine kinase genes were generated by homologous recombination between the two deletion mutants.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Small, J -- Scangos, G -- New York, N.Y. -- Science. 1983 Jan 14;219(4581):174-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6294829" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cells, Cultured ; Chromosome Deletion ; *Genetic Engineering ; Mice ; Mutation ; *Plasmids ; *Recombination, Genetic ; Simplexvirus ; Thymidine Kinase/*genetics
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  • 77
    Publication Date: 1983-08-26
    Description: Macrophages isolated from tumor-bearing patients as well as cultured human monocytes express Fc receptors that cross-react strongly with murine immunoglobulins of the G2a but only slightly or not at all with the G1, G2b, or G3 subclasses. Such macrophages in the presence of murine immunoglobulin G2a monoclonal antibodies to tumors mediated the killing of tumor cells in vitro. These data suggest that monoclonal antibodies of the G2a subclass may be useful in the immunotherapy of human cancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Steplewski, Z -- Lubeck, M D -- Koprowski, H -- CA-10815/CA/NCI NIH HHS/ -- CA-21124/CA/NCI NIH HHS/ -- CA-25874/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1983 Aug 26;221(4613):865-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6879183" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/*immunology ; Cells, Cultured ; Cytotoxicity, Immunologic ; Humans ; *Immunity, Cellular ; Immunoglobulin G/immunology ; Immunotherapy ; Macrophages/*immunology ; Mice ; Monocytes/immunology ; Neoplasms, Experimental/immunology/therapy ; Receptors, Fc/*immunology ; Species Specificity
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  • 78
    Publication Date: 1984-09-14
    Description: Nuclear estrogen receptor from MCF-7 cells undergoes a time-dependent, hormone-inducible transformation to a form that is less extractable from nuclei and less exchangeable with ligand. This receptor-modifying, intranuclear event is independent of receptor loss (processing) and appears associated with hormone responsiveness (progesterone-receptor induction) in these cells. The magnitude of receptor loss, however, is variable and apparently not a prerequisite for hormone action to induce progesterone receptor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kasid, A -- Strobl, J S -- Huff, K -- Greene, G L -- Lippman, M E -- New York, N.Y. -- Science. 1984 Sep 14;225(4667):1162-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6474170" target="_blank"〉PubMed〈/a〉
    Keywords: Breast Neoplasms/*metabolism ; Cell Nucleus/metabolism ; Cells, Cultured ; Female ; Humans ; Receptors, Estradiol ; Receptors, Estrogen/*metabolism ; Receptors, Progesterone/biosynthesis ; Time Factors
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  • 79
    Publication Date: 1984-05-04
    Description: Peripheral blood lymphocytes from patients with the acquired immunodeficiency syndrome (AIDS) or with signs or symptoms that frequently precede AIDS (pre-AIDS) were grown in vitro with added T-cell growth factor and assayed for the expression and release of human T-lymphotropic retroviruses (HTLV). Retroviruses belonging to the HTLV family and collectively designated HTLV-III were isolated from a total of 48 subjects including 18 of 21 patients wih pre-AIDS, three of four clinically normal mothers of juveniles with AIDS, 26 of 72 adult and juvenile patients with AIDS, and from one of 22 normal male homosexual subjects. No HTLV-III was detected in or isolated from 115 normal heterosexual subjects. The number of HTLV-III isolates reported here underestimates the true prevalence of the virus since many specimens were received in unsatisfactory condition. Other data show that serum samples from a high proportion of AIDS patients contain antibodies to HTLV-III. That these new isolates are members of the HTLV family but differ from the previous isolates known as HTLV-I and HTLV-II is indicated by their morphological, biological, and immunological characteristics. These results and those reported elsewhere in this issue suggest that HTLV-III may be the primary cause of AIDS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gallo, R C -- Salahuddin, S Z -- Popovic, M -- Shearer, G M -- Kaplan, M -- Haynes, B F -- Palker, T J -- Redfield, R -- Oleske, J -- Safai, B -- New York, N.Y. -- Science. 1984 May 4;224(4648):500-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6200936" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/blood/*microbiology ; Adult ; Antigens, Viral/analysis ; Cells, Cultured ; Cytopathogenic Effect, Viral ; Deltaretrovirus/*isolation & purification/physiology/ultrastructure ; Female ; Homosexuality ; Humans ; Immune Sera/pharmacology ; Interferon Type I/immunology ; Male ; RNA-Directed DNA Polymerase/metabolism ; Risk ; T-Lymphocytes/microbiology
