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  • Mice  (145)
  • United States  (113)
  • American Association for the Advancement of Science (AAAS)  (257)
  • American Meteorological Society
  • 1995-1999  (257)
  • 1997  (257)
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Publisher
  • American Association for the Advancement of Science (AAAS)  (257)
  • American Meteorological Society
  • Springer  (6)
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  • 1995-1999  (257)
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  • 1
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-06-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Taubes, G -- New York, N.Y. -- Science. 1997 Jun 27;276(5321):1993.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9221506" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; DNA, Recombinant ; Diagnostic Imaging/*methods ; *Gene Expression Regulation ; Genetic Therapy ; HIV/physiology ; HIV Infections/virology ; Luciferases/*genetics ; Luminescence ; Mice ; Mice, Transgenic ; Salmonella Infections, Animal/drug therapy/microbiology ; Virus Replication
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
    Publication Date: 1997-03-07
    Description: The DED1 gene, which encodes a putative RNA helicase, has been implicated in nuclear pre-messenger RNA splicing in the yeast Saccharomyces cerevisiae. It is shown here by genetic and biochemical analysis that translation, rather than splicing, is severely impaired in two newly isolated ded1 conditional mutants. Preliminary evidence suggests that the protein Ded1p may be required for the initiation step of translation, as is the distinct DEAD-box protein, eukaryotic initiation factor 4A (eIF4A). The DED1 gene could be functionally replaced by a mouse homolog, PL10, which suggests that the function of Ded1p in translation is evolutionarily conserved.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chuang, R Y -- Weaver, P L -- Liu, Z -- Chang, T H -- GM48752/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1997 Mar 7;275(5305):1468-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular, Cellular, and Developmental Biology Program, Ohio State University, Columbus, OH 43210, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9045610" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cytoplasm/metabolism ; DEAD-box RNA Helicases ; Eukaryotic Initiation Factor-4A ; Genes, Fungal ; Mice ; Mutation ; Peptide Initiation Factors/genetics/metabolism ; Phenotype ; *Protein Biosynthesis ; RNA Helicases ; RNA Nucleotidyltransferases/genetics/*metabolism ; RNA Splicing ; RNA, Fungal/*genetics ; RNA, Messenger/*genetics ; Recombinant Fusion Proteins/metabolism ; Saccharomyces cerevisiae/enzymology/*genetics ; *Saccharomyces cerevisiae Proteins
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  • 3
    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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  • 4
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-10-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, J -- New York, N.Y. -- Science. 1997 Oct 10;278(5336):218.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9340767" target="_blank"〉PubMed〈/a〉
    Keywords: *Acquired Immunodeficiency Syndrome ; History, 20th Century ; National Institutes of Health (U.S.)/*organization & administration ; Research ; United States
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  • 5
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-04-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Taubes, G -- New York, N.Y. -- Science. 1997 Apr 4;276(5309):27-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9122702" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Age Factors ; Breast Neoplasms/*prevention & control/radiography ; Consensus Development Conferences, NIH as Topic ; Female ; Humans ; *Mammography ; *Mass Screening ; Middle Aged ; *National Institutes of Health (U.S.) ; Randomized Controlled Trials as Topic ; Risk Factors ; United States
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-01-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lorimer, B G -- New York, N.Y. -- Science. 1997 Jan 31;275(5300):601-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9019811" target="_blank"〉PubMed〈/a〉
    Keywords: Academies and Institutes ; Base Sequence ; DNA, Complementary/*genetics ; Databases, Factual ; *Genome, Human ; Humans ; Intellectual Property ; Publishing ; Research Support as Topic ; Sequence Analysis, DNA ; United States
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  • 7
    Publication Date: 1997-09-26
    Description: To determine which proteinases are responsible for the lung destruction characteristic of pulmonary emphysema, macrophage elastase-deficient (MME-/-) mice were subjected to cigarette smoke. In contrast to wild-type mice, MME-/- mice did not have increased numbers of macrophages in their lungs and did not develop emphysema in response to long-term exposure to cigarette smoke. Smoke-exposed MME-/- mice that received monthly intratracheal instillations of monocyte chemoattractant protein-1 showed accumulation of alveolar macrophages but did not develop air space enlargement. Thus, macrophage elastase is probably sufficient for the development of emphysema that results from chronic inhalation of cigarette smoke.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hautamaki, R D -- Kobayashi, D K -- Senior, R M -- Shapiro, S D -- New York, N.Y. -- Science. 1997 Sep 26;277(5334):2002-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Internal Medicine, Washington University School of Medicine at Barnes-Jewish Hospital, St. Louis, MO 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9302297" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Count ; Chemokine CCL2/pharmacology ; Gene Targeting ; Lung/pathology ; Macrophages, Alveolar/*enzymology/physiology ; Matrix Metalloproteinase 12 ; Metalloendopeptidases/genetics/*metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Inbred Strains ; Neutrophils ; Plants, Toxic ; Pulmonary Alveoli/pathology ; Pulmonary Emphysema/enzymology/*etiology/pathology ; Smoke/adverse effects ; Smoking/*adverse effects ; Tobacco
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  • 8
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-02-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, J -- New York, N.Y. -- Science. 1997 Feb 7;275(5301):773.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9036538" target="_blank"〉PubMed〈/a〉
    Keywords: Biotechnology/history/*organization & administration ; Genetics, Medical/history/*organization & administration ; Genome, Human ; History, 20th Century ; Humans ; Industry/history/organization & administration ; Molecular Biology/history/*organization & administration ; United States
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  • 9
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-05-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rall, J E -- New York, N.Y. -- Science. 1997 May 30;276(5317):1319-20.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9190671" target="_blank"〉PubMed〈/a〉
    Keywords: *Drug Evaluation ; National Institutes of Health (U.S.) ; Professional Competence ; Research Personnel ; United States ; *United States Food and Drug Administration
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  • 10
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-09-26
    Description: A selection strategy was devised to identify bacterial genes preferentially expressed when a bacterium associates with its host cell. Fourteen Salmonella typhimurium genes, which were under the control of at least four independent regulatory circuits, were identified to be selectively induced in host macrophages. Four genes encode virulence factors, including a component of a type III secretory apparatus. This selection methodology should be generally applicable to the identification of genes from pathogenic organisms that are induced upon association with host cells or tissues.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Valdivia, R H -- Falkow, S -- AI26195/AI/NIAID NIH HHS/ -- DK38707/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1997 Sep 26;277(5334):2007-11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA. valdivia@cmgm.stanford.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9302299" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacterial Proteins/genetics ; Cell Line ; Cloning, Molecular ; Female ; Flow Cytometry ; Fluorescence ; *Gene Expression Regulation, Bacterial ; Green Fluorescent Proteins ; HeLa Cells ; Humans ; Luminescent Proteins/genetics ; Macrophages/*microbiology ; Mice ; Mice, Inbred BALB C ; Microscopy, Fluorescence ; Molecular Sequence Data ; Open Reading Frames ; Promoter Regions, Genetic ; Recombinant Fusion Proteins ; Salmonella Infections, Animal/microbiology ; Salmonella typhimurium/*genetics/isolation & purification/*pathogenicity ; Spleen/microbiology ; Transcription Factors/genetics ; Virulence/genetics
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  • 11
    Publication Date: 1997-01-17
    Description: Familial combined hyperlipidemia (FCHL) is a common inherited lipid disorder, affecting 1 to 2 percent of the population in Westernized societies. Individuals with FCHL have large quantities of very low density lipoprotein (VLDL) and low density lipoprotein (LDL) and develop premature coronary heart disease. A mouse model displaying some of the features of FCHL was created by crossing mice carrying the human apolipoprotein C-III (APOC3) transgene with mice deficient in the LDL receptor. A synergistic interaction between the apolipoprotein C-III and the LDL receptor defects produced large quantities of VLDL and LDL and enhanced the development of atherosclerosis. This mouse model may provide clues to the origin of human FCHL.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Masucci-Magoulas, L -- Goldberg, I J -- Bisgaier, C L -- Serajuddin, H -- Francone, O L -- Breslow, J L -- Tall, A R -- HL 21006/HL/NHLBI NIH HHS/ -- HL 54591/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1997 Jan 17;275(5298):391-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Columbia University, 630 West 168 Street, New York, NY 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8994037" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apolipoprotein C-III ; Apolipoproteins B/blood ; Apolipoproteins C/*genetics ; Apolipoproteins E/blood ; Arteriosclerosis/etiology ; Carrier Proteins/genetics ; Cholesterol/blood ; Cholesterol Ester Transfer Proteins ; Cholesterol, HDL/blood ; Cholesterol, LDL/blood ; Cholesterol, VLDL/blood ; Diet ; *Disease Models, Animal ; Disease Susceptibility ; Female ; *Glycoproteins ; Humans ; *Hyperlipidemia, Familial Combined/blood/genetics ; Hyperlipoproteinemia Type IV/genetics ; Lipoproteins/blood ; Lipoproteins, VLDL/blood ; Male ; Mice ; Mice, Inbred C57BL ; *Mice, Transgenic ; Receptors, LDL/*genetics/metabolism ; Transgenes ; Triglycerides/blood
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  • 12
    Publication Date: 1997-02-28
    Description: The small guanosine triphosphatase (GTPase) Rho is implicated in the formation of stress fibers and focal adhesions in fibroblasts stimulated by extracellular signals such as lysophosphatidic acid (LPA). Rho-kinase is activated by Rho and may mediate some biological effects of Rho. Microinjection of the catalytic domain of Rho-kinase into serum-starved Swiss 3T3 cells induced the formation of stress fibers and focal adhesions, whereas microinjection of the inactive catalytic domain, the Rho-binding domain, or the pleckstrin-homology domain inhibited the LPA-induced formation of stress fibers and focal adhesions. Thus, Rho-kinase appears to mediate signals from Rho and to induce the formation of stress fibers and focal adhesions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Amano, M -- Chihara, K -- Kimura, K -- Fukata, Y -- Nakamura, N -- Matsuura, Y -- Kaibuchi, K -- New York, N.Y. -- Science. 1997 Feb 28;275(5304):1308-11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Signal Transduction, Nara Institute of Science and Technology, Ikoma 630-01, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9036856" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Actins/*metabolism ; Adenosine Triphosphate/metabolism ; Animals ; Binding Sites ; *Cell Adhesion ; Cell Line ; DNA, Complementary/genetics ; Enzyme Inhibitors/pharmacology ; GTP Phosphohydrolases/metabolism ; Intracellular Signaling Peptides and Proteins ; Lysophospholipids/pharmacology ; Mice ; Mutation ; Protein-Serine-Threonine Kinases/antagonists & inhibitors/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Staurosporine/pharmacology ; rho-Associated Kinases
