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  • Female  (103)
  • Transfection  (57)
  • American Association for the Advancement of Science (AAAS)  (158)
  • American Meteorological Society
  • PANGAEA
  • 1995-1999  (158)
  • 1997  (158)
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  • American Association for the Advancement of Science (AAAS)  (158)
  • American Meteorological Society
  • PANGAEA
  • Springer  (1)
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  • 1995-1999  (158)
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  • 1
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    Genetic testing for cancer risk (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-11-14
    Description: Genetic testing for cancer susceptibility is already part of the clinical management of families with some of the well-defined (but uncommon) inherited cancer syndromes. In cases where the risks associated with a predisposing mutation are less certain, or where there is no clearly effective intervention to offer those with a positive result, its use is more controversial. Careful evaluation of costs and benefits, and of the efficacy of interventions in those found to be at risk, is essential and is only just beginning. An immediate challenge is to ensure that both health professionals and the public understand clearly the issues involved.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ponder, B -- New York, N.Y. -- Science. 1997 Nov 7;278(5340):1050-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Oncology, University of Cambridge, Addenbrooke's Hospital, Box 238, Level 3 Lab Block, Hills Road, Cambridge CB2 2QQ, UK. bajp@mole.bio.cam.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9353178" target="_blank"〉PubMed〈/a〉
    Keywords: Confidentiality ; Cost-Benefit Analysis ; Female ; Genetic Counseling ; Genetic Predisposition to Disease ; Genetic Services ; *Genetic Testing ; Genetic Variation ; Humans ; Insurance, Health ; Insurance, Life ; Male ; Mutation ; Neoplasms/*diagnosis/*genetics ; Resource Allocation ; Risk Assessment ; Risk Factors ; Uncertainty
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Spectral technique paints cells in vivid new colors (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    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):1990.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9221504" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Nucleus/ultrastructure ; Chromosomes, Human/ultrastructure ; Coloring Agents ; *Cytological Techniques ; Female ; Humans ; Image Processing, Computer-Assisted ; Microscopy, Interference/*methods ; Spectrum Analysis ; Uterine Cervical Dysplasia/pathology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    Can cloning help save beleaguered species? (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-05-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, J -- New York, N.Y. -- Science. 1997 May 30;276(5317):1329-30.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9190674" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Zoo/genetics ; Cloning, Molecular ; *Conservation of Natural Resources ; Costs and Cost Analysis ; Cryopreservation ; Female ; Fibroblasts/cytology ; *Genetic Engineering/economics ; Genetic Variation ; Reproduction, Asexual ; Sheep ; Species Specificity
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    Sexual selection in Asian elephants (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-12-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tiedemann, R -- New York, N.Y. -- Science. 1997 Nov 28;278(5343):1550-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9411772" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Elephants/*anatomy & histology/*physiology ; Female ; Incisor/anatomy & histology ; India ; Male ; Models, Biological ; Models, Statistical ; *Sexual Behavior, Animal ; Sri Lanka
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    Angiopoietin-2, a natural antagonist for Tie2 that disrupts in vivo angiogenesis (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    NCI reverses one expert panel, sides with another (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
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    Pain affect encoded in human anterior cingulate but not somatosensory cortex (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-08-15
    Description: Recent evidence demonstrating multiple regions of human cerebral cortex activated by pain has prompted speculation about their individual contributions to this complex experience. To differentiate cortical areas involved in pain affect, hypnotic suggestions were used to alter selectively the unpleasantness of noxious stimuli, without changing the perceived intensity. Positron emission tomography revealed significant changes in pain-evoked activity within anterior cingulate cortex, consistent with the encoding of perceived unpleasantness, whereas primary somatosensory cortex activation was unaltered. These findings provide direct experimental evidence in humans linking frontal-lobe limbic activity with pain affect, as originally suggested by early clinical lesion studies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rainville, P -- Duncan, G H -- Price, D D -- Carrier, B -- Bushnell, M C -- New York, N.Y. -- Science. 1997 Aug 15;277(5328):968-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉D-epartement de Psychologie and Centre de Recherche en Sciences Neurologiques, Universite de Montreal, Montreal, Quebec, Canada H3C 3J7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9252330" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Affect/*physiology ; *Brain Mapping ; Female ; Frontal Lobe/blood supply/*physiology/radionuclide imaging ; Gyrus Cinguli/blood supply/*physiology/radionuclide imaging ; Humans ; Hypnosis ; Male ; Middle Aged ; Pain/*physiopathology/*psychology ; Pain Measurement ; Regional Blood Flow ; Regression Analysis ; Somatosensory Cortex/blood supply/*physiology/radionuclide imaging ; Thermosensing ; Tomography, Emission-Computed
    Print ISSN: 0036-8075
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  • 8
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    Ethics of AZT studies in poorer countries attacked (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-05-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, J -- New York, N.Y. -- Science. 1997 May 16;276(5315):1022.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9173534" target="_blank"〉PubMed〈/a〉
    Keywords: Africa ; Anti-HIV Agents/administration & dosage/*therapeutic use ; *Bioethics ; Caribbean Region ; *Control Groups ; Controlled Clinical Trials as Topic/*standards ; Female ; HIV Infections/drug therapy/prevention & control/*transmission ; Humans ; Infectious Disease Transmission, Vertical/*prevention & control ; Placebos ; Pregnancy ; Pregnancy Complications, Infectious/drug therapy ; *Pregnant Women ; Thailand ; Therapeutic Human Experimentation ; Withholding Treatment ; Zidovudine/administration & dosage/*therapeutic use
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