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  • 80
    Publication Date: 1984-11-02
    Description: Smooth muscle cells with 4C (double diploid) DNA content have been found in major arteries. The proportion of 4C cells increases with normal aging and with hypertension. These cells may represent a state of arrest at the G2 phase of the cell cycle or may be examples of true tetraploidy. Flow cytometric cell sorting was used to isolate 4C smooth muscle cells from the rat aorta, and the cells were cultured. Flow cytometry, Feulgen microdensitometry, and karyotyping of the progeny of the 4C cells established the presence of true tetraploid cells. These findings demonstrate the presence of reproductively viable tetraploid cells in a normal mammalian tissue.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Goldberg, I D -- Rosen, E M -- Shapiro, H M -- Zoller, L C -- Myrick, K -- Levenson, S E -- Christenson, L -- 5-P01-CA-12662/CA/NCI NIH HHS/ -- AG00599/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 1984 Nov 2;226(4674):559-61.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6494901" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aorta, Thoracic/analysis/*cytology ; Cells, Cultured ; DNA/analysis ; Flow Cytometry ; Humans ; Karyotyping ; Muscle, Smooth, Vascular/analysis/*cytology ; *Polyploidy ; Rats ; Rats, Inbred Strains
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  • 81
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1984-10-05
    Description: The human malarial parasite Plasmodium falciparum can produce surface protrusions (knobs) on infected erythrocytes; however, long-term culturing of the parasite results in the appearance of knobless cells. In this study it was found that a knob-producing clone lost the ability to produce knobs in vitro. Furthermore, a clone not producing knobs derived from the knob-producing clone regained the capacity to produce knobby cells in vitro. Certain parasite proteins were associated with the knobby phenotype but not with the knobless type. These results indicate that the parasites change in vitro in a spontaneous and reversible manner independent of immunological selection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gritzmacher, C A -- Reese, R T -- AI 18695/AI/NIAID NIH HHS/ -- DRR 00833/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1984 Oct 5;226(4670):65-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6382613" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Clone Cells ; Erythrocytes/*parasitology/ultrastructure ; Humans ; Mutation ; Phenotype ; Plasmodium falciparum/analysis/genetics/growth & development/*physiology ; Proteins/analysis
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  • 82
    Publication Date: 1984-11-02
    Description: The motile activity of growth cones of specific identified neurons is inhibited by the neurotransmitter serotonin, although other identified neurons are unaffected. As a consequence, affected neurons are unable to form electrical synapses, whereas other neurons whose growth is unaffected can still interconnect. This result demonstrates that neurotransmitters can play a prominent role in regulating neuronal architecture and connectivity in addition to their classical role in neurotransmission.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Haydon, P G -- McCobb, D P -- Kater, S B -- HD18577/HD/NICHD NIH HHS/ -- NS15350/NS/NINDS NIH HHS/ -- NS18819/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1984 Nov 2;226(4674):561-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6093252" target="_blank"〉PubMed〈/a〉
    Keywords: Animal Population Groups ; Animals ; Cells, Cultured ; Neurons/*drug effects/growth & development ; Serotonin/*pharmacology ; Snails ; Synapses/*drug effects ; Synaptic Transmission
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  • 83
    Publication Date: 1984-04-20
    Description: Ganglion cells were dissociated from postnatal rat retinas, identified by specific fluorescent labels, and maintained in culture on a variety of substrates. Regeneration of processes by retinal ganglion cells was enhanced when the cells were plated on glass coated with a monoclonal antibody against the Thy-1 determinant. Plain glass and glass coated with polylysine, collagen, fibronectin, or other monoclonal antibodies supported the growth of neural processes, but were less effective than antibody to Thy-1.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Leifer, D -- Lipton, S A -- Barnstable, C J -- Masland, R H -- EY01075/EY/NEI NIH HHS/ -- EY03735/EY/NEI NIH HHS/ -- EY04179/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 1984 Apr 20;224(4646):303-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6143400" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/*physiology ; Antigens, Surface/*immunology ; Antigens, Thy-1 ; Cell Adhesion ; Cells, Cultured ; Isoantibodies/*physiology ; *Nerve Regeneration ; Polylysine/pharmacology ; Rats ; Retina/cytology/*physiology ; Retinal Ganglion Cells/*physiology