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  • 13
    Publication Date: 1997-02-14
    Description: For the past decade the immune system has been exploited as a rich source of de novo catalysts. Catalytic antibodies have been shown to have chemoselectivity, enantioselectivity, large rate accelerations, and even an ability to reroute chemical reactions. In many instances catalysts have been made for reactions for which there are no known natural or man-made enzymes. Yet, the full power of this combinatorial system can only be exploited if there was a system that allows for the direct selection of a particular function. A method that allows for the direct chemical selection for catalysis from antibody libraries was so devised, whereby the positive aspects of hybridoma technology were preserved and re-formatted in the filamentous phage system to allow direct selection of catalysis. This methodology is based on a purely chemical selection process, making it more general than biologically based selection systems because it is not limited to reaction products that perturb cellular machinery.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Janda, K D -- Lo, L C -- Lo, C H -- Sim, M M -- Wang, R -- Wong, C H -- Lerner, R A -- GM-43858/GM/NIGMS NIH HHS/ -- GM-44154/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1997 Feb 14;275(5302):945-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Scripps Research Institute, Department of Chemistry, 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/9020070" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antibodies, Catalytic/genetics/metabolism ; Catalysis ; Cloning, Molecular ; Coliphages ; Dithiothreitol ; Enzyme-Linked Immunosorbent Assay ; Escherichia coli/genetics/metabolism ; Galactosides/metabolism ; Haptens ; Hybridomas ; Immunoglobulin Fab Fragments/genetics/metabolism ; Indoles/metabolism ; Isopropyl Thiogalactoside/metabolism ; Mice ; Nitrophenylgalactosides/metabolism ; *Peptide Library ; Polymerase Chain Reaction ; Serum Albumin, Bovine ; Transformation, Bacterial ; beta-Galactosidase/metabolism
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  • 14
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-03-28
    Description: Neuroendocrine hormones of the hypothalamus-pituitary-thyroid axis can exert positive or negative immunoregulatory effects on intestinal lymphocytes. Small intestine epithelial cells were found to express receptors for thyrotropin-releasing hormone (TRH) and to be a primary source of intestine-derived thyroid-stimulating hormone (TSH). The gene for the TSH receptor (TSH-R) was expressed in intestinal T cells but not in epithelial cells, which suggested a hormone-mediated link between lymphoid and nonhematopoietic components of the intestine. Because mice with congenitally mutant TSH-R (hyt/hyt mice) have a selectively impaired intestinal T cell repertoire, TSH may be a key immunoregulatory mediator in the intestine.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, J -- Whetsell, M -- Klein, J R -- DK35566/DK/NIDDK NIH HHS/ -- R01 DK035566/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1997 Mar 28;275(5308):1937-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Science and Mervin Bovaird Center for Studies in Molecular Biology and Biotechnology, University of Tulsa, Tulsa, OK 74104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9072972" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Homeostasis ; *Immunity, Mucosal ; Intestinal Mucosa/cytology/*immunology/metabolism ; Intestine, Small/cytology/immunology/metabolism ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Nude ; Point Mutation ; Receptors, Thyrotropin/genetics/metabolism ; Receptors, Thyrotropin-Releasing Hormone/genetics/metabolism ; T-Lymphocyte Subsets/immunology/metabolism ; T-Lymphocytes/*immunology/metabolism ; Thyrotropin/genetics/*metabolism ; Thyrotropin-Releasing Hormone/*metabolism/pharmacology
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  • 15
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-12-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Husten, L -- New York, N.Y. -- Science. 1997 Nov 14;278(5341):1228.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9411750" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenal Glands/metabolism ; Animals ; Antigens, CD36/genetics/*metabolism ; Arteriosclerosis/etiology/metabolism ; *Carrier Proteins ; Cholesterol/blood/metabolism ; Cloning, Molecular ; Humans ; Lipoproteins, HDL/blood/*metabolism ; Liver/metabolism ; *Membrane Proteins ; Mice ; Mice, Knockout ; *RNA-Binding Proteins ; *Receptors, Immunologic ; Receptors, Lipoprotein/genetics/*metabolism ; Receptors, Scavenger ; Scavenger Receptors, Class B
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  • 16
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-03-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marshall, E -- New York, N.Y. -- Science. 1997 Mar 21;275(5307):1733.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9122675" target="_blank"〉PubMed〈/a〉
    Keywords: Advisory Committees ; Animal Husbandry ; Animals ; Animals, Genetically Modified ; *Bioethics ; Cloning, Molecular ; Federal Government ; *Genetic Engineering ; Genetic Research ; Government Regulation ; Humans ; Public Policy ; Risk Assessment ; United States
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  • 17
    Publication Date: 1997-12-31
    Description: A lymphocyte subpopulation, the Valpha14 natural killer T (NKT) cells, expresses both NK1.1 and a single invariant T cell receptor encoded by the Valpha14 and Jalpha281 gene segments. Mice with a deletion of the Jalpha281 gene segment were found to exclusively lack this subpopulation. The Valpha14 NKT cell-deficient mice could no longer mediate the interleukin-12 (IL-12)-induced rejection of tumors. Although the antitumor effect of IL-12 was thought to be mediated through natural killer cells and T cells, Valpha14 NKT cells were found to be an essential target of IL-12, and they mediated their cytotoxicity by an NK-like effector mechanism after activation with IL-12.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cui, J -- Shin, T -- Kawano, T -- Sato, H -- Kondo, E -- Toura, I -- Kaneko, Y -- Koseki, H -- Kanno, M -- Taniguchi, M -- New York, N.Y. -- Science. 1997 Nov 28;278(5343):1623-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Core Research for Evolutional Science and Technology (CREST) Project, Japan Science and Technology Corporation (JST), 1-8-1 Inohana, Chuo-ku, Chiba, Japan 260.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9374462" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anti-Bacterial Agents/pharmacology ; *Cytotoxicity, Immunologic ; Gene Deletion ; Gene Targeting ; Genes, RAG-1 ; Genes, T-Cell Receptor alpha ; Interferon-gamma/immunology ; Interleukin-12/*immunology ; Killer Cells, Natural/*immunology ; *Macrolides ; Melanoma, Experimental/immunology ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Neoplasms, Experimental/*immunology ; Poly I-C/pharmacology ; Proton-Translocating ATPases/antagonists & inhibitors ; Receptors, Antigen, T-Cell, alpha-beta/genetics/*immunology ; T-Lymphocyte Subsets/*immunology
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-05-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marshall, E -- New York, N.Y. -- Science. 1997 May 23;276(5316):1189-90.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9182326" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Computer Communication Networks ; *Dna ; Europe ; Germany ; Humans ; *Information Dissemination ; Intellectual Property ; *Internationality ; *Patents as Topic ; Time Factors ; United States
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-05-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marshall, E -- New York, N.Y. -- Science. 1997 May 23;276(5316):1189.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9182325" target="_blank"〉PubMed〈/a〉
    Keywords: *Academies and Institutes/economics/organization & administration ; Financial Management ; Maryland ; Research Personnel ; *Research Support as Topic ; United States
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-05-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marshall, E -- New York, N.Y. -- Science. 1997 May 9;276(5314):888-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9163031" target="_blank"〉PubMed〈/a〉
    Keywords: *National Institutes of Health (U.S.) ; *Peer Review, Research/methods/standards ; Research Support as Topic ; United States
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  • 21
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-11-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vogel, G -- New York, N.Y. -- Science. 1997 Sep 19;277(5333):1753-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9324757" target="_blank"〉PubMed〈/a〉
    Keywords: Advisory Committees ; *Bioethics ; Federal Government ; *Genetic Engineering ; *Genetic Enhancement ; *Genetic Research ; *Genetic Therapy ; *Genetics, Medical ; Government Regulation ; Humans ; National Institutes of Health (U.S.) ; Social Change ; United States ; Wedge Argument
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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〉New York, N.Y. -- Science. 1997 May 2;276(5313):667.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9157541" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/*drug therapy/virology ; Anti-HIV Agents/*pharmacology/therapeutic use ; Drug Resistance, Microbial ; HIV/*drug effects ; Humans ; *National Institutes of Health (U.S.) ; United States
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-04-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marshall, E -- New York, N.Y. -- Science. 1997 Apr 18;276(5311):344-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9139352" target="_blank"〉PubMed〈/a〉
    Keywords: *Budgets ; Financing, Government ; Lobbying ; National Institutes of Health (U.S.)/*economics ; *Research Support as Topic ; United States
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-03-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cullen, S E -- New York, N.Y. -- Science. 1997 Mar 28;275(5308):1861-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9122683" target="_blank"〉PubMed〈/a〉
    Keywords: *Amino Acid Sequence ; *Base Sequence ; *Dna ; National Institutes of Health (U.S.)/*legislation & jurisprudence ; *Patents as Topic ; United States
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-06-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vogel, G -- New York, N.Y. -- Science. 1997 Jun 27;276(5321):1973.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9221499" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromosome Mapping ; Chromosomes, Human, Pair 4 ; Genetic Markers ; Humans ; Lewy Bodies/chemistry ; Mice ; Mice, Transgenic ; Nerve Tissue Proteins/analysis/chemistry/*genetics ; Oxidative Stress ; Parkinson Disease/etiology/*genetics ; Point Mutation ; Protein Conformation ; Protein Folding ; Rats ; Synucleins
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-02-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marshall, E -- New York, N.Y. -- Science. 1997 Feb 21;275(5303):1062-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9054005" target="_blank"〉PubMed〈/a〉
    Keywords: Environmental Exposure ; Financing, Government ; Humans ; International Cooperation ; *Nuclear Reactors ; Occupational Exposure ; Plutonium/adverse effects ; *Radiation Dosage ; Radiation Effects ; Radiation Injuries/*etiology ; Radioactive Waste/*adverse effects ; Russia ; Strontium Radioisotopes/adverse effects ; United States
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-02-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marshall, E -- New York, N.Y. -- Science. 1997 Feb 7;275(5301):782.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9036543" target="_blank"〉PubMed〈/a〉
    Keywords: Advisory Committees ; Centers for Medicare and Medicaid Services (U.S.) ; Confidentiality ; Federal Government ; Genetic Counseling ; Genetic Services ; Genetic Testing/*standards ; *Government ; *Government Regulation ; Humans ; Reproducibility of Results ; *Social Control, Formal ; United States ; United States Food and Drug Administration
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-03-14
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉New York, N.Y. -- Science. 1997 Mar 14;275(5306):1573.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9072823" target="_blank"〉PubMed〈/a〉