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    Fluorescence-based isolation of bacterial genes expressed within host cells (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
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    Regulation of replicon size in Xenopus egg extracts (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-02-14
    Description: Once a specific number of cells have been produced in the early Xenopus laevis embryo, replicon size during the S phase of the cell cycle increases. Here, it is reported that similar increase in replicon size occurred when the concentration of nuclei in replication-competent Xenopus egg extracts exceeded a critical threshold. In this system, the origin recognition complex (ORC) did not become stoichiometrically limiting for initiation, and similar amounts of this complex bound to chromatin regardless of replicon size. These data suggest that in early development, an unidentified factor controls how many preformed ORC-DNA complexes initiate DNA replication.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Walter, J -- Newport, J W -- 1F32FM17980-01/PHS HHS/ -- R01FM44656/PHS HHS/ -- New York, N.Y. -- Science. 1997 Feb 14;275(5302):993-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, University of California, San Diego, La Jolla, CA 92093-0347, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9020085" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Cycle Proteins/metabolism ; Chromatin/metabolism ; Cyclin-Dependent Kinase Inhibitor p21 ; Cyclins/pharmacology ; Cytarabine/pharmacology ; DNA/*metabolism ; *DNA Replication ; DNA-Binding Proteins/*metabolism ; Enzyme Inhibitors/pharmacology ; Female ; Origin Recognition Complex ; Ovum/*metabolism ; Replication Origin ; *Replicon ; S Phase ; Xenopus laevis
    Print ISSN: 0036-8075
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  • 11
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    A mouse model with features of familial combined hyperlipidemia (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    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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  • 12
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    Conditional mutator phenotypes in hMSH2-deficient tumor cell lines (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-09-05
    Description: Two human tumor cell lines that are deficient in the mismatch repair protein hMSH2 show little or no increase in mutation rate relative to that of a mismatch repair-proficient cell line when the cells are maintained in culture conditions allowing rapid growth. However, mutations accumulate at a high rate in these cells when they are maintained at high density. Thus the mutator phenotype of some mismatch repair-deficient cell lines is conditional and strongly depends on growth conditions. These observations have implications for tumor development because they suggest that mutations may accumulate in tumor cells when growth is limited.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Richards, B -- Zhang, H -- Phear, G -- Meuth, M -- R01-CA-62244/CA/NCI NIH HHS/ -- T32-CA-09602/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1997 Sep 5;277(5331):1523-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Oncological Sciences, Eccles Institute of Human Genetics, University of Utah, Salt Lake City, UT, 84112, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9278518" target="_blank"〉PubMed〈/a〉
    Keywords: *Cell Count ; *Cell Division ; *DNA Repair ; DNA Replication ; *DNA-Binding Proteins ; Drug Resistance, Neoplasm ; Female ; Frameshift Mutation ; Humans ; Hypoxanthine Phosphoribosyltransferase/genetics ; Microsatellite Repeats ; MutS Homolog 2 Protein ; *Mutation ; Neoplasms/*genetics/pathology ; Ouabain/pharmacology ; Ovarian Neoplasms/genetics/pathology ; Phenotype ; Proto-Oncogene Proteins/genetics/*physiology ; Tumor Cells, Cultured ; Uterine Neoplasms/genetics/pathology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 13
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    Group brands AIDS trials unethical (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-04-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉New York, N.Y. -- Science. 1997 Apr 25;276(5312):519.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9148403" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/*drug therapy/transmission ; Anti-HIV Agents/*therapeutic use ; *Controlled Clinical Trials as Topic/standards ; *Developing Countries ; *Ethics, Medical ; Female ; Humans ; Infant ; Infant, Newborn ; Placebos ; Pregnancy ; Pregnancy Complications, Infectious/*drug therapy ; Zidovudine/therapeutic use
    Print ISSN: 0036-8075
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  • 14
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    Peptide agonist of the thrombopoietin receptor as potent as the natural cytokine (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 15
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    Publishing sensitive data: who calls the shots? Long-suppressed study finally sees light of day (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-04-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vogel, G -- New York, N.Y. -- Science. 1997 Apr 25;276(5312):525-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9148408" target="_blank"〉PubMed〈/a〉
    Keywords: California ; *Drug Industry ; Drugs, Generic/*pharmacokinetics ; Female ; Humans ; *Publishing ; Randomized Controlled Trials as Topic ; Therapeutic Equivalency ; Thyroxine/*pharmacokinetics ; Universities
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 16
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    Thanks to a parasite, asexual reproduction catches on (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-03-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Enserink, M -- New York, N.Y. -- Science. 1997 Mar 21;275(5307):1743.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9122678" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Evolution ; Butterflies/parasitology ; Female ; Male ; Moths/parasitology ; Ovum/parasitology ; *Parthenogenesis ; Rickettsiaceae/*physiology ; Wasps/microbiology/*physiology
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  • 17
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    How much pain for cardiac gain? (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    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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  • 18
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    New insights into how babies learn language (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-08-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1997 Aug 1;277(5326):641.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9254430" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Female ; Humans ; Infant ; *Language Development ; Mothers ; *Phonetics ; Speech Acoustics ; *Speech Perception
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 19