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  • 84
    Publication Date: 1984-08-24
    Description: Infectious retroviruses have been detected in 22 of 45 randomly selected patients with acquired immune deficiency syndrome (AIDS) and in other individuals from San Francisco. The AIDS-associated retroviruses (ARV) studied in detail had a type D morphology, Mg2+-dependent reverse transcriptase, and cytopathic effects on lymphocytes. The viruses can be propagated in an established adult human T cell line, HUT-78. They cross-react with antiserum to the lymphadenopathy-associated retrovirus isolated from AIDS patients in France. Antibodies to ARV were found in all 86 AIDS patients and in a high percentage of 88 other homosexual men in San Francisco. This observation indicates the widespread presence of these lymphocytopathic retroviruses and their close association with AIDS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Levy, J A -- Hoffman, A D -- Kramer, S M -- Landis, J A -- Shimabukuro, J M -- Oshiro, L S -- CA-34980/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1984 Aug 24;225(4664):840-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6206563" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/immunology/*microbiology ; Antibodies, Viral/analysis ; Bone Marrow/microbiology ; California ; Cell Line ; Cells, Cultured ; Cross Reactions ; Cytopathogenic Effect, Viral ; Deltaretrovirus/immunology/*isolation & purification/physiology/ultrastructure ; *Homosexuality ; Humans ; Leukocytes/microbiology ; Lymphatic Diseases/immunology ; Male ; RNA-Directed DNA Polymerase/metabolism ; Syndrome ; T-Lymphocytes ; Virus Cultivation
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  • 85
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1984-02-24
    Description: Human fibroblasts have exhibited enhanced DNA synthesis when exposed to sinusoidally varying magnetic fields for a wide range of frequencies (15 hertz to 4 kilohertz) and amplitudes (2.3 X 10(-6) to 5.6 X 10(-4) tesla). This effect, which is at maximum during the middle of the S phase of the cell cycle, appears to be independent of the time derivative of the magnetic field, suggesting an underlying mechanism other than Faraday's law. The threshold is estimated to be between 0.5 X 10(-5) and 2.5 X 10(-5) tesla per second. These results bring into question the allegedly specific magnetic wave shapes now used in therapeutic devices for bone nonunion. The range of magnetic field amplitudes tested encompass the geomagnetic field, suggesting the possibility of mutagenic interactions directly arising from short-term changes in the earth's field.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liboff, A R -- Williams, T Jr -- Strong, D M -- Wistar, R Jr -- New York, N.Y. -- Science. 1984 Feb 24;223(4638):818-20.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6695183" target="_blank"〉PubMed〈/a〉
    Keywords: Cells, Cultured ; DNA/*biosynthesis ; Humans ; *Magnetics ; Mutation ; Periodicity
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  • 86
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1984-03-30
    Description: Astroblasts in culture proliferated when exposed to glia maturation factor for at least 2 hours and then to insulin, but not when exposed in the reverse order. The sequential relation suggests that glia maturation factor is a competence factor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lim, R -- Miller, J F -- CA-31796/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1984 Mar 30;223(4643):1419-20.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6367047" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Astrocytes/drug effects/physiology ; Cell Division/drug effects ; Cells, Cultured ; Drug Interactions ; Glia Maturation Factor ; Growth Substances/*pharmacology/physiology ; Insulin/*pharmacology/physiology ; Mice ; Mice, Inbred BALB C ; Nerve Tissue Proteins/*pharmacology/physiology ; Rats
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  • 87
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1984-12-14