    Keywords: *AIDS Vaccines ; Animals ; Humans ; National Institutes of Health (U.S.)/economics ; *Research Support as Topic ; United States
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  • 29
    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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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-12-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1997 Nov 21;278(5342):1404-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9411764" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/metabolism ; Copper/*metabolism/toxicity ; Copper Sulfate/poisoning ; Mice ; Mice, Knockout ; Neurons/drug effects/physiology ; PrPC Proteins/genetics/*metabolism ; Prion Diseases/etiology
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-09-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1997 Sep 5;277(5331):1430-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9304209" target="_blank"〉PubMed〈/a〉
    Keywords: Administration, Cutaneous ; Biomedical Research ; California ; Federal Government ; Government Regulation ; Heart/physiology ; Humans ; *Intellectual Property ; Nicotine/administration & dosage ; *Plagiarism ; *Research Support as Topic ; Smoking Cessation ; United States ; United States Office of Research Integrity ; *Universities
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-05-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1997 May 30;276(5317):1324-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9190672" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aged ; Centers for Disease Control and Prevention (U.S.) ; Exercise/*physiology/psychology ; Female ; Guidelines as Topic ; Heart Diseases/epidemiology/*prevention & control ; Humans ; Male ; Middle Aged ; Risk Factors ; United States
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  • 33
    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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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-05-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1997 May 16;276(5315):1030-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9173537" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Biological Clocks/*genetics ; CLOCK Proteins ; Chromosome Mapping ; Circadian Rhythm/*genetics ; Cloning, Molecular ; Gene Expression Regulation ; Mice ; Mutation ; Trans-Activators/chemistry/*genetics/physiology
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-08-22
    Description: Tuberculosis is the leading cause of death due to an infectious organism, killing an estimated 3 million people annually. Mycobacterium tuberculosis, the causative agent of tuberculosis, and other pathogenic mycobacteria require entry into host macrophages to initiate infection. An invasion mechanism was defined that was shared among pathogenic mycobacteria including M. tuberculosis, M. leprae, and M. avium but not by nonpathogenic mycobacteria or nonmycobacterial intramacrophage pathogens. This pathway required the association of the complement cleavage product C2a with mycobacteria resulting in the formation of a C3 convertase. The mycobacteria-associated C2a cleaved C3, resulting in C3b opsonization of the mycobacteria and recognition by macrophages.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schorey, J S -- Carroll, M C -- Brown, E J -- AI33348/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1997 Aug 22;277(5329):1091-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Internal Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9262476" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Complement C2/*physiology ; Complement C2a ; Complement C3/metabolism ; Complement C3-C5 Convertases/metabolism ; Complement C3b/immunology ; Horses ; Humans ; In Vitro Techniques ; Isoflurophate/pharmacology ; Macrophages/immunology/*microbiology ; Mice ; Molecular Sequence Data ; Mycobacterium/*pathogenicity ; Mycobacterium avium Complex/immunology/*pathogenicity ; Mycobacterium bovis/immunology/pathogenicity ; Mycobacterium leprae/immunology/pathogenicity ; Mycobacterium tuberculosis/immunology/pathogenicity ; Opsonin Proteins ; Virulence
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-01-17
    Description: The proto-oncogene-encoded transcription factor c-Jun activates genes in response to a number of inducers that act through mitogen-activated protein kinase (MAPK) signal transduction pathways. The activation of c-Jun after phosphorylation by MAPK is accompanied by a reduction in c-Jun ubiquitination and consequent stabilization of the protein. These results illustrate the relevance of regulated protein degradation in the signal-dependent control of gene expression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Musti, A M -- Treier, M -- Bohmann, D -- New York, N.Y. -- Science. 1997 Jan 17;275(5298):400-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉European Molecular Biology Laboratory, Meyerhofstr. 1, 69117 Heidelberg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8994040" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Animals ; Calcium-Calmodulin-Dependent Protein Kinases/*metabolism ; Cell Cycle Proteins/metabolism ; GTP-Binding Proteins/metabolism ; Gene Expression Regulation ; JNK Mitogen-Activated Protein Kinases ; Mice ; *Mitogen-Activated Protein Kinases ; Phosphorylation ; Proto-Oncogene Proteins c-jun/*metabolism ; Signal Transduction ; Transfection ; Ubiquitins/*metabolism ; cdc42 GTP-Binding Protein, Saccharomyces cerevisiae
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-10-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaiser, J -- New York, N.Y. -- Science. 1997 Oct 3;278(5335):26.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9340750" target="_blank"〉PubMed〈/a〉
    Keywords: Advertising as Topic ; *American Medical Association/economics/organization & administration ; Contracts ; Equipment and Supplies ; *Ethics ; *Ethics, Business ; *Industry ; United States
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  • 38
    Publication Date: 1997-02-14
    Description: Mutations in the Caenorhabditis elegans gene clk-1 affect biological timing and extend longevity. The gene clk-1 was identified, and the cloned gene complemented the clk-1 phenotypes and restored normal longevity. The CLK-1 protein was found to be conserved among eukaryotes, including humans, and structurally similar to the yeast metabolic regulator Cat5p (also called Coq7p). These proteins contain a tandem duplication of a core 82-residue domain. clk-1 complemented the phenotype of cat5/coq7 null mutants, demonstrating that clk-1 and CAT5/COQ7 share biochemical function and that clk-1 acts at the level of cellular physiology.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ewbank, J J -- Barnes, T M -- Lakowski, B -- Lussier, M -- Bussey, H -- Hekimi, S -- New York, N.Y. -- Science. 1997 Feb 14;275(5302):980-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, McGill University, 1205 Avenue Docteur Penfield, Montreal, Quebec, Canada H3A 1B1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9020081" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Caenorhabditis elegans/*genetics/metabolism/*physiology ; *Caenorhabditis elegans Proteins ; Cell Aging/*genetics ; Chromosome Mapping ; Conserved Sequence ; Exons ; Fungal Proteins/chemistry/genetics/physiology ; *Genes, Helminth ; Genetic Complementation Test ; Glycerol/metabolism ; Helminth Proteins/chemistry/*genetics/physiology ; Humans ; Longevity/genetics ; Mice ; Molecular Sequence Data ; Phenotype ; Protein Structure, Secondary ; Protein Structure, Tertiary ; RNA Splicing ; *Saccharomyces cerevisiae Proteins
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  • 39
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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〉Service, R F -- New York, N.Y. -- Science. 1997 Apr 25;276(5312):533.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9148412" target="_blank"〉PubMed〈/a〉
    Keywords: Adhesins, Bacterial/*immunology ; *Adhesins, Escherichia coli ; Animals ; Antibodies, Bacterial/biosynthesis ; *Bacterial Vaccines/administration & dosage/immunology ; Clinical Trials as Topic ; Escherichia coli/*immunology ; Escherichia coli Infections/*prevention & control ; Female ; *Fimbriae Proteins ; Humans ; Immunoglobulin G/biosynthesis ; Mice ; Urinary Tract Infections/immunology/*prevention & control ; Vaccination ; Vaccines, Inactivated/administration & dosage/immunology ; *Vaccines, Synthetic/administration & dosage/immunology
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  • 40
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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〉O'Gorman, S -- Wahl, G M -- New York, N.Y. -- Science. 1997 Aug 22;277(5329):1025.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9289845" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; DNA Nucleotidyltransferases/*metabolism ; *Genetic Engineering ; Integrases/metabolism ; Licensure ; Mice ; *Mice, Transgenic ; *Viral Proteins
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  • 41
    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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  • 42
    Publication Date: 1997-10-06
    Description: Familial adenomatous polyposis coli (FAP) is a disease characterized by the development of multiple colorectal adenomas, and affected individuals carry germline mutations in the APC gene. With the use of a conditional gene targeting system, a mouse model of FAP was created that circumvents the embryonic lethality of Apc deficiency and directs Apc inactivation specifically to the colorectal epithelium. loxP sites were inserted into the introns around Apc exon 14, and the resultant mutant allele (Apc580S) was introduced into the mouse germline. Mice homozygous for Apc580S were normal; however, upon infection of the colorectal region with an adenovirus encoding the Cre recombinase, the mice developed adenomas within 4 weeks. The adenomas showed deletion of Apc exon 14, indicating that the loss of Apc function was caused by Cre-loxP-mediated recombination.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shibata, H -- Toyama, K -- Shioya, H -- Ito, M -- Hirota, M -- Hasegawa, S -- Matsumoto, H -- Takano, H -- Akiyama, T -- Toyoshima, K -- Kanamaru, R -- Kanegae, Y -- Saito, I -- Nakamura, Y -- Shiba, K -- Noda, T -- New York, N.Y. -- Science. 1997 Oct 3;278(5335):120-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Cancer Institute, Toshima-ku, Tokyo 170, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9311916" target="_blank"〉PubMed〈/a〉
    Keywords: Adenomatous Polyposis Coli/*genetics ; Adenomatous Polyposis Coli Protein ; Adenoviridae/genetics ; Animals ; Colon/metabolism ; Cytoskeletal Proteins/biosynthesis ; Disease Models, Animal ; Exons ; Female ; Frameshift Mutation ; Gene Deletion ; *Gene Targeting ; *Genes, APC ; Genetic Vectors ; Germ-Line Mutation ; Homozygote ; Integrases/genetics/metabolism ; Introns ; Male ; Mice ; Mice, Inbred C57BL ; Recombination, Genetic ; *Viral Proteins
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  • 43
    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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  • 44
    Publication Date: 1997-09-05
    Description: In response to DNA damage, mammalian cells prevent cell cycle progression through the control of critical cell cycle regulators. A human gene was identified that encodes the protein Chk1, a homolog of the Schizosaccharomyces pombe Chk1 protein kinase, which is required for the DNA damage checkpoint. Human Chk1 protein was modified in response to DNA damage. In vitro Chk1 bound to and phosphorylated the dual-specificity protein phosphatases Cdc25A, Cdc25B, and Cdc25C, which control cell cycle transitions by dephosphorylating cyclin-dependent kinases. Chk1 phosphorylates Cdc25C on serine-216. As shown in an accompanying paper by Peng et al. in this issue, serine-216 phosphorylation creates a binding site for 14-3-3 protein and inhibits function of the phosphatase. These results suggest a model whereby in response to DNA damage, Chk1 phosphorylates and inhibits Cdc25C, thus preventing activation of the Cdc2-cyclin B complex and mitotic entry.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sanchez, Y -- Wong, C -- Thoma, R S -- Richman, R -- Wu, Z -- Piwnica-Worms, H -- Elledge, S J -- GM17763/GM/NIGMS NIH HHS/ -- GM44664/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1997 Sep 5;277(5331):1497-501.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Verna and Marrs McLean Department of Biochemistry, Howard Hughes Medical Institute, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9278511" target="_blank"〉PubMed〈/a〉