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    Life and death of neurons in the aging brain (1997)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1997-10-23
    Description: Neurodegenerative disorders are characterized by extensive neuron death that leads to functional decline, but the neurobiological correlates of functional decline in normal aging are less well defined. For decades, it has been a commonly held notion that widespread neuron death in the neocortex and hippocampus is an inevitable concomitant of brain aging, but recent quantitative studies suggest that neuron death is restricted in normal aging and unlikely to account for age-related impairment of neocortical and hippocampal functions. In this article, the qualitative and quantitative differences between aging and Alzheimer's disease with respect to neuron loss are discussed, and age-related changes in functional and biochemical attributes of hippocampal circuits that might mediate functional decline in the absence of neuron death are explored. When these data are viewed comprehensively, it appears that the primary neurobiological substrates for functional impairment in aging differ in important ways from those in neurodegenerative disorders such as Alzheimer's disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Morrison, J H -- Hof, P R -- AG05138/AG/NIA NIH HHS/ -- AG06647/AG/NIA NIH HHS/ -- MHDA52145/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1997 Oct 17;278(5337):412-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neurobiology of Aging Laboratories, the Fishberg Research Center for Neurobiology, and the Department of Geriatrics and Adult Development, Mount Sinai School of Medicine, New York, NY 10029, USA. morrison@cortex.neuro.mssm.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9334292" target="_blank"〉PubMed〈/a〉
    Keywords: *Aging ; Alzheimer Disease/pathology ; Animals ; Cell Death ; Cell Survival ; Entorhinal Cortex/pathology ; Estrogens/physiology ; Female ; Hippocampus/cytology/pathology/*physiology ; Humans ; Male ; Memory ; Neocortex/cytology/pathology/*physiology ; *Nerve Degeneration ; Neurofibrillary Tangles/pathology ; Neurofilament Proteins/metabolism ; Neurons/cytology/pathology/*physiology
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  • 20
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    Reduced ubiquitin-dependent degradation of c-Jun after phosphorylation by MAP kinases (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 21
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    Longer tusks are healthy signs (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-06-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bagla, P -- New York, N.Y. -- Science. 1997 Jun 27;276(5321):1972.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9221498" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Commerce ; Elephants/*anatomy & histology/genetics/*parasitology ; Female ; Helminthiasis, Animal/*immunology ; Immunity, Innate ; Incisor/anatomy & histology ; Male ; Parasite Egg Count/veterinary ; Sexual Behavior, Animal
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  • 22
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    Interaction and regulation of subcellular localization of CED-4 by CED-9 (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-02-21
    Description: The Caenorhabditis elegans survival gene ced-9 regulates ced-4 activity and inhibits cell death, but the mechanism by which this occurs is unknown. Through a genetic screen for CED-4-binding proteins, CED-9 was identified as an interacting partner of CED-4. CED-9, but not loss-of-function mutants, associated specifically with CED-4 in yeast or mammalian cells. The CED-9 protein localized primarily to intracellular membranes and the perinuclear region, whereas CED-4 was distributed in the cytosol. Expression of CED-9, but not a mutant lacking the carboxy-terminal hydrophobic domain, targeted CED-4 from the cytosol to intracellular membranes in mammalian cells. Thus, the actions of CED-4 and CED-9 are directly linked, which could provide the basis for the regulation of programmed cell death in C. elegans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wu, D -- Wallen, H D -- Nunez, G -- CA-64556/CA/NCI NIH HHS/ -- T32A107413-03/PHS HHS/ -- New York, N.Y. -- Science. 1997 Feb 21;275(5303):1126-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and Comprehensive Cancer Center, The University of Michigan Medical School, Ann Arbor, MI 48109, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9027313" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Apoptosis Regulatory Proteins ; Caenorhabditis elegans/*cytology/genetics ; *Caenorhabditis elegans Proteins ; Calcium-Binding Proteins/analysis/genetics/*metabolism ; Cell Fractionation ; Cell Line ; Cytosol/chemistry ; Genes, Helminth ; Helminth Proteins/analysis/genetics/*metabolism ; Humans ; Intracellular Membranes/chemistry ; Mutation ; Proto-Oncogene Proteins/analysis/genetics/*metabolism ; *Proto-Oncogene Proteins c-bcl-2 ; Transfection ; bcl-X Protein
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 23
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    Study shows one-fifth of female bison infected (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-06-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Baskin, Y -- New York, N.Y. -- Science. 1997 Jun 20;276(5320):1786.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9206836" target="_blank"〉PubMed〈/a〉
    Keywords: Abortion, Veterinary/microbiology ; Animals ; *Bison ; *Brucella abortus ; Brucellosis/*epidemiology/transmission ; Brucellosis, Bovine/*transmission ; Cattle ; Female ; Montana/epidemiology ; Pregnancy ; Risk Factors
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 24
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    Estrogen stakes claim to cognition (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-05-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wickelgren, I -- New York, N.Y. -- Science. 1997 May 2;276(5313):675-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9157544" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/*drug therapy ; Animals ; Antioxidants/pharmacology ; Brain/cytology/metabolism ; Choline O-Acetyltransferase/metabolism ; Cognition/drug effects/*physiology ; Controlled Clinical Trials as Topic ; Estrogens/pharmacology/*physiology/therapeutic use ; Female ; Humans ; Male ; Memory/drug effects/*physiology ; Nerve Growth Factors/metabolism ; Receptors, N-Methyl-D-Aspartate/metabolism ; Synapses/physiology
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  • 25
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    Subtle, secret female chimpanzees (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-08-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wrangham, R W -- New York, N.Y. -- Science. 1997 Aug 8;277(5327):774-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anthropology, Harvard University, Cambridge, MA 02138, USA. wrangham@fas.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9273699" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Female ; Male ; Pan troglodytes/*psychology ; *Reproduction ; *Sexual Behavior, Animal ; *Social Dominance