    Description: The electrophysiological properties of glial cells were examined in primary culture in the presence of tetraethylammonium and Ba2+, a treatment that reduces K+ permeability of the membrane and enhances currents through voltage-dependent Ca2+ channels. Under these conditions, glial cells showed both spontaneous action potentials and action potentials evoked by the injections of current. These responses appear to represent entry of Ba2+ through Ca2+ channels because they were resistant to tetrodotoxin but were blocked by Mn2+ or Cd2+.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉MacVicar, B A -- New York, N.Y. -- Science. 1984 Dec 14;226(4680):1345-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6095454" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Barium/pharmacology ; Cadmium/pharmacology ; Calcium/*metabolism ; Cells, Cultured ; Evoked Potentials ; Ion Channels/*physiology ; Microelectrodes ; Neuroglia/*physiology ; Tetraethylammonium Compounds/pharmacology ; Tetrodotoxin/pharmacology
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  • 88
    Publication Date: 1984-11-30
    Description: Intraperitoneal administration of insulin to control rats and to rats with pituitary stalk transections or with lesions of the median eminence resulted in increased plasma adrenocorticotropin (ACTH) levels. The insulin-induced stimulation of ACTH release was blocked in both the control and lesioned animals by prior treatment with either the beta-adrenergic antagonist propranolol or the glucocorticoid analog dexamethasone. The direct application of insulin to primary cultures of the anterior pituitary did not evoke ACTH release or affect the maximal ability of corticotropin-releasing factor or epinephrine to stimulate ACTH secretion. The results suggest that insulin stimulates ACTH release by a mechanism in which catecholamines of peripheral origin act directly on the anterior pituitary.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mezey, E -- Reisine, T D -- Brownstein, M J -- Palkovits, M -- Axelrod, J -- New York, N.Y. -- Science. 1984 Nov 30;226(4678):1085-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6093262" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenocorticotropic Hormone/blood/*secretion ; Animals ; Cells, Cultured ; Corticotropin-Releasing Hormone/pharmacology ; Dexamethasone/pharmacology ; Epinephrine/pharmacology ; Insulin/*pharmacology ; Median Eminence/physiology ; Pituitary Gland/physiology ; Pituitary Gland, Anterior/drug effects/*secretion ; Propranolol/*pharmacology ; Rats ; Receptors, Adrenergic, beta/drug effects/*physiology
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  • 89
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1984-06-29
    Description: Normal human colon mucosal epithelial cells were cultured in vitro and treated with the oncogenic simian DNA virus (SV40) and the chemical carcinogen azoxymethane. Both SV40 and azoxymethane altered a number of phenotypic characteristics of the normal human colon cells, including their morphology, culture longevity, growth in soft agar, substrate adherence, and peanut agglutinin binding. The SV40 transformants synthesized intranuclear T antigen. These data indicate that normal human colon mucosal cells were transformed toward the malignant phenotype.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Moyer, M P -- Aust, J B -- RRO5654/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1984 Jun 29;224(4656):1445-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6328655" target="_blank"〉PubMed〈/a〉
    Keywords: Antigens, Viral, Tumor/metabolism ; Azoxymethane/pharmacology ; Cell Transformation, Neoplastic/*physiopathology ; Cells, Cultured ; Colon/*cytology/drug effects ; Colonic Neoplasms/physiopathology ; Fibroblasts/drug effects ; Humans ; Lectins/pharmacology ; Simian virus 40/metabolism
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  • 90
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1984-02-10
    Description: When human lymphocytes were cultured with [3H]thymidine, which acts as a source of low-level chronic radiation, and then exposed to 150 rad of x-rays at 5, 7, 9, or 11 hours before fixation, the yield of chromatid aberrations was less than the sum of the yields of aberrations induced by [3H]thymidine and x-rays separately. Often fewer aberrations were found after exposure to radiation from both sources than were found after exposure to x-rays alone. At the same fixation times, nonradioactive thymidine did not affect the yield of x-ray-induced aberrations. The same phenomenon occurred at earlier fixation times, after exposure to 30 or 40 rad of x-rays and [3H]thymidine. This response is analogous to the adaptive response to alkylating agents whereby prior treatment with small doses for a long period reduces the damage occurring from large doses of similar agents given for a short time.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Olivieri, G -- Bodycote, J -- Wolff, S -- New York, N.Y. -- Science. 1984 Feb 10;223(4636):594-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6695170" target="_blank"〉PubMed〈/a〉