    Keywords: 14-3-3 Proteins ; Amino Acid Sequence ; Animals ; CDC2 Protein Kinase/*metabolism ; Cell Cycle Proteins/antagonists & inhibitors/*metabolism ; Chromosome Mapping ; Chromosomes, Human, Pair 11 ; Cytoskeletal Proteins ; *DNA Damage ; *F-Box Proteins ; G2 Phase ; HeLa Cells ; Humans ; Mice ; *Mitosis ; Molecular Sequence Data ; Phosphoprotein Phosphatases/metabolism ; Phosphorylation ; Phosphoserine/metabolism ; Protein Kinases/chemistry/genetics/*metabolism ; Protein Tyrosine Phosphatases/metabolism ; Proteins/metabolism ; Recombinant Fusion Proteins/metabolism ; Schizosaccharomyces pombe Proteins ; Signal Transduction ; Transfection ; *Tyrosine 3-Monooxygenase ; *Ubiquitin-Protein Ligases ; *cdc25 Phosphatases
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  • 45
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-03-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Balter, M -- New York, N.Y. -- Science. 1997 Mar 28;275(5308):1871-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9122686" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Child ; Drug Utilization ; France ; Humans ; Iodine Radioisotopes/adverse effects ; Neoplasms, Radiation-Induced/etiology/*prevention & control ; Potassium Iodide/*administration & dosage ; *Power Plants ; *Radioactive Hazard Release ; Thyroid Neoplasms/etiology/*prevention & control ; United States
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  • 46
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-08-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ehrenstein, D -- New York, N.Y. -- Science. 1997 Aug 8;277(5327):762.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9273696" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Chromosome Mapping ; *Computer Communication Networks ; *Databases, Factual ; *Genes ; Genome, Human ; Humans ; National Institutes of Health (U.S.) ; National Library of Medicine (U.S.) ; Neoplasms/*genetics ; United States
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  • 47
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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〉Kaiser, Jocelyn -- New York, N.Y. -- Science. 1997 Jan 31;275(5300):605.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11644893" target="_blank"〉PubMed〈/a〉
    Keywords: Ethics Committees ; Ethics Committees, Research ; Federal Government ; Government ; *Government Regulation ; *Human Experimentation ; Humans ; Informed Consent ; Legislation as Topic ; Private Sector ; Public Sector ; *Social Control, Formal ; United States ; United States Dept. of Health and Human Services
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  • 48
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-10-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Williams, N -- New York, N.Y. -- Science. 1997 Oct 3;278(5335):31.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9340753" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*pathology ; Brain Chemistry ; Cattle ; Creutzfeldt-Jakob Syndrome/pathology/*transmission ; Encephalopathy, Bovine Spongiform/pathology/*transmission ; Humans ; Mice ; Mice, Transgenic ; Prions/*chemistry
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  • 49
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-10-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Novelli, W D -- New York, N.Y. -- Science. 1997 Oct 10;278(5336):203.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9340761" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Advertising as Topic ; Child ; Health Policy ; Humans ; *Plants, Toxic ; Smoking/legislation & jurisprudence/*prevention & control ; Smoking Cessation ; *Tobacco ; Tobacco Industry/*legislation & jurisprudence ; Tobacco Smoke Pollution/prevention & control ; Tobacco, Smokeless ; United States ; United States Food and Drug Administration
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  • 50
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-01-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Frank, E -- New York, N.Y. -- Science. 1997 Jan 17;275(5298):324-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, University of Pittsburgh, Pittsburgh, PA 15261, USA. efrank+@pitt.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9005555" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcholine/metabolism ; Action Potentials ; Animals ; Axons/physiology ; Central Nervous System/physiology ; Mice ; Motor Neurons/*physiology ; Muscle Fibers, Skeletal/physiology ; Neuromuscular Junction/*physiology ; Receptors, Cholinergic/metabolism ; Synapses/*physiology ; *Synaptic Transmission
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  • 51
    Publication Date: 1997-07-18
    Description: CD1 represents a third lineage of antigen-presenting molecules that are distantly related to major histocompatibility complex (MHC) molecules in the immune system. The crystal structure of mouse CD1d1, corresponding to human CD1d, at 2.8 resolution shows that CD1 adopts an MHC fold that is more closely related to that of MHC class I than to that of MHC class II. The binding groove, although significantly narrower, is substantially larger because of increased depth and it has only two major pockets that are almost completely hydrophobic. The extreme hydrophobicity and shape of the binding site are consistent with observations that human CD1b and CD1c can present mycobacterial cell wall antigens, such as mycolic acid and lipoarabinomannans. However, mouse CD1d1 can present very hydrophobic peptides, but must do so in a very different way from MHC class Ia and class II molecules.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zeng, Z -- Castano, A R -- Segelke, B W -- Stura, E A -- Peterson, P A -- Wilson, I A -- CA-58896/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1997 Jul 18;277(5324):339-45.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology and the Skaggs Institute for Chemical Biology at the Scripps Research Institute, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9219685" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antigen Presentation ; Antigens, CD1/*chemistry/immunology/metabolism ; Binding Sites ; Crystallization ; Crystallography, X-Ray ; Glycolipids/chemistry/immunology/metabolism ; Histocompatibility Antigens Class I/chemistry ; Histocompatibility Antigens Class II/chemistry ; Humans ; Hydrogen Bonding ; Ligands ; Lipid Metabolism ; Lipids/chemistry/immunology ; Mice ; Models, Molecular ; *Protein Conformation ; *Protein Folding ; Protein Structure, Secondary ; Protein Structure, Tertiary ; T-Lymphocyte Subsets/immunology
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  • 52
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-03-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shanahan, F -- New York, N.Y. -- Science. 1997 Mar 28;275(5308):1897-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, National University of Ireland, Cork, University Hospital, Cork, Ireland. fshanahan@iruccvax.ucc.ie〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9122691" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CD8-Positive T-Lymphocytes/cytology/immunology/metabolism ; Cell Communication ; Cell Division ; *Immunity, Mucosal ; Intestinal Mucosa/cytology/*immunology/metabolism ; Lymphocyte Activation ; Mice ; Receptors, Thyrotropin-Releasing Hormone/metabolism ; T-Lymphocytes/cytology/*immunology/metabolism ; Thyrotropin/*metabolism/pharmacology ; Thyrotropin-Releasing Hormone/*metabolism/pharmacology
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  • 53
    Publication Date: 1997-10-10
    Description: The caspase-3 (CPP32, apopain, YAMA) family of cysteinyl proteases has been implicated as key mediators of apoptosis in mammalian cells. Gelsolin was identified as a substrate for caspase-3 by screening the translation products of small complementary DNA pools for sensitivity to cleavage by caspase-3. Gelsolin was cleaved in vivo in a caspase-dependent manner in cells stimulated by Fas. Caspase-cleaved gelsolin severed actin filaments in vitro in a Ca2+-independent manner. Expression of the gelsolin cleavage product in multiple cell types caused the cells to round up, detach from the plate, and undergo nuclear fragmentation. Neutrophils isolated from mice lacking gelsolin had delayed onset of both blebbing and DNA fragmentation, following apoptosis induction, compared with wild-type neutrophils. Thus, cleaved gelsolin may be one physiological effector of morphologic change during apoptosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kothakota, S -- Azuma, T -- Reinhard, C -- Klippel, A -- Tang, J -- Chu, K -- McGarry, T J -- Kirschner, M W -- Koths, K -- Kwiatkowski, D J -- Williams, L T -- P01 HL48743/HL/NHLBI NIH HHS/ -- R01 HL54188/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1997 Oct 10;278(5336):294-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Chiron Corporation, Emeryville, CA 94608, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9323209" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/metabolism ; Amino Acid Chloromethyl Ketones/pharmacology ; Animals ; Antigens, CD95/physiology ; *Apoptosis ; Caspase 3 ; *Caspases ; Cell Line ; *Cell Size ; Cycloheximide/pharmacology ; Cysteine Endopeptidases/*metabolism ; Cysteine Proteinase Inhibitors/pharmacology ; Cytoskeleton/metabolism ; DNA Fragmentation ; Gelsolin/*metabolism ; Humans ; Mice ; Neutrophils/cytology/metabolism ; Recombinant Proteins/metabolism ; Transfection ; Tumor Cells, Cultured ; Tumor Necrosis Factor-alpha/pharmacology
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  • 54
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-08-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bevan, M W -- New York, N.Y. -- Science. 1997 Aug 15;277(5328):885-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9281065" target="_blank"〉PubMed〈/a〉
    Keywords: Arabidopsis/*genetics ; European Union ; *Genome, Plant ; International Cooperation ; Japan ; *Sequence Analysis, DNA ; United States
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  • 55
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-12-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zonana, H -- New York, N.Y. -- Science. 1997 Nov 14;278(5341):1248-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Yale Law School, New Haven, CT 06519, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9411753" target="_blank"〉PubMed〈/a〉
    Keywords: Antisocial Personality Disorder/psychology/therapy ; Commitment of Mentally Ill/*legislation & jurisprudence ; Humans ; *Mental Disorders/psychology/therapy ; Paraphilic Disorders/psychology/therapy ; Sex Offenses/*legislation & jurisprudence/prevention & control/psychology ; United States
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 56
    Publication Date: 1997-10-06
    Description: Expression of Agouti protein is normally limited to the skin where it affects pigmentation, but ubiquitous expression causes obesity. An expressed sequence tag was identified that encodes Agouti-related protein, whose RNA is normally expressed in the hypothalamus and whose levels were increased eightfold in ob/ob mice. Recombinant Agouti-related protein was a potent, selective antagonist of Mc3r and Mc4r, melanocortin receptor subtypes implicated in weight regulation. Ubiquitous expression of human AGRP complementary DNA in transgenic mice caused obesity without altering pigmentation. Thus, Agouti-related protein is a neuropeptide implicated in the normal control of body weight downstream of leptin signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ollmann, M M -- Wilson, B D -- Yang, Y K -- Kerns, J A -- Chen, Y -- Gantz, I -- Barsh, G S -- EY07106/EY/NEI NIH HHS/ -- GM07365/GM/NIGMS NIH HHS/ -- P30DK-34933/DK/NIDDK NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1997 Oct 3;278(5335):135-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatrics, Howard Hughes Medical Institute, Stanford University School of Medicine, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9311920" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenal Glands/metabolism ; Amino Acid Sequence ; Animals ; Female ; Humans ; Hypothalamus/metabolism ; Male ; Melanocyte-Stimulating Hormones/antagonists & inhibitors/pharmacology ; Melanophores/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Inbred CBA ; Mice, Obese ; Mice, Transgenic ; Molecular Sequence Data ; Obesity/etiology ; Organophosphorus Compounds/pharmacology ; Proteins/chemistry/genetics/pharmacology/*physiology ; RNA/genetics/metabolism ; Receptor, Melanocortin, Type 3 ; Receptor, Melanocortin, Type 4 ; Receptors, Corticotropin/*antagonists & inhibitors/metabolism ; Receptors, Peptide/*antagonists & inhibitors/metabolism ; Recombinant Proteins/metabolism ; Signal Transduction ; Xenopus