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 26
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    New vaccines may ward off urinary tract infections (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    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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  • 27
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    Quantitative trait loci for refractoriness of Anopheles gambiae to Plasmodium cynomolgi B (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-04-18
    Description: The severity of the malaria pandemic in the tropics is aggravated by the ongoing spread of parasite resistance to antimalarial drugs and mosquito resistance to insecticides. A strain of Anopheles gambiae, normally a major vector for human malaria in Africa, can encapsulate and kill the malaria parasites within a melanin-rich capsule in the mosquito midgut. Genetic mapping revealed one major and two minor quantitative trait loci (QTLs) for this encapsulation reaction. Understanding such antiparasite mechanisms in mosquitoes may lead to new strategies for malaria control.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zheng, L -- Cornel, A J -- Wang, R -- Erfle, H -- Voss, H -- Ansorge, W -- Kafatos, F C -- Collins, F H -- New York, N.Y. -- Science. 1997 Apr 18;276(5311):425-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉European Molecular Biology Laboratory, Meyerhofstrasse 1, 69117 Heidelberg, Germany. Disease Control and Prevention, 4770 Buford Hi.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9103203" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anopheles/*genetics/immunology/*parasitology ; Chromosome Mapping ; Crosses, Genetic ; Female ; *Genes, Insect ; Genotype ; Insect Vectors/*genetics/immunology/*parasitology ; Lod Score ; Male ; Melanins/physiology ; Microsatellite Repeats ; Phenotype ; Plasmodium cynomolgi/*immunology
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  • 28
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    Rapid colorectal adenoma formation initiated by conditional targeting of the Apc gene (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    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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  • 29
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    Transmission of hepatitis C by intrahepatic inoculation with transcribed RNA (1997)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1997-07-25
    Description: More than 1% of the world's population is chronically infected with hepatitis C virus (HCV). HCV infection can result in acute hepatitis, chronic hepatitis, and cirrhosis, which is strongly associated with development of hepatocellular carcinoma. Genetic studies of HCV replication have been hampered by lack of a bona fide infectious molecular clone. Full-length functional clones of HCV complementary DNA were constructed. RNA transcripts from the clones were found to be infectious and to cause disease in chimpanzees after direct intrahepatic inoculation. This work defines the structure of a functional HCV genome RNA and proves that HCV alone is sufficient to cause disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kolykhalov, A A -- Agapov, E V -- Blight, K J -- Mihalik, K -- Feinstone, S M -- Rice, C M -- AI40034/AI/NIAID NIH HHS/ -- CA57973/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1997 Jul 25;277(5325):570-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Microbiology, Washington University School of Medicine, 660 South Euclid Avenue, St. Louis, MO 63110-1093, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9228008" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cloning, Molecular ; Consensus Sequence ; DNA, Complementary ; Hepacivirus/*genetics/physiology ; Hepatitis C/*transmission/*virology ; Liver/*virology ; Molecular Sequence Data ; Pan troglodytes ; Polymerase Chain Reaction ; RNA, Messenger/*genetics ; RNA, Viral/blood/*genetics ; Transfection ; Viremia ; Virus Replication
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  • 30
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    Conservation of the Chk1 checkpoint pathway in mammals: linkage of DNA damage to Cdk regulation through Cdc25 (1997)
    American Association for the Advancement of Science (AAAS)
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    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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  • 31
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    Caspase-3-generated fragment of gelsolin: effector of morphological change in apoptosis (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    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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    Evidence for a role of CRM1 in signal-mediated nuclear protein export (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-10-06
    Description: Chromosome maintenance region 1 (CRM1), a protein that shares sequence similarities with the karyopherin beta family of proteins involved in nuclear import pathway, was shown to form a complex with the leucine-rich nuclear export signal (NES). This interaction was inhibited by leptomycin B, a drug that prevents the function of the CRM1 protein in yeast. To analyze the role of the CRM1-NES interaction in nuclear export, a transport assay based on semipermeabilized cells was developed. In this system, which reconstituted NES-, cytosol-, and energy-dependent nuclear export, leptomycin B specifically blocked export of NES-containing proteins. Thus, the CRM1 protein could act as a NES receptor involved in nuclear protein export.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ossareh-Nazari, B -- Bachelerie, F -- Dargemont, C -- New York, N.Y. -- Science. 1997 Oct 3;278(5335):141-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut Curie-CNRS Unite Mixte de Recherche 144, 26 rue d'Ulm, 75248 Paris Cedex 05, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9311922" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Amino Acid Sequence ; Biological Transport/drug effects ; Carrier Proteins/*physiology ; Cell Nucleus/*metabolism ; DNA-Binding Proteins/chemistry/*metabolism ; Fatty Acids, Unsaturated/pharmacology ; Fluorescent Antibody Technique, Indirect ; HeLa Cells ; Humans ; *I-kappa B Proteins ; Immunoblotting ; *Karyopherins ; Nuclear Localization Signals ; Nuclear Proteins/*metabolism ; Protein Sorting Signals/chemistry/*metabolism ; Pyruvate Kinase/metabolism ; *Receptors, Cytoplasmic and Nuclear ; Recombinant Fusion Proteins/metabolism ; Transfection
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    Antagonism of central melanocortin receptors in vitro and in vivo by agouti-related protein (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    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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    Immune hyperactivation of HIV-1-infected T cells mediated by Tat and the CD28 pathway (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-03-07