    Keywords: Cells, Cultured ; *Chromosome Aberrations ; Chromosome Deletion ; Humans ; Lymphocytes/drug effects/physiology/*radiation effects ; Metaphase/drug effects/radiation effects ; Thymidine/*toxicity ; Tritium
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  • 91
    Publication Date: 1984-02-17
    Description: Cell-free conditioned media from human T cells transformed by human T-cell leukemia-lymphoma virus (HTLV-I) were tested for the production of soluble biologically active factors, including several known lymphokines. The cell lines used were established from patients with T-cell leukemia-lymphoma and from human umbilical cord blood and bone marrow leukocytes transformed by HTLV-I in vitro. All of the cell lines liberated constitutively one or more of the 12 biological activities assayed. These included macrophage migration inhibitory factor (MIF), leukocyte migration inhibitory factor (LIF), leukocyte migration enhancing factor (MEF), macrophage activating factor (MAF), differentiation inducing factor (DIF), colony stimulating factor (CSF), eosinophil growth and maturation activity (eos. GMA), fibroblast activating factor (FAF), gamma-interferon and, in rare instances, T-cell growth factor (TCGF). Some cell lines produced interleukin 3 (IL-3), platelet-derived growth factor (PDGF), or B-cell growth factors (BCGF). Such cells should prove useful for the production of lymphokines and as sources of specific messenger RNA's for their genetic cloning.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Salahuddin, S Z -- Markham, P D -- Lindner, S G -- Gootenberg, J -- Popovic, M -- Hemmi, H -- Sarin, P S -- Gallo, R C -- New York, N.Y. -- Science. 1984 Feb 17;223(4637):703-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6320367" target="_blank"〉PubMed〈/a〉
    Keywords: Antibodies, Monoclonal ; Antigens, Neoplasm/analysis ; Bone Marrow ; Cell Line ; *Cell Transformation, Neoplastic ; Cells, Cultured ; Deltaretrovirus/*genetics ; Female ; Humans ; Leukemia/*microbiology ; Lymphokines/*biosynthesis ; Lymphoma/*microbiology ; Phenotype ; Pregnancy ; T-Lymphocytes/*immunology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 92
    Publication Date: 1983-08-12
    Description: Since it has been postulated that liver hepatocytes may become infected by hepatitis B virus (HBV) in vivo through direct contact with infected macrophages, the possibility that a circulating cell of hematopoietic origin might be susceptible to infection with HBV was investigated. Cells positive for HBV surface antigen were identified in aspirates of bone marrow cells from people infected with HBV. These cells were used to prepare a lymphoblastoid suspension culture that contains HBV-infected cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Romet-Lemonne, J L -- McLane, M F -- Elfassi, E -- Haseltine, W A -- Azocar, J -- Essex, M -- New York, N.Y. -- Science. 1983 Aug 12;221(4611):667-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6867736" target="_blank"〉PubMed〈/a〉
    Keywords: Cells, Cultured ; Hepatitis B/*microbiology/pathology ; Hepatitis B Surface Antigens/immunology ; Hepatitis B virus/growth & development ; Humans ; Liver/pathology ; Lymphocytes/*microbiology/pathology ; Male ; Middle Aged
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 93
    Publication Date: 1984-11-16
    Description: The benzodiazepine-gamma-aminobutyric acid receptor complex was used to study functional receptor synthesis and degradation in primary cultures of neurons. Fifty percent of the receptors turned over with an unusually rapid half-life (4 hours); this was followed by a second, slower phase (32 hours). These results provide the basis for elucidating the mechanism by which neurons derived from the central nervous system control neurotransmitter receptor number, an important problem in cellular neurobiology. The findings may be of significance in the study of neurological and psychiatric disorders.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Borden, L A -- Czajkowski, C -- Chan, C Y -- Farb, D H -- New York, N.Y. -- Science. 1984 Nov 16;226(4676):857-60.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6093257" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Chick Embryo ; Flunitrazepam/metabolism ; Half-Life ; Kinetics ; Neurons/*metabolism ; Receptors, GABA-A/biosynthesis/*metabolism ; Spinal Cord/cytology ; gamma-Aminobutyric Acid/physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 94