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  • 57
    Publication Date: 1997-03-21
    Description: The adenomatous polyposis coli (APC) tumor suppressor protein binds to beta-catenin, a protein recently shown to interact with Tcf and Lef transcription factors. The gene encoding hTcf-4, a Tcf family member that is expressed in colonic epithelium, was cloned and characterized. hTcf-4 transactivates transcription only when associated with beta-catenin. Nuclei of APC-/- colon carcinoma cells were found to contain a stable beta-catenin-hTcf-4 complex that was constitutively active, as measured by transcription of a Tcf reporter gene. Reintroduction of APC removed beta-catenin from hTcf-4 and abrogated the transcriptional transactivation. Constitutive transcription of Tcf target genes, caused by loss of APC function, may be a crucial event in the early transformation of colonic epithelium.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Korinek, V -- Barker, N -- Morin, P J -- van Wichen, D -- de Weger, R -- Kinzler, K W -- Vogelstein, B -- Clevers, H -- CA57345/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1997 Mar 21;275(5307):1784-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, University Hospital, Post Office Box 85500, 3508 GA Utrecht, Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9065401" target="_blank"〉PubMed〈/a〉
    Keywords: Adenomatous Polyposis Coli Protein ; Amino Acid Sequence ; Animals ; Cell Line ; Cell Transformation, Neoplastic ; Cloning, Molecular ; Colon/metabolism ; Colonic Neoplasms/*genetics/metabolism ; Cytoskeletal Proteins/genetics/*metabolism ; Gene Expression Regulation, Neoplastic ; *Genes, APC ; Genes, Reporter ; Humans ; Intestinal Mucosa/metabolism ; Mice ; Molecular Sequence Data ; Signal Transduction ; TCF Transcription Factors ; *Trans-Activators ; Transcription Factor 7-Like 2 Protein ; Transcription Factors/chemistry/genetics/*metabolism ; *Transcriptional Activation ; Transfection ; Tumor Cells, Cultured ; beta Catenin
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  • 58
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-07-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Boullin, J M -- New York, N.Y. -- Science. 1997 Jul 18;277(5324):297-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9518352" target="_blank"〉PubMed〈/a〉
    Keywords: Computer Communication Networks ; Costs and Cost Analysis ; Great Britain ; National Institutes of Health (U.S.) ; *Neoplasms ; *Periodicals as Topic/economics ; Private Sector ; *Publishing/economics ; United States ; Universities
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  • 59
    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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  • 60
    Publication Date: 1997-08-01
    Description: In the early months of life, infants acquire information about the phonetic properties of their native language simply by listening to adults speak. The acoustic properties of phonetic units in language input to young infants in the United States, Russia, and Sweden were examined. In all three countries, mothers addressing their infants produced acoustically more extreme vowels than they did when addressing adults, resulting in a "stretching" of vowel space. The findings show that language input to infants provides exceptionally well-specified information about the linguistic units that form the building blocks for words.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kuhl, P K -- Andruski, J E -- Chistovich, I A -- Chistovich, L A -- Kozhevnikova, E V -- Ryskina, V L -- Stolyarova, E I -- Sundberg, U -- Lacerda, F -- DC 00520/DC/NIDCD NIH HHS/ -- New York, N.Y. -- Science. 1997 Aug 1;277(5326):684-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Speech and Hearing Sciences, University of Washington, Box 357920, Seattle, WA 98195, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9235890" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Female ; Humans ; Infant ; *Language Development ; Mothers ; *Phonetics ; Russia ; Speech Acoustics ; *Speech Perception ; Sweden ; United States
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  • 61
    Publication Date: 1997-07-11
    Description: Platelet-derived growth factor (PDGF)-B-deficient mouse embryos were found to lack microvascular pericytes, which normally form part of the capillary wall, and they developed numerous capillary microaneurysms that ruptured at late gestation. Endothelial cells of the sprouting capillaries in the mutant mice appeared to be unable to attract PDGF-Rbeta-positive pericyte progenitor cells. Pericytes may contribute to the mechanical stability of the capillary wall. Comparisons made between PDGF null mouse phenotypes suggest a general role for PDGFs in the development of myofibroblasts.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lindahl, P -- Johansson, B R -- Leveen, P -- Betsholtz, C -- New York, N.Y. -- Science. 1997 Jul 11;277(5323):242-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Biochemistry, University of Goteborg, Medicinaregatan 9A, S-413 90 Goteborg, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9211853" target="_blank"〉PubMed〈/a〉
    Keywords: Aneurysm/*etiology ; Animals ; Brain/blood supply ; Capillaries/*cytology/embryology/metabolism ; Cell Movement ; Endothelium, Vascular/cytology/metabolism ; Hemorrhage/etiology ; Mice ; Mice, Inbred C57BL ; Mutation ; Neovascularization, Physiologic ; Platelet-Derived Growth Factor/deficiency/genetics/*physiology ; Proto-Oncogene Proteins/deficiency/genetics/*physiology ; Proto-Oncogene Proteins c-sis ; Receptor Protein-Tyrosine Kinases/metabolism ; Receptor, Platelet-Derived Growth Factor beta ; Receptor, TIE-2 ; Receptors, Platelet-Derived Growth Factor/metabolism ; Signal Transduction ; Stem Cells/cytology/metabolism ; Up-Regulation
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  • 62
    Publication Date: 1997-06-13
    Description: Extracellular levels of the excitatory neurotransmitter glutamate in the nervous system are maintained by transporters that actively remove glutamate from the extracellular space. Homozygous mice deficient in GLT-1, a widely distributed astrocytic glutamate transporter, show lethal spontaneous seizures and increased susceptibility to acute cortical injury. These effects can be attributed to elevated levels of residual glutamate in the brains of these mice.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tanaka, K -- Watase, K -- Manabe, T -- Yamada, K -- Watanabe, M -- Takahashi, K -- Iwama, H -- Nishikawa, T -- Ichihara, N -- Kikuchi, T -- Okuyama, S -- Kawashima, N -- Hori, S -- Takimoto, M -- Wada, K -- New York, N.Y. -- Science. 1997 Jun 13;276(5319):1699-702.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Degenerative Neurological Diseases, National Institute of Neuroscience, Kodaira, Tokyo 187, Japan. tanaka@ncnaxp.ncap.go.jp〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9180080" target="_blank"〉PubMed〈/a〉
    Keywords: ATP-Binding Cassette Transporters/genetics/*metabolism ; Amino Acid Transport System X-AG ; Animals ; Biological Transport ; Brain/*metabolism/pathology ; Brain Injuries/*metabolism/pathology ; Electroencephalography ; Epilepsy/*metabolism/pathology ; Gene Targeting ; Glutamic Acid/*metabolism ; Hippocampus/metabolism/pathology ; Mice ; Mice, Inbred C57BL ; Nerve Degeneration ; Pyramidal Cells/pathology/physiology ; Synapses/metabolism ; Synaptic Transmission
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  • 63
    Publication Date: 1997-10-06
    Description: Immunotherapy of mice with preexisting cancers with heat shock protein preparations derived from autologous cancer resulted in retarded progression of the primary cancer, a reduced metastatic load, and prolongation of life-span. Treatment with heat shock protein preparations derived from cancers other than the autologous cancer did not provide significant protection. Spontaneous cancers (lung cancer and melanoma), chemically induced cancers (fibrosarcoma and colon carcinoma), and an ultraviolet radiation-induced spindle cell carcinoma were tested, and the results support the efficacy of autologous cancer-derived heat shock protein-peptide complexes in immunotherapy of cancers without the need to identify specific tumor antigenic epitopes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tamura, Y -- Peng, P -- Liu, K -- Daou, M -- Srivastava, P K -- CA44786/CA/NCI NIH HHS/ -- CA64394/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1997 Oct 3;278(5335):117-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Immunotherapy of Cancer and Infectious Diseases, MC1601, University of Connecticut School of Medicine, Farmington, CT 06030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9311915" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Neoplasm/*immunology/therapeutic use ; Autoimmunity ; CD4-Positive T-Lymphocytes/immunology ; CD8-Positive T-Lymphocytes/immunology ; HSP70 Heat-Shock Proteins/immunology ; Heat-Shock Proteins/*immunology/therapeutic use ; Immunization ; *Immunotherapy ; Killer Cells, Natural/immunology ; Lung Neoplasms/immunology/pathology/secondary/therapy ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Neoplasm Metastasis ; Neoplasms/immunology/pathology/*therapy ; Neoplasms, Experimental/immunology/pathology/*therapy
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  • 64
    Publication Date: 1997-12-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kang, S M -- Hoffmann, A -- Le, D -- Springer, M L -- Stock, P G -- Blau, H M -- F32 HL08991/HL/NHLBI NIH HHS/ -- R01-CA59717/CA/NCI NIH HHS/ -- R01-HD18179/HD/NICHD NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1997 Nov 14;278(5341):1322-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9411754" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD95/biosynthesis ; Apoptosis ; Cell Differentiation ; Cell Transplantation ; Fas Ligand Protein ; *Graft Rejection ; Immune Tolerance ; Islets of Langerhans/cytology ; *Islets of Langerhans Transplantation ; Membrane Glycoproteins/genetics/*physiology ; Mice ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Muscle Fibers, Skeletal/*cytology/metabolism ; Muscle, Skeletal/*cytology/metabolism ; Neutrophils/*immunology ; Transfection
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  • 65
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-05-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Morell, V -- New York, N.Y. -- Science. 1997 May 2;276(5313):699-702.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9157549" target="_blank"〉PubMed〈/a〉
    Keywords: Archaea/*classification/genetics/physiology ; Bacteria/*classification/genetics ; Base Sequence ; Biological Evolution ; History, 20th Century ; Origin of Life ; *Phylogeny ; RNA, Bacterial/genetics ; RNA, Ribosomal/genetics ; Sequence Analysis, RNA ; Temperature ; United States
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  • 66
    Publication Date: 1997-08-15
    Description: The epithelium that lines the gut is impermeable to macromolecules and microorganisms, except in Peyer's patches (PPs), where the lymphoid follicle-associated epithelium (FAE) contains M cells that transport antigens and microorganisms. A cultured system that reproduces the main characteristics of FAE and M cells was established by cultivation of PP lymphocytes with the differentiated human intestinal cell line Caco-2. Lymphocytes settled into the epithelial monolayer, inducing reorganization of the brush border and a temperature-dependent transport of particles and Vibrio cholerae. This model system could prove useful for intestinal physiology, vaccine research, and drug delivery studies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kerneis, S -- Bogdanova, A -- Kraehenbuhl, J P -- Pringault, E -- New York, N.Y. -- Science. 1997 Aug 15;277(5328):949-52.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Swiss Institute for Experimental Cancer Research, and Institute of Biochemistry, University of Lausanne, CH-1066 Epalinges-Lausanne, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9252325" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/immunology ; *Bacterial Translocation ; Caco-2 Cells ; Carrier Proteins/analysis ; Cell Polarity ; Coculture Techniques ; Fluorescein-5-isothiocyanate ; Humans ; *Immunity, Mucosal ; Intestinal Mucosa/*cytology/*immunology/microbiology ; Lymphocytes/*immunology ; Mice ; Mice, Inbred BALB C ; Microfilament Proteins/analysis ; Microspheres ; Microvilli/chemistry/ultrastructure ; Peyer's Patches/cytology/*immunology ; Sucrase-Isomaltase Complex/analysis ; T-Lymphocytes/immunology ; Temperature ; Vibrio cholerae/*metabolism