    Description: Human immunodeficiency virus-type 1 (HIV-1) infection is characterized by a chronic state of immune hyperactivation in patients. Infection of human peripheral blood lymphocytes with HIV-1 in vitro resulted in increased interleukin-2 (IL-2) secretion in response to T cell activation via the CD3 and CD28 receptors. Expression of the HIV-1 transactivator Tat recapitulated this phenotype and was associated with increased IL-2 secretion in response to costimulation with CD3 plus CD28. IL-2 superinduction by Tat occurred at the transcriptional level, was mediated by the CD28-responsive element in the IL-2 promoter, and was exclusively dependent on the 29 amino acids encoded by the second exon of Tat.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ott, M -- Emiliani, S -- Van Lint, C -- Herbein, G -- Lovett, J -- Chirmule, N -- McCloskey, T -- Pahwa, S -- Verdin, E -- New York, N.Y. -- Science. 1997 Mar 7;275(5305):1481-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Picower Institute for Medical Research, 350 Community Drive, Manhasset, NY 11030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9045614" target="_blank"〉PubMed〈/a〉
    Keywords: Anti-HIV Agents/pharmacology ; Antibodies, Monoclonal/immunology ; Antigens, CD28/*immunology ; Antigens, CD3/immunology ; Exons ; Gene Products, tat/genetics/*physiology ; HIV Infections/immunology ; HIV-1/drug effects/genetics/*physiology ; Humans ; Interleukin-2/genetics/*secretion ; Jurkat Cells ; Leukocytes, Mononuclear/virology ; *Lymphocyte Activation ; Promoter Regions, Genetic ; T-Lymphocytes/*immunology/*virology ; Transcription Factors/metabolism ; Transcription, Genetic ; Transfection ; Zidovudine/pharmacology ; tat Gene Products, Human Immunodeficiency Virus
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    Constitutive transcriptional activation by a beta-catenin-Tcf complex in APC-/- colon carcinoma (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    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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    When should fatherhood stop? (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-07-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gavrilov, L A -- Gavrilova, N S -- New York, N.Y. -- Science. 1997 Jul 4;277(5322):17-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9229762" target="_blank"〉PubMed〈/a〉
    Keywords: Female ; Humans ; *Longevity ; Male ; *Nuclear Family ; *Paternal Age
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    Cross-language analysis of phonetic units in language addressed to infants (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    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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    The origin of dogs: running with the wolves (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-06-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Morell, V -- New York, N.Y. -- Science. 1997 Jun 13;276(5319):1647-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9206828" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Breeding ; Carnivora/*genetics ; Crosses, Genetic ; DNA, Mitochondrial/*genetics ; Dogs/*genetics ; Female ; Haplotypes ; Male
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    Immune response and myoblasts that express Fas ligand (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    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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  • 40
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    Activation of heat shock transcription factor 3 by c-Myb in the absence of cellular stress (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-07-11
    Description: In vertebrates, the presence of multiple heat shock transcription factors (HSFs) indicates that these factors may be regulated by distinct stress signals. HSF3 was specifically activated in unstressed proliferating cells by direct binding to the c-myb proto-oncogene product (c-Myb). These factors formed a complex through their DNA binding domains that stimulated the nuclear entry and formation of the transcriptionally active trimer of HSF3. Because c-Myb participates in cellular proliferation, this regulatory pathway may provide a link between cellular proliferation and the stress response.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kanei-Ishii, C -- Tanikawa, J -- Nakai, A -- Morimoto, R I -- Ishii, S -- New York, N.Y. -- Science. 1997 Jul 11;277(5323):246-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Genetics, Tsukuba Life Science Center, RIKEN, Tsukuba, Ibaraki 305, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9211854" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Cycle ; Cell Line ; Cell Nucleus/metabolism ; DNA/*metabolism ; DNA-Binding Proteins/chemistry/*metabolism ; Promoter Regions, Genetic ; Proto-Oncogene Proteins/*metabolism ; Proto-Oncogene Proteins c-myb ; Recombinant Fusion Proteins/metabolism ; Trans-Activators/chemistry/*metabolism ; Transcriptional Activation ; Transfection
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    Bangkok study adds fuel to AIDS ethics debate (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-12-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaiser, J -- New York, N.Y. -- Science. 1997 Nov 28;278(5343):1553.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9411773" target="_blank"〉PubMed〈/a〉
    Keywords: Anti-HIV Agents/*therapeutic use ; Controlled Clinical Trials as Topic ; Ethics, Medical ; Female ; HIV Infections/*drug therapy/transmission ; Humans ; Infant ; Infectious Disease Transmission, Vertical ; *Placebos ; Pregnancy ; Pregnancy Complications, Infectious/*drug therapy ; Pregnant Women ; Thailand ; Zidovudine/*therapeutic use
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    Requirement for the transcription factor LSIRF/IRF4 for mature B and T lymphocyte function (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    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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    Control of TRAIL-induced apoptosis by a family of signaling and decoy receptors (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-08-08
    Description: TRAIL (also called Apo2L) belongs to the tumor necrosis factor family, activates rapid apoptosis in tumor cells, and binds to the death-signaling receptor DR4. Two additional TRAIL receptors were identified. The receptor designated death receptor 5 (DR5) contained a cytoplasmic death domain and induced apoptosis much like DR4. The receptor designated decoy receptor 1 (DcR1) displayed properties of a glycophospholipid-anchored cell surface protein. DcR1 acted as a decoy receptor that inhibited TRAIL signaling. Thus, a cell surface mechanism exists for the regulation of cellular responsiveness to pro-apoptotic stimuli.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sheridan, J P -- Marsters, S A -- Pitti, R M -- Gurney, A -- Skubatch, M -- Baldwin, D -- Ramakrishnan, L -- Gray, C L -- Baker, K -- Wood, W I -- Goddard, A D -- Godowski, P -- Ashkenazi, A -- New York, N.Y. -- Science. 1997 Aug 8;277(5327):818-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Oncology, Genentech, South San Francisco, CA 94080-4918, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9242611" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; *Apoptosis ; Apoptosis Regulatory Proteins ; Cell Membrane/metabolism ; Cells, Cultured ; GPI-Linked Proteins ; Glycosylphosphatidylinositols/metabolism ; HeLa Cells ; Humans ; Ligands ; Membrane Glycoproteins/*metabolism ; Molecular Sequence Data ; NF-kappa B/metabolism ; Receptors, TNF-Related Apoptosis-Inducing Ligand ; Receptors, Tumor Necrosis Factor/chemistry/genetics/*metabolism ; Signal Transduction ; TNF-Related Apoptosis-Inducing Ligand ; Transfection ; Tumor Cells, Cultured ; Tumor Necrosis Factor Decoy Receptors ; Tumor Necrosis Factor-alpha/*metabolism