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1983-04-29
    Description: Cultured hippocampal neurons, when exposed to cyanide or an anoxic atmosphere in the early stages of differentiation, were not visibly affected. However, neurons in the mature cultures died when exposed to cyanide or anoxia. Cell death could be prevented by treatment with magnesium, which eliminates synaptic activity. These observations suggest that damage in hypoxic neurons is mediated by synaptic activity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rothman, S M -- 5 K07 N500568-02/PHS HHS/ -- New York, N.Y. -- Science. 1983 Apr 29;220(4596):536-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6836300" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials/drug effects ; Animals ; Anoxia/*metabolism/physiopathology ; Cells, Cultured ; Hippocampus/cytology ; Magnesium/pharmacology ; Magnesium Chloride ; Membrane Potentials/drug effects ; Neurons/metabolism/*physiology ; Rats ; Sodium Cyanide/pharmacology ; Synapses/drug effects/*physiology
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  • 95
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1983-03-11
    Description: Primary cultures of epithelial cells were grown from the tonsils and adenoids of patients with diseases not related to Epstein-Barr virus. The cells could not be infected by Epstein-Barr virus. Fluorescein-labeled Epstein-Barr virus and a cytofluorograph were then used to show that the epithelial cells do not have detectable receptors for the virus. However, implantation with Epstein-Barr virus receptors gave the cells the ability to bind the labeled virus. One to 5 percent of receptor-implanted cells exposed to the transforming B95-8 substrain of the virus expressed Epstein-Barr nuclear antigen. The early and viral capsid Epstein-Barr virus-determined antigens were not detected in the virus-infected cultures. The results show that normal human epithelial cells from the nasopharynx become susceptible to infection by Epstein-Barr virus when the membrane barrier resulting from the lack of viral receptors is overcome by receptor implantation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shapiro, I M -- Volsky, D J -- 1R01 CA33386-01/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1983 Mar 11;219(4589):1225-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6298935" target="_blank"〉PubMed〈/a〉
    Keywords: Cells, Cultured ; Epithelium/*microbiology ; Herpesviridae Infections/*microbiology ; Herpesvirus 4, Human/growth & development ; Humans ; Receptors, Virus/metabolism ; Virus Replication
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  • 96
    Publication Date: 1984-11-30
    Description: Complementary DNA clones of genes induced by platelet-derived growth factor (PDGF) in BALB/c-3T3 cells were isolated; one such clone contains a domain having nucleotide sequence homology with the third exon of c-fos. This nucleotide sequence homology is reflected in the predicted amino acid sequences of the gene products. Under low stringency conditions, the mouse v-fos gene cross-hybridizes with the PDGF-inducible complementary DNA clone. However, the messenger RNA transcripts of mouse c-fos and the new fos-related gene can be distinguished by gel electrophoresis and by S1 nuclease analysis. Expression of the authentic c-fos gene is induced by PDGF and superinduced by the combination of PDGF and cycloheximide.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cochran, B H -- Zullo, J -- Verma, I M -- Stiles, C D -- New York, N.Y. -- Science. 1984 Nov 30;226(4678):1080-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6093261" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cells, Cultured ; *Cloning, Molecular ; DNA/analysis ; DNA Restriction Enzymes ; DNA Transposable Elements ; Endonucleases ; Genes/drug effects ; Mice ; Mice, Inbred BALB C ; Nucleic Acid Hybridization ; Oncogenes/*drug effects ; Platelet-Derived Growth Factor/*pharmacology ; Single-Strand Specific DNA and RNA Endonucleases ; Transcription, Genetic/drug effects
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 97
    Publication Date: 1983-09-23