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  • 67
    Publication Date: 1997-01-24
    Description: Lymphocyte-specific interferon regulatory factor (LSIRF) (now called IRF4) is a transcription factor expressed only in lymphocytes. Mice deficient in IRF4 showed normal distribution of B and T lymphocyes at 4 to 5 weeks of age but developed progressive generalized lymphadenopathy. IRF4-deficient mice exhibited a profound reduction in serum immunoglobulin concentrations and did not mount detectable antibody responses. T lymphocyte function was also impaired in vivo; these mice could not generate cytotoxic or antitumor responses. Thus, IRF4 is essential for the function and homeostasis of both mature B and mature T lymphocytes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mittrucker, H W -- Matsuyama, T -- Grossman, A -- Kundig, T M -- Potter, J -- Shahinian, A -- Wakeham, A -- Patterson, B -- Ohashi, P S -- Mak, T W -- New York, N.Y. -- Science. 1997 Jan 24;275(5299):540-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, University of Toronto, Toronto, Ontario, M5G 2C1, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8999800" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen Presentation ; B-Lymphocytes/*immunology ; Bone Marrow Cells ; Cytotoxicity, Immunologic ; DNA-Binding Proteins/genetics/*physiology ; Female ; Gene Targeting ; Graft vs Host Reaction ; Immunization ; Immunoglobulins/blood ; Interferon Regulatory Factors ; Lymphatic Diseases/etiology ; Lymphocyte Activation ; Lymphocyte Subsets/cytology ; Lymphoid Tissue/cytology ; Male ; Mast-Cell Sarcoma/immunology ; Mice ; Mice, Inbred C57BL ; Mice, SCID ; Neoplasm Transplantation ; T-Lymphocytes/*immunology ; T-Lymphocytes, Cytotoxic/immunology ; Transcription Factors/genetics/*physiology
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  • 68
    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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  • 69
    Publication Date: 1997-10-24
    Description: Animals vary in their sensitivity to ethanol, a trait at least partly determined by genetic factors. In order to identify possible responsible genes, mice lacking Fyn, a non-receptor type tyrosine kinase, were investigated. These mice were hypersensitive to the hypnotic effect of ethanol. The administration of ethanol enhanced tyrosine phosphorylation of the N-methyl-D-aspartate receptor (NMDAR) in the hippocampus of control mice but not in Fyn-deficient mice. An acute tolerance to ethanol inhibition of NMDAR-mediated excitatory postsynaptic potentials in hippocampal slices developed in control mice but not in Fyn-deficient mice. These results indicate that Fyn affects behavioral, biochemical, and physiological responses to ethanol.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miyakawa, T -- Yagi, T -- Kitazawa, H -- Yasuda, M -- Kawai, N -- Tsuboi, K -- Niki, H -- New York, N.Y. -- Science. 1997 Oct 24;278(5338):698-701.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory for Neurobiology of Emotion, Brain Science Institute, RIKEN, Hirosawa, Wako-shi, Saitama-ken 351-01, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9381182" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Central Nervous System Depressants/*pharmacology ; Ethanol/*pharmacology ; Excitatory Postsynaptic Potentials/drug effects ; Flurazepam/pharmacology ; Hippocampus/metabolism ; Hypnotics and Sedatives/pharmacology ; In Vitro Techniques ; Male ; Mice ; Mice, Knockout ; Motor Activity/*drug effects ; N-Methylaspartate/pharmacology ; Phosphorylation ; Phosphotyrosine/metabolism ; Protein-Tyrosine Kinases/deficiency/genetics/*metabolism ; Proto-Oncogene Proteins/deficiency/genetics/*metabolism ; Proto-Oncogene Proteins c-fyn ; Receptors, N-Methyl-D-Aspartate/*metabolism
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  • 70
    Publication Date: 1997-12-31
    Description: Lhx3 and Lhx4 (Gsh4), two closely related LIM homeobox genes, determine formation of the pituitary gland in mice. Rathke's pouch is formed in two steps-first as a rudiment and later as a definitive pouch. Lhx3 and Lhx4 have redundant control over formation of the definitive pouch. Lhx3 controls a subsequent step of pituitary fate commitment. Thereafter, Lhx3 and Lhx4 together regulate proliferation and differentiation of pituitary-specific cell lineages. Thus, Lhx3 and Lhx4 dictate pituitary organ identity by controlling developmental decisions at multiple stages of organogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sheng, H Z -- Moriyama, K -- Yamashita, T -- Li, H -- Potter, S S -- Mahon, K A -- Westphal, H -- New York, N.Y. -- Science. 1997 Dec 5;278(5344):1809-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Mammalian Genes and Development, National Institute of Child Health and Human Development, 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/9388186" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cell Division ; Cell Lineage ; Embryonic and Fetal Development/genetics ; Gene Expression Regulation, Developmental ; *Genes, Homeobox ; Homeodomain Proteins/*genetics/physiology ; LIM-Homeodomain Proteins ; Mice ; Mutation ; Pituitary Gland/chemistry/cytology/*embryology ; Pituitary Hormones/analysis/genetics ; Stem Cells/cytology ; *Transcription Factors
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  • 71
    Publication Date: 1997-10-06
    Description: Apoptosis of mouse neocortical neurons induced by serum deprivation or by staurosporine was associated with an early enhancement of delayed rectifier (IK) current and loss of total intracellular K+. This IK augmentation was not seen in neurons undergoing excitotoxic necrosis or in older neurons resistant to staurosporine-induced apoptosis. Attenuating outward K+ current with tetraethylammonium or elevated extracellular K+, but not blockers of Ca2+, Cl-, or other K+ channels, reduced apoptosis, even if associated increases in intracellular Ca2+ concentration were prevented. Furthermore, exposure to the K+ ionophore valinomycin or the K+-channel opener cromakalim induced apoptosis. Enhanced K+ efflux may mediate certain forms of neuronal apoptosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yu, S P -- Yeh, C H -- Sensi, S L -- Gwag, B J -- Canzoniero, L M -- Farhangrazi, Z S -- Ying, H S -- Tian, M -- Dugan, L L -- Choi, D W -- 30337/PHS HHS/ -- New York, N.Y. -- Science. 1997 Oct 3;278(5335):114-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for the Study of Nervous System Injury and Department of Neurology, Washington University School of Medicine, St. Louis, MO 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9311914" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Chloromethyl Ketones/pharmacology ; Animals ; *Apoptosis/drug effects ; Benzopyrans/pharmacology ; Calcium/metabolism ; Cerebral Cortex/cytology ; Cromakalim ; Cycloheximide/pharmacology ; Cysteine Proteinase Inhibitors/pharmacology ; Gadolinium/pharmacology ; Mice ; N-Methylaspartate/pharmacology ; Neurons/*cytology/metabolism ; Neuroprotective Agents/pharmacology ; Nifedipine/pharmacology ; Patch-Clamp Techniques ; Potassium/*metabolism ; Potassium Channels/drug effects/*metabolism ; Pyrroles/pharmacology ; Staurosporine/pharmacology ; Tetraethylammonium ; Tetraethylammonium Compounds/pharmacology ; Veratridine/pharmacology
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  • 72
    Publication Date: 1997-01-31
    Description: The regulation of the serine-threonine kinase Akt by lipid products of phosphoinositide 3-kinase (PI 3-kinase) was investigated. Akt activity was found to correlate with the amount of phosphatidylinositol-3,4-bisphosphate (PtdIns-3,4-P2) in vivo, and synthetic PtdIns-3,4-P2 activated Akt both in vitro and in vivo. Binding of PtdIns-3,4-P2 occurred within the Akt pleckstrin homology (PH) domain and facilitated dimerization of Akt. Akt mutated in the PH domain was not activated by PI 3-kinase in vivo or by PtdIns-3, 4-P2 in vitro, and it was impaired in binding to PtdIns-3,4-P2. Examination of the binding to other phosphoinositides revealed that they bound to the Akt PH domain with much lower affinity than did PtdIns-3,4-P2 and failed to increase Akt activity. Thus, Akt is apparently regulated by the direct interaction of PtdIns-3,4-P2 with the Akt PH domain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Franke, T F -- Kaplan, D R -- Cantley, L C -- Toker, A -- GM41890/GM/NIGMS NIH HHS/ -- N01-CO-74101/CO/NCI NIH HHS/ -- R01 GM041890/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1997 Jan 31;275(5300):665-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉ABL-Basic Research Program, National Cancer Institute-Frederick Cancer Research Facility and Development Center (NCI-FCRFDC), Frederick, MD 21702, USA. tfranke@bidmc.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9005852" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Animals ; COS Cells ; Dimerization ; Enzyme Activation ; Mice ; Phosphatidylinositol 3-Kinases ; Phosphatidylinositol Phosphates/*metabolism/pharmacology ; Phosphorylation ; Phosphotransferases (Alcohol Group Acceptor)/metabolism ; Platelet-Derived Growth Factor/pharmacology ; Point Mutation ; Protein-Serine-Threonine Kinases/chemistry/genetics/*metabolism ; Proto-Oncogene Proteins/chemistry/genetics/*metabolism ; Proto-Oncogene Proteins c-akt ; Recombinant Fusion Proteins/chemistry/metabolism
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  • 73
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-10-06
    Description: Modern approaches to the treatment of addiction have been influenced by several important factors. These include advances in our understanding of the nature of addiction based on longitudinal studies, and progress in elucidating the biological underpinnings of addictive behavior. In addition, changes in the system for delivery of services have begun to shape the way that addiction is treated.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉O'Brien, C P -- P60-05186/PHS HHS/ -- New York, N.Y. -- Science. 1997 Oct 3;278(5335):66-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of Pennsylvania VA Medical Center, 3900 Chestnut Street, Philadelphia, PA 19104-6178, USA. obrien@research.trc.upenn.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9311929" target="_blank"〉PubMed〈/a〉
    Keywords: Alcoholism/drug therapy ; Animals ; Behavior, Addictive ; Clinical Trials as Topic ; Delivery of Health Care ; Humans ; Narcotic Antagonists/pharmacology/therapeutic use ; Receptors, Opioid/agonists ; Recurrence ; Substance Withdrawal Syndrome/drug therapy ; Substance-Related Disorders/*drug therapy/prevention & control/psychology ; United States ; Vaccines
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 74
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-10-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Freitas, A A -- Rocha, B -- New York, N.Y. -- Science. 1997 Sep 26;277(5334):1950.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratoire des Dynamiques Lymphocytaires, Institut Pasteur CNRS URA 1961, 75015 Paris, France. afreitas@pasteur.fr〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9333949" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; CD8-Positive T-Lymphocytes/cytology/immunology ; Cell Survival ; Histocompatibility Antigens Class I/physiology ; Histocompatibility Antigens Class II/physiology ; Immunologic Memory ; Kruppel-Like Transcription Factors ; Lymphocyte Activation ; Mice ; T-Lymphocytes/*cytology/*immunology/metabolism ; Trans-Activators/*physiology ; Zinc Fingers
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  • 75
    Publication Date: 1997-04-25