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    Genetic feminization of pheromones and its behavioral consequences in Drosophila males (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-06-06
    Description: Pheromones are intraspecific chemical signals important for mate attraction and discrimination. In the fruit fly Drosophila melanogaster, hydrocarbons on the cuticular surface of the animal are sexually dimorphic in both their occurrence and their effects: Female-specific molecules stimulate male sexual excitation, whereas the predominant male-specific molecule tends to inhibit male excitation. Complete feminization of the pheromone mixture produced by males was induced by targeted expression of the transformer gene in adult oenocytes (subcuticular abdominal cells) or by ubiquitous expression during early imaginal life. The resulting flies generally exhibited male heterosexual orientation but elicited homosexual courtship from other males.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ferveur, J F -- Savarit, F -- O'Kane, C J -- Sureau, G -- Greenspan, R J -- Jallon, J M -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 1997 Jun 6;276(5318):1555-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Mecanismes de communication, Unite de Recherche Associee-CNRS 1491, Batiment 446, Universite Paris-Sud, 91405, Orsay-Cedex, France. ferveur@ext.jussieu.fr〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9171057" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Drosophila melanogaster ; Female ; Gene Expression Regulation, Developmental ; Homosexuality ; Male ; Nuclear Proteins/genetics/physiology ; Recombinant Fusion Proteins ; Sex Attractants/genetics/*physiology ; *Sex Characteristics ; Sex Differentiation ; *Sexual Behavior, Animal/physiology ; Transgenes
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Neighborhoods and violent crime: a multilevel study of collective efficacy (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-08-15
    Description: It is hypothesized that collective efficacy, defined as social cohesion among neighbors combined with their willingness to intervene on behalf of the common good, is linked to reduced violence. This hypothesis was tested on a 1995 survey of 8782 residents of 343 neighborhoods in Chicago, Illinois. Multilevel analyses showed that a measure of collective efficacy yields a high between-neighborhood reliability and is negatively associated with variations in violence, when individual-level characteristics, measurement error, and prior violence are controlled. Associations of concentrated disadvantage and residential instability with violence are largely mediated by collective efficacy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sampson, R J -- Raudenbush, S W -- Earls, F -- New York, N.Y. -- Science. 1997 Aug 15;277(5328):918-24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Sociology, University of Chicago, Chicago, IL 60637, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9252316" target="_blank"〉PubMed〈/a〉
    Keywords: Chicago ; Female ; Humans ; Male ; Models, Statistical ; *Residence Characteristics ; Social Conditions ; *Social Control, Informal ; *Social Environment ; Social Values ; Socioeconomic Factors ; *Violence
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    Separate neural bases of two fundamental memory processes in the human medial temporal lobe (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-04-11
    Description: The participation of medial temporal-lobe structures in memory performance was examined by functional magnetic resonance imaging of local blood oxygenation level-dependent signals. Signals were measured during encoding into memory complex scenes or line drawings and during retrieval from memory of previously studied line drawings or words. Encoding tasks yielded increased signals for unfamiliar information in a posterior medial-temporal region that were focused in the parahippocampal cortex. Retrieval tasks yielded increased signals for successfully remembered information in an anterior medial-temporal region that were focused in the subiculum. These results indicate that separate components of the human medial temporal-lobe memory system are active during distinct memory processes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gabrieli, J D -- Brewer, J B -- Desmond, J E -- Glover, G H -- New York, N.Y. -- Science. 1997 Apr 11;276(5310):264-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychology and Neuroscience Program, Stanford University, Stanford, CA 94305, USA. gabrieli@psych.stanford.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9092477" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Brain Mapping ; Female ; Hippocampus/physiology ; Humans ; Magnetic Resonance Imaging ; Male ; Memory/*physiology ; Mental Recall/*physiology ; Temporal Lobe/*physiology
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    Independent and additive effects of central POMC and leptin pathways on murine obesity (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    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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    Environment and cancer: who are susceptible? (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-11-14
    Description: Acting in concert with individual susceptibility, environmental factors such as smoking, diet, and pollutants play a role in most human cancer. However, new molecular evidence indicates that specific groups-characterized by predisposing genetic traits or ethnicity, the very young, and women-may have heightened risk from certain exposures. This is illustrated by molecular epidemiologic studies of environmental carcinogens such as polycyclic aromatic hydrocarbons and aromatic amines. Individual genetic screening for rare high-risk traits or for more common, low-penetrant susceptibility genes is problematic and not routinely recommended. However, knowledge of the full spectrum of both genetic and acquired susceptibility in the population will be instrumental in developing health and regulatory policies that increase protection of the more susceptible groups from risks of environmental carcinogens. This will necessitate revision of current risk assessment methodologies to explicitly account for individual variation in susceptibility to environmental carcinogens.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Perera, F P -- New York, N.Y. -- Science. 1997 Nov 7;278(5340):1068-73.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Environmental Health Sciences, Columbia University School of Public Health, 60 Haven Avenue, B-1, New York, NY 10032, USA. fpp1@columbia.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9353182" target="_blank"〉PubMed〈/a〉