    Description: Changes occur in the synthesis and axonal transport of neuronal proteins in dorsal-root ganglia axons as a result of contact with cells from the spinal cord during synapse formation. Dorsal-root ganglia cells were cultured in a compartmental cel culture system that allows separate access to neuronal cell bodies and their axons. When cells from the ventral spinal cord were cultured with the dorsal-root ganglia axons, synapses were established within a few days. Metabolic labeling and two-dimensional electrophoresis revealed that four of more than 300 axonal proteins had changed in their expression by the time synapses were established. The highly selective nature of these changes suggests that the proteins involved may be important in the processes of axon growth and synapse formation and their regulation by the regional environment.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sonderegger, P -- Fishman, M C -- Bokoum, M -- Bauer, H C -- Nelson, P G -- New York, N.Y. -- Science. 1983 Sep 23;221(4617):1294-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6612344" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/*metabolism ; Cells, Cultured ; Chick Embryo ; Isoelectric Point ; Molecular Weight ; Nerve Tissue Proteins/*biosynthesis ; Synapses/*metabolism
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  • 98
    Publication Date: 1983-02-04
    Description: Two toxins, latrunculins A and B, which contain a new class of 16- and 14-membered marine macrolides attached to the rare 2-thiazolidinone moiety, were purified recently from the Red Sea sponge Latrunculia magnifica. The effects of these toxins on cultured mouse neuroblastoma and fibroblast cells have been evaluated. In both types of cells, submicromolar toxin concentrations rapidly induce striking changes in cell morphology that are reversible upon removal of the toxin. Immunofluorescence studies with antibodies specific for cytoskeletal proteins reveal that the toxins cause major alterations in the organization of microfilaments without obvious effects on the organization of the microtubular system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Spector, I -- Shochet, N R -- Kashman, Y -- Groweiss, A -- New York, N.Y. -- Science. 1983 Feb 4;219(4584):493-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6681676" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/metabolism ; Animals ; *Bicyclo Compounds, Heterocyclic ; Cells, Cultured ; Cytoskeleton/*drug effects ; Fibroblasts/ultrastructure ; Marine Toxins/*pharmacology ; Microscopy, Fluorescence ; Microtubules/drug effects ; Neuroblastoma/ultrastructure ; Thiazoles/*pharmacology ; Thiazolidines
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 99
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1984-05-11
    Description: Protozoan parasites of the genus Cryptosporidium cause a short-term, flu-like, gastrointestinal illness in immunocompetent persons and severe, persistent, life-threatening diarrhea in immunodeficient individuals. No effective therapy is available for the treatment of cryptosporidiosis in the immunodeficient host. Complete development (from sporozoite to sporulated oocyst) of a human isolate of Cryptosporidium was achieved in cultured human fetal lung cells and primary chicken kidney and porcine kidney cells. The growth of this newly recognized zoonotic agent in cell culture now provides a means of studying its behavior, development, and metabolism, and a mechanism for evaluation of potentially useful therapeutic agents.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Current, W L -- Haynes, T B -- New York, N.Y. -- Science. 1984 May 11;224(4649):603-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6710159" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/complications ; Animals ; Cattle ; Cells, Cultured ; Coccidia/*growth & development ; Coccidiosis/etiology/parasitology ; Culture Media ; Humans ; Mice
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 100
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1984-12-07
    Description: An assay was developed to detect recombination events taking place in an in vitro reaction. Extracts of cultured mouse preB lymphocytes were found to catalyze homologous recombination between substrate DNA molecules but not site-specific recombination between cloned mouse immunoglobulin D and J genes. Addition of deoxyribonucleoside triphosphates increased the frequency of homologous recombination. This recombination activity was not observed in two differentiated lymphocyte cell lines.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Darby, V -- Blattner, F -- AI19325/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1984 Dec 7;226(4679):1213-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6334360" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes ; Cells, Cultured ; Crossing Over, Genetic ; DNA, Viral ; Immunoglobulin Variable Region/genetics ; Mice ; Mutation ; Nucleoproteins/genetics ; *Recombination, Genetic
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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