    Description: ARIA (for acetylcholine receptor-inducing activity), a protein purified on the basis of its ability to stimulate acetylcholine receptor (AChR) synthesis in cultured myotubes, is a member of the neuregulin family and is present at motor endplates. This suggests an important role for neuregulins in mediating the nerve-dependent accumulation of AChRs in the postsynaptic membrane. Nerve-muscle synapses have now been analyzed in neuregulin-deficient animals. Mice that are heterozygous for the deletion of neuregulin isoforms containing an immunoglobulin-like domain are myasthenic. Postsynaptic AChR density is significantly reduced, as judged by the decrease in the mean amplitude of spontaneous miniature endplate potentials and bungarotoxin binding. On the other hand, the mean amplitude of evoked endplate potentials was not decreased, due to an increase in the number of quanta released per impulse, a compensation that has been observed in other myasthenic states. Thus, the density of AChRs in the postsynaptic membrane depends on immunoglobulin-containing neuregulin isoforms throughout the life of the animal.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sandrock, A W Jr -- Dryer, S E -- Rosen, K M -- Gozani, S N -- Kramer, R -- Theill, L E -- Fischbach, G D -- K08-NS01580/NS/NINDS NIH HHS/ -- R01-NS18458/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1997 Apr 25;276(5312):599-603.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉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/9110980" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcholine/metabolism ; Animals ; Bungarotoxins/metabolism ; Glycoproteins/genetics/*physiology ; Heterozygote ; Immunoglobulins/analysis ; In Vitro Techniques ; Membrane Potentials ; Mice ; Motor Endplate/metabolism/physiology ; Muscle Weakness/etiology ; Nerve Tissue Proteins/genetics/*physiology ; Neuregulin-1 ; Neuregulins ; Neuromuscular Junction/*metabolism ; Receptors, Cholinergic/genetics/*metabolism ; Synaptic Transmission
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  • 76
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-03-14
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gallagher, R -- New York, N.Y. -- Science. 1997 Mar 14;275(5306):1615.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9072827" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Humans ; Immunophenotyping ; Interferons/pharmacology ; Interleukin-12/pharmacology ; Mice ; Receptors, Interleukin/*analysis/biosynthesis ; Receptors, Interleukin-12 ; Th2 Cells/*immunology
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  • 77
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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〉Gallagher, R B -- New York, N.Y. -- Science. 1997 Jun 20;276(5320):1817.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9206842" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/*cytology/immunology/physiology ; Gene Rearrangement ; Genes, Immunoglobulin ; Homeostasis ; Lymphocyte Count ; Mice ; Mice, Transgenic ; Receptors, Antigen, B-Cell/analysis
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  • 78
    Publication Date: 1997-12-31
    Description: The lethal yellow (AY/a) mouse has a defect in proopiomelanocortin (POMC) signaling in the brain that leads to obesity, and is resistant to the anorexigenic effects of the hormone leptin. It has been proposed that the weight-reducing effects of leptin are thus transmitted primarily by way of POMC neurons. However, the central effects of defective POMC signaling, and the absence of leptin, on weight gain in double-mutant lethal yellow (AY/a) leptin-deficient (lepob/lepob) mice were shown to be independent and additive. Furthermore, deletion of the leptin gene restored leptin sensitivity to AY/a mice. This result implies that in the AY/a mouse, obesity is independent of leptin action, and resistance to leptin results from desensitization of leptin signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Boston, B A -- Blaydon, K M -- Varnerin, J -- Cone, R D -- DK/AR517330/DK/NIDDK NIH HHS/ -- DK02404/DK/NIDDK NIH HHS/ -- HD33703/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1997 Nov 28;278(5343):1641-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatrics, Oregon Health Sciences University, Portland, OR 97201, USA. Laboratories, Rahway, NJ 07065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9374468" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenalectomy ; Agouti Signaling Protein ; Alleles ; Animals ; Arcuate Nucleus of Hypothalamus/*metabolism ; Blood Glucose/analysis ; Corticosterone/blood ; Crosses, Genetic ; Eating/drug effects ; Energy Metabolism ; Female ; Homeostasis ; Insulin/blood ; *Intercellular Signaling Peptides and Proteins ; Leptin ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Obese ; Neurons/metabolism ; Obesity/genetics/*metabolism ; Pro-Opiomelanocortin/*metabolism ; Proteins/genetics/*metabolism/pharmacology ; Signal Transduction ; Weight Gain
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  • 79
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-07-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chappell, J -- New York, N.Y. -- Science. 1997 Jul 18;277(5324):298-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9518353" target="_blank"〉PubMed〈/a〉
    Keywords: Copyright ; Costs and Cost Analysis ; Great Britain ; National Institutes of Health (U.S.) ; *Neoplasms ; *Periodicals as Topic/economics/legislation & jurisprudence ; Private Sector ; *Publishing/economics/legislation & jurisprudence ; United States ; Universities
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  • 80
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-07-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Abelson, P H -- New York, N.Y. -- Science. 1997 Jul 4;277(5322):15.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9229761" target="_blank"〉PubMed〈/a〉
    Keywords: Air/*standards ; Air Pollutants/*analysis ; Environmental Monitoring ; Humans ; Maximum Allowable Concentration ; Ozone/*analysis ; United States ; United States Environmental Protection Agency
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  • 81
    Publication Date: 1997-07-11
    Description: An integrated human-mouse positional candidate approach was used to identify the gene responsible for the phenotypes observed in a mouse model of Niemann-Pick type C (NP-C) disease. The predicted murine NPC1 protein has sequence homology to the putative transmembrane domains of the Hedgehog signaling molecule Patched, to the cholesterol-sensing regions of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase and SREBP cleavage-activating protein (SCAP), and to the NPC1 orthologs identified in human, the nematode Caenorhabditis elegans, and the yeast Saccharomyces cerevisiae. The mouse model may provide an important resource for studying the role of NPC1 in cholesterol homeostasis and neurodegeneration and for assessing the efficacy of new drugs for NP-C disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Loftus, S K -- Morris, J A -- Carstea, E D -- Gu, J Z -- Cummings, C -- Brown, A -- Ellison, J -- Ohno, K -- Rosenfeld, M A -- Tagle, D A -- Pentchev, P G -- Pavan, W J -- New York, N.Y. -- Science. 1997 Jul 11;277(5323):232-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Genetic Disease Research, National Human Genome Research Institute, National Institutes of Health (NIH), Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9211850" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cholesterol/*metabolism ; *Disease Models, Animal ; Homeostasis ; Humans ; Hydroxymethylglutaryl CoA Reductases/chemistry ; Intracellular Signaling Peptides and Proteins ; Lysosomes/metabolism ; Membrane Proteins/chemistry ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Mutant Strains ; Molecular Sequence Data ; Mutation ; Niemann-Pick Diseases/*genetics/metabolism ; Phenotype ; Protein Sorting Signals/chemistry ; Proteins/chemistry/*genetics/physiology ; Sequence Homology, Amino Acid
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  • 82
    Publication Date: 1997-10-10
    Description: Reexpression of the V(D)J recombinase-activating genes RAG1 and RAG2 in germinal center B cells creates the potential for immunoglobulin gene rearrangement and the generation of new antigen receptor specificities. Intermediate products of V(D)J recombination are abundant in a subset of germinal center B cells, demonstrating that the kappa immunoglobulin light-chain locus becomes a substrate for renewed V(D)J recombinase activity. This recombinationally active cell compartment contains many heavy-chain VDJ rearrangements that encode low-affinity or nonfunctional antibody. In germinal centers, secondary V(D)J recombination may be induced by diminished binding to antigen ligands, thereby limiting abrupt changes in receptor specificity to B cells that are usually eliminated from the germinal center reaction. This restriction preserves efficient antigen-driven selection in germinal centers while allowing for saltations in the somatic evolution of B cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Han, S -- Dillon, S R -- Zheng, B -- Shimoda, M -- Schlissel, M S -- Kelsoe, G -- AI24335/AI/NIAID NIH HHS/ -- AI40227/AI/NIAID NIH HHS/ -- HL48722/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1997 Oct 10;278(5336):301-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology and Program in Molecular and Cell Biology, University of Maryland School of Medicine, 655 West Baltimore Street, Baltimore, MD 21201, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9323211" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibody Diversity ; B-Lymphocytes/*enzymology/immunology ; DNA Nucleotidyltransferases/*metabolism ; DNA-Binding Proteins/genetics ; *Gene Rearrangement, B-Lymphocyte ; *Genes, Immunoglobulin ; Genes, RAG-1 ; Germinal Center/cytology/*immunology ; Immunization ; Immunoglobulin Joining Region/genetics ; Immunoglobulin Variable Region/genetics ; Immunoglobulin kappa-Chains/genetics ; Lymphocyte Activation ; Mice ; Mice, Inbred C57BL ; *Recombination, Genetic ; VDJ Recombinases
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  • 83
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-07-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hanahan, D -- New York, N.Y. -- Science. 1997 Jul 4;277(5322):48-50.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, University of California at San Francisco, San Francisco, CA 94143-0534, USA. dougvhanahan@biochem.ucsf.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9229772" target="_blank"〉PubMed〈/a〉
    Keywords: Angiopoietin-1 ; Angiopoietin-2 ; Animals ; Apoptosis ; Blood Vessels/*embryology/growth & development/metabolism ; Cell Division ; Endothelial Growth Factors/metabolism ; Endothelium, Vascular/*cytology/metabolism ; Lymphokines/metabolism ; Membrane Glycoproteins/metabolism ; Mice ; Mice, Knockout ; Morphogenesis ; *Neovascularization, Physiologic ; Phosphorylation ; Proteins/metabolism ; Proto-Oncogene Proteins/metabolism ; Receptor Protein-Tyrosine Kinases/*metabolism ; Receptor, TIE-2 ; Receptors, Growth Factor/metabolism ; Receptors, Vascular Endothelial Growth Factor ; *Signal Transduction ; Vascular Endothelial Growth Factor A ; Vascular Endothelial Growth Factor Receptor-1 ; Vascular Endothelial Growth Factors
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  • 84
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-02-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marshall, E -- New York, N.Y. -- Science. 1997 Feb 7;275(5301):780-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9036542" target="_blank"〉PubMed〈/a〉
    Keywords: *Dna ; DNA, Complementary ; Databases, Nucleic Acid ; Federal Government ; *Genes ; Genetic Research ; *Genome, Human ; Humans ; Information Dissemination ; National Institutes of Health (U.S.)/legislation & jurisprudence ; *Patents as Topic ; United States
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  • 85
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-02-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Taubes, G -- New York, N.Y. -- Science. 1997 Feb 21;275(5303):1056-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9054004" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Age Factors ; Aged ; Breast Neoplasms/*mortality/prevention & control/radiography ; Consensus Development Conferences, NIH as Topic ; Female ; Humans ; *Mammography/statistics & numerical data ; *Mass Screening/statistics & numerical data ; Middle Aged ; Randomized Controlled Trials as Topic ; United States
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  • 86
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-03-07