    Keywords: *Aging ; Amines/adverse effects ; Carcinogens, Environmental/*adverse effects ; Continental Population Groups ; Female ; *Genetic Predisposition to Disease ; Humans ; Male ; Neoplasms/chemically induced/ethnology/*etiology/genetics/prevention & control ; Nutritional Physiological Phenomena ; Polycyclic Hydrocarbons, Aromatic/adverse effects ; Risk Factors ; *Sex Characteristics
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    Identification of a chemokine receptor encoded by human cytomegalovirus as a cofactor for HIV-1 entry (1997)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1997-06-20
    Description: The human cytomegalovirus encodes a beta-chemokine receptor (US28) that is distantly related to the human chemokine receptors CCR5 and CXCR4, which also serve as cofactors for the entry into cells of human immunodeficiency virus-type 1 (HIV-1). Like CCR5, US28 allowed infection of CD4-positive human cell lines by primary isolates of HIV-1 and HIV-2, as well as fusion of these cell lines with cells expressing the viral envelope proteins. In addition, US28 mediated infection by cell line-adapted HIV-1 for which CXCR4 was an entry cofactor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pleskoff, O -- Treboute, C -- Brelot, A -- Heveker, N -- Seman, M -- Alizon, M -- New York, N.Y. -- Science. 1997 Jun 20;276(5320):1874-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Inserm U.332, Institut Cochin de Genetique Moleculaire, 22 rue Mechain, 75014 Paris, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9188536" target="_blank"〉PubMed〈/a〉
    Keywords: AIDS-Related Opportunistic Infections/virology ; Amino Acid Sequence ; Cell Fusion ; Chemokines ; Coculture Techniques ; Cytomegalovirus/*genetics/physiology ; Cytomegalovirus Infections/virology ; Giant Cells ; HIV Infections/virology ; HIV-1/*physiology ; HIV-2/*physiology ; HeLa Cells ; Humans ; Membrane Proteins/physiology ; Molecular Sequence Data ; Receptors, CCR2 ; Receptors, CCR5 ; Receptors, CXCR4 ; *Receptors, Chemokine ; Receptors, Cytokine/genetics/*physiology ; Receptors, HIV/genetics/*physiology ; Transfection ; Tumor Cells, Cultured ; Viral Proteins/genetics/*physiology
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    The breast-screening brawl (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    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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    PTG, a protein phosphatase 1-binding protein with a role in glycogen metabolism (1997)
    American Association for the Advancement of Science (AAAS)
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    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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    A mammalian telomerase-associated protein (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    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
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    NF-AT activation induced by a CAML-interacting member of the tumor necrosis factor receptor superfamily (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-10-06
    Description: Activation of the nuclear factor of activated T cells transcription factor (NF-AT) is a key event underlying lymphocyte action. The CAML (calcium-modulator and cyclophilin ligand) protein is a coinducer of NF-AT activation when overexpressed in Jurkat T cells. A member of the tumor necrosis factor receptor superfamily was isolated by virtue of its affinity for CAML. Cross-linking of this lymphocyte-specific protein, designated TACI (transmembrane activator and CAML-interactor), on the surface of transfected Jurkat cells with TACI-specific antibodies led to activation of the transcription factors NF-AT, AP-1, and NFkappaB. TACI-induced activation of NF-AT was specifically blocked by a dominant-negative CAML mutant, thus implicating CAML as a signaling intermediate.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉von Bulow, G U -- Bram, R J -- CA21765/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1997 Oct 3;278(5335):138-41.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Experimental Oncology, St. Jude Children's Research Hospital, 332 North Lauderdale, Memphis, TN 38105, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9311921" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptor Proteins, Signal Transducing ; Amino Acid Sequence ; Calcineurin ; Calmodulin-Binding Proteins/metabolism ; Carrier Proteins/genetics/*metabolism ; Cell Line ; Cell Membrane/metabolism ; DNA-Binding Proteins/*metabolism ; Humans ; Jurkat Cells ; Lymphocyte Activation ; *Membrane Proteins ; Molecular Sequence Data ; Mutation ; NF-kappa B/metabolism ; NFATC Transcription Factors ; *Nuclear Proteins ; Phosphoprotein Phosphatases/metabolism ; Receptors, Tumor Necrosis Factor/chemistry/genetics/*metabolism ; Sequence Alignment ; Signal Transduction ; T-Lymphocytes/immunology/*metabolism ; Transcription Factor AP-1/metabolism ; Transcription Factors/*metabolism ; Transcription, Genetic ; Transfection ; Transmembrane Activator and CAML Interactor Protein
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    Requirement for GD3 ganglioside in CD95- and ceramide-induced apoptosis (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-09-12
    Description: Gangliosides participate in development and tissue differentiation. Cross-linking of the apoptosis-inducing CD95 protein (also called Fas or APO-1) in lymphoid and myeloid tumor cells triggered GD3 ganglioside synthesis and transient accumulation. CD95-induced GD3 accumulation depended on integral receptor "death domains" and on activation of a family of cysteine proteases called caspases. Cell-permeating ceramides, which are potent inducers of apoptosis, also triggered GD3 synthesis. GD3 disrupted mitochondrial transmembrane potential (DeltaPsim), and induced apoptosis, in a caspase-independent fashion. Transient overexpression of the GD3 synthase gene directly triggered apoptosis. Pharmacological inhibition of GD3 synthesis and exposure to GD3 synthase antisense oligodeoxynucleotides prevented CD95-induced apoptosis. Thus, GD3 ganglioside mediates the propagation of CD95-generated apoptotic signals in hematopoietic cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉De Maria, R -- Lenti, L -- Malisan, F -- d'Agostino, F -- Tomassini, B -- Zeuner, A -- Rippo, M R -- Testi, R -- New York, N.Y. -- Science. 1997 Sep 12;277(5332):1652-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Experimental Medicine and Biochemical Sciences, University of Rome "Tor Vergata," 00133 Rome, Italy.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9287216" target="_blank"〉PubMed〈/a〉
    Keywords: Antigens, CD95/metabolism/*physiology ; *Apoptosis ; Ceramides/pharmacology/*physiology ; Cysteine Endopeptidases/metabolism ; Cysteine Proteinase Inhibitors/pharmacology ; Enzyme Inhibitors/pharmacology ; Gangliosides/biosynthesis/*metabolism/pharmacology ; Golgi Apparatus/metabolism ; Humans ; Membrane Potentials ; Mitochondria/physiology ; Morpholines/pharmacology ; Oligonucleotides, Antisense/pharmacology ; Sialyltransferases/genetics/metabolism ; Signal Transduction ; Transfection ; Tumor Cells, Cultured
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    CD4-independent binding of SIV gp120 to rhesus CCR5 (1997)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1997-12-31
    Description: CCR5 and CD4 are coreceptors for immunodeficiency virus entry into target cells. The gp120 envelope glycoprotein from human immunodeficiency virus strain HIV-1(YU2) bound human CCR5 (CCR5hu) or rhesus macaque CCR5 (CCR5rh) only in the presence of CD4. The gp120 from simian immunodeficiency virus strain SIVmac239 bound CCR5rh without CD4, but CCR5hu remained CD4-dependent. The CD4-independent binding of SIVmac239 gp120 depended on a single amino acid, Asp13, in the CCR5rh amino-terminus. Thus, CCR5-binding moieties on the immunodeficiency virus envelope glycoprotein can be generated by interaction with CD4 or by direct interaction with the CCR5 amino-terminus. These results may have implications for the evolution of receptor use among lentiviruses as well as utility in the development of effective intervention.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Martin, K A -- Wyatt, R -- Farzan, M -- Choe, H -- Marcon, L -- Desjardins, E -- Robinson, J -- Sodroski, J -- Gerard, C -- Gerard, N P -- AI41581/AI/NIAID NIH HHS/ -- HL36162/HL/NHLBI NIH HHS/ -- HL51366/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1997 Nov 21;278(5342):1470-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Perlmutter Laboratory, Children's Hospital, Department of Medicine, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9367961" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antibodies, Monoclonal ; Antigens, CD4/*physiology ; Cell Line ; HIV Antibodies/immunology ; HIV Envelope Protein gp120/chemistry/*metabolism ; HIV-2/immunology ; Humans ; Macaca mulatta ; Macrophages/virology ; *Membrane Glycoproteins ; Mutation ; Receptors, CCR5/chemistry/*metabolism ; Simian Immunodeficiency Virus/*metabolism ; Transfection ; *Viral Envelope Proteins
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    Attentional activation of the cerebellum independent of motor involvement (1997)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1997-03-28
    Description: The cerebellum traditionally has been viewed as a neural device dedicated to motor control. Although recent evidence shows that it is involved in nonmotor operations as well, an important question is whether this involvement is independent of motor control and motor guidance. Functional magnetic resonance imaging was used to demonstrate that attention and motor performance independently activate distinct cerebellar regions. These findings support a broader concept of cerebellar function, in which the cerebellum is involved in diverse cognitive and noncognitive neurobehavioral systems, including the attention and motor systems, in order to anticipate imminent information acquisition, analysis, or action.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Allen, G -- Buxton, R B -- Wong, E C -- Courchesne, E -- R01-MH36840/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1997 Mar 28;275(5308):1940-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉San Diego State University-University of California, San Diego Joint Doctoral Program in Clinical Psychology, San Diego, CA 92120, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9072973" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; *Attention ; Brain Mapping ; Cerebellar Cortex/physiology ; Cerebellum/*physiology ; *Cognition ; Female ; Humans ; Magnetic Resonance Imaging ; Male ; *Motor Activity ; *Psychomotor Performance
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    Regulation of protein phosphatase 2A by direct interaction with casein kinase 2alpha (1997)
    American Association for the Advancement of Science (AAAS)
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    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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    Nonsyndromic deafness DFNA1 associated with mutation of a human homolog of the Drosophila gene diaphanous (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-11-21
    Description: The gene responsible for autosomal dominant, fully penetrant, nonsyndromic sensorineural progressive hearing loss in a large Costa Rican kindred was previously localized to chromosome 5q31 and named DFNA1. Deafness in the family is associated with a protein-truncating mutation in a human homolog of the Drosophila gene diaphanous. The truncation is caused by a single nucleotide substitution in a splice donor, leading to a four-base pair insertion in messenger RNA and a frameshift. The diaphanous protein is a profilin ligand and target of Rho that regulates polymerization of actin, the major component of the cytoskeleton of hair cells of the inner ear.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lynch, E D -- Lee, M K -- Morrow, J E -- Welcsh, P L -- Leon, P E -- King, M C -- R01-DC01076/DC/NIDCD NIH HHS/ -- New York, N.Y. -- Science. 1997 Nov 14;278(5341):1315-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of Washington, Seattle, WA 98195, USA. eric@lynch.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9360932" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/*metabolism ; *Adaptor Proteins, Signal Transducing ; Amino Acid Sequence ; Animals ; Base Sequence ; Carrier Proteins/chemistry/*genetics/physiology ; Chromosome Mapping ; Chromosomes, Human, Pair 5 ; Cochlea/metabolism ; *Contractile Proteins ; Deafness/*genetics/metabolism/pathology ; Drosophila/genetics ; *Drosophila Proteins ; Female ; Frameshift Mutation ; GTP-Binding Proteins/metabolism ; Gene Expression ; Hair Cells, Auditory/*metabolism/ultrastructure ; Humans ; Male ; Microfilament Proteins/metabolism ; Molecular Sequence Data ; Pedigree ; Profilins ; RNA Splicing ; RNA, Messenger/genetics/metabolism ; X Chromosome
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    Possible function found for breast cancer genes (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Mutation of the Stargardt disease gene (ABCR) in age-related macular degeneration (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-09-20
    Description: Age-related macular degeneration (AMD) is the leading cause of severe central visual impairment among the elderly and is associated both with environmental factors such as smoking and with genetic factors. Here, 167 unrelated AMD patients were screened for alterations in ABCR, a gene that encodes a retinal rod photoreceptor protein and is defective in Stargardt disease, a common hereditary form of macular dystrophy. Thirteen different