    Description: Protein dephosphorylation by phosphatase PP1 plays a central role in mediating the effects of insulin on glucose and lipid metabolism. A PP1C-targeting protein expressed in 3T3-L1 adipocytes (called PTG, for protein targeting to glycogen) was cloned and characterized. PTG was expressed predominantly in insulin-sensitive tissues. In addition to binding and localizing PP1C to glycogen, PTG formed complexes with phosphorylase kinase, phosphorylase a, and glycogen synthase, the primary enzymes involved in the hormonal regulation of glycogen metabolism. Overexpression of PTG markedly increased basal and insulin-stimulated glycogen synthesis in Chinese hamster ovary cells overexpressing the insulin receptor, which do not express endogenous PTG. These results suggest that PTG is critical for glycogen metabolism, possibly functioning as a molecular scaffold.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Printen, J A -- Brady, M J -- Saltiel, A R -- New York, N.Y. -- Science. 1997 Mar 7;275(5305):1475-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, University of Michigan School of Medicine, Ann Arbor, MI 48109, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9045612" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Amino Acid Sequence ; Animals ; CHO Cells ; Carrier Proteins/chemistry/genetics/*metabolism ; Cloning, Molecular ; Cricetinae ; DNA, Complementary/genetics ; Glycogen/biosynthesis/*metabolism ; Glycogen Synthase/metabolism ; Insulin/pharmacology ; *Intracellular Signaling Peptides and Proteins ; Mice ; Molecular Sequence Data ; Phosphoprotein Phosphatases/*metabolism ; Phosphorylase Kinase/metabolism ; Phosphorylase a/metabolism ; Phosphorylation ; Protein Binding ; Protein Phosphatase 1 ; Recombinant Fusion Proteins/metabolism ; Substrate Specificity ; Transfection
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 87
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-06-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, J -- New York, N.Y. -- Science. 1997 Jun 27;276(5321):1960-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9221492" target="_blank"〉PubMed〈/a〉
    Keywords: Arabidopsis/genetics ; DNA, Complementary/genetics ; DNA, Plant/genetics ; Databases, Factual ; Financing, Government ; Gene Expression ; *Genome, Plant ; International Cooperation ; Oryza/genetics ; Research Support as Topic ; Sequence Analysis, DNA ; United States ; Zea mays/*genetics
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 88
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-04-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hayflick, L -- New York, N.Y. -- Science. 1997 Apr 18;276(5311):337-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9139350" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; *Cell Transformation, Neoplastic ; *Cell Transformation, Viral ; Haplorhini ; Humans ; Poliovirus/growth & development ; *Poliovirus Vaccine, Inactivated ; Simian virus 40/*pathogenicity ; United States ; United States Food and Drug Administration ; Virus Cultivation
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 89
    Publication Date: 1997-02-14
    Description: The telomerase ribonucleoprotein catalyzes the addition of new telomeres onto chromosome ends. A gene encoding a mammalian telomerase homolog called TP1 (telomerase-associated protein 1) was identified and cloned. TP1 exhibited extensive amino acid similarity to the Tetrahymena telomerase protein p80 and was shown to interact specifically with mammalian telomerase RNA. Antiserum to TP1 immunoprecipitated telomerase activity from cell extracts, suggesting that TP1 is associated with telomerase in vivo. The identification of TP1 suggests that telomerase-associated proteins are conserved from ciliates to humans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Harrington, L -- McPhail, T -- Mar, V -- Zhou, W -- Oulton, R -- Bass, M B -- Arruda, I -- Robinson, M O -- New York, N.Y. -- Science. 1997 Feb 14;275(5302):973-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Arruda, Ontario Cancer Institute-Amgen Institute, Department of Medical Biophysics, University of Toronto, 620 University Avenue, Toronto, Ontario M5G 2C1, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9020079" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Blotting, Northern ; Carrier Proteins/*chemistry/genetics/immunology/*metabolism ; Cell Line ; Cloning, Molecular ; DNA, Complementary/genetics ; Humans ; Mice ; Molecular Sequence Data ; Precipitin Tests ; RNA/*metabolism ; RNA, Messenger/genetics/metabolism ; Sequence Homology, Amino Acid ; Telomerase/*chemistry/genetics/metabolism ; Tetrahymena/chemistry/genetics ; Transfection ; Tumor Cells, Cultured
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 90
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-12-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, J -- New York, N.Y. -- Science. 1997 Nov 28;278(5343):1565-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9411779" target="_blank"〉PubMed〈/a〉
    Keywords: *Acquired Immunodeficiency Syndrome/epidemiology/immunology/therapy ; Belgium ; Budgets ; Centers for Disease Control and Prevention (U.S.) ; Democratic Republic of the Congo ; Humans ; International Cooperation ; National Institutes of Health (U.S.) ; *Research ; Research Support as Topic ; United States
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 91
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-09-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marshall, E -- Bagla, P -- New York, N.Y. -- Science. 1997 Sep 5;277(5331):1429.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9304208" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Curcumin/*therapeutic use ; Humans ; India ; *Patents as Topic ; *Plants, Medicinal ; United States ; Wound Healing
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 92
    Publication Date: 1997-03-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rothenberg, K -- Fuller, B -- Rothstein, M -- Duster, T -- Ellis Kahn, M J -- Cunningham, R -- Fine, B -- Hudson, K -- King, M C -- Murphy, P -- Swergold, G -- Collins, F -- New York, N.Y. -- Science. 1997 Mar 21;275(5307):1755-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Law and Health Care Program, University of Maryland School of Law, 500 West Baltimore Street, Baltimore, MD 21201, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9122681" target="_blank"〉PubMed〈/a〉
    Keywords: Confidentiality ; Disclosure ; Employment/*legislation & jurisprudence ; Federal Government ; Genetic Diseases, Inborn ; *Genetic Privacy ; *Genetic Testing ; *Genetics, Medical ; *Government Regulation ; Humans ; Insurance Selection Bias ; Insurance, Health/legislation & jurisprudence ; *Prejudice ; *Public Policy ; United States
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 93
    Publication Date: 1997-05-09
    Description: Timely deactivation of kinase cascades is crucial to the normal control of cell signaling and is partly accomplished by protein phosphatase 2A (PP2A). The catalytic (alpha) subunit of the serine-threonine kinase casein kinase 2 (CK2) bound to PP2A in vitro and in mitogen-starved cells; binding required the integrity of a sequence motif common to CK2alpha and SV40 small t antigen. Overexpression of CK2alpha resulted in deactivation of mitogen-activated protein kinase kinase (MEK) and suppression of cell growth. Moreover, CK2alpha inhibited the transforming activity of oncogenic Ras, but not that of constitutively activated MEK. Thus, CK2alpha may regulate the deactivation of the mitogen-activated protein kinase pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Heriche, J K -- Lebrin, F -- Rabilloud, T -- Leroy, D -- Chambaz, E M -- Goldberg, Y -- New York, N.Y. -- Science. 1997 May 9;276(5314):952-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Commissariat a l'Energie Atomique, Departement de Biologie Moleculaire et Structurale, Laboratoire de Biochimie des Regulations Cellulaires Endocrines, Unite 244, F-38054 Grenoble Cedex 9, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9139659" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Amino Acid Sequence ; Animals ; Antigens, Polyomavirus Transforming ; Binding Sites ; Casein Kinase II ; Cell Division ; Cell Transformation, Neoplastic ; MAP Kinase Kinase 1 ; Mice ; *Mitogen-Activated Protein Kinase Kinases ; Mutation ; Okadaic Acid/pharmacology ; Phosphoprotein Phosphatases/*metabolism ; Phosphorylation ; Platelet-Derived Growth Factor/pharmacology ; Protein Phosphatase 2 ; Protein-Serine-Threonine Kinases/*metabolism/pharmacology ; Protein-Tyrosine Kinases/metabolism/pharmacology ; Recombinant Fusion Proteins/metabolism ; Transfection ; ras Proteins/pharmacology
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  • 94
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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〉Marx, G -- New York, N.Y. -- Science. 1997 Apr 25;276(5312):531-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9148411" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; BRCA1 Protein/genetics/*metabolism ; BRCA2 Protein ; Breast Neoplasms/*genetics/metabolism ; Cell Division ; *DNA Repair ; DNA-Binding Proteins/genetics/metabolism ; Female ; Gene Expression Regulation ; *Genes, BRCA1 ; Humans ; Mice ; Mice, Knockout ; Mutation ; Neoplasm Proteins/*genetics/*metabolism ; Ovarian Neoplasms/genetics ; Rad51 Recombinase ; Transcription Factors/*genetics/*metabolism
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  • 95
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-04-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, J -- New York, N.Y. -- Science. 1997 Apr 18;276(5311):345.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9139353" target="_blank"〉PubMed〈/a〉
    Keywords: *Acquired Immunodeficiency Syndrome ; *Budgets ; Financing, Government ; Humans ; National Institutes of Health (U.S.)/*economics ; *Research Support as Topic ; United States
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  • 96
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-05-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Himms-Hagen, J -- New York, N.Y. -- Science. 1997 May 16;276(5315):1132-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9173544" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue ; Animals ; Body Composition ; Body Weight ; *Eating ; Energy Intake ; *Energy Metabolism ; Leptin ; Mice ; Mice, Obese ; Neuropeptide Y/genetics/physiology ; Obesity/*metabolism ; *Oxygen Consumption ; Proteins/pharmacology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 97
    Publication Date: 1997-05-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cork, L C -- Clarkson, T B -- Jacoby, R O -- Gaertner, D J -- Leary, S L -- Linn, J M -- Pakes, S P -- Ringler, D H -- Strandberg, J D -- Swindle, M M -- New York, N.Y. -- Science. 1997 May 2;276(5313):758-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Comparative Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9157554" target="_blank"〉PubMed〈/a〉
    Keywords: Animal Welfare ; Animals ; *Animals, Laboratory ; Costs and Cost Analysis ; Financing, Government ; Laboratory Animal Science/*economics/education ; National Institutes of Health (U.S.)/economics ; Research/*economics ; *Research Support as Topic ; United States ; Veterinary Medicine/economics
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  • 98
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-07-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marshall, E -- New York, N.Y. -- Science. 1997 Jul 4;277(5322):24-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9229765" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacteriophage P1/genetics ; DNA, Complementary ; Gene Expression ; *Gene Targeting ; Genetic Engineering/*methods ; Integrases/genetics ; Mice ; *Mice, Transgenic ; National Institutes of Health (U.S.) ; *Patents as Topic ; Polymerase Chain Reaction ; United States ; *Viral Proteins
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 99
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-12-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marshall, E -- New York, N.Y. -- Science. 1997 Nov 14;278(5341):1218.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9411744" target="_blank"〉PubMed〈/a〉
    Keywords: *Budgets ; Financing, Government ; Human Genome Project ; Humans ; National Institutes of Health (U.S.)/*economics ; Parkinson Disease ; Research Support as Topic ; United States
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  • 100
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-08-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roush, W -- New York, N.Y. -- Science. 1997 Aug 15;277(5328):897-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9281069" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caenorhabditis elegans/*genetics/growth & development/metabolism ; Caenorhabditis elegans Proteins ; Cloning, Molecular ; Energy Intake ; *Genes, Helminth ; Glucose/metabolism ; Humans ; Insulin/metabolism ; Longevity/*genetics ; Mice ; Mutation ; Phosphatidylinositol 3-Kinases ; Phosphotransferases (Alcohol Group Acceptor)/genetics/metabolism ; Receptor, Insulin/*genetics/metabolism ; Second Messenger Systems ; Signal Transduction
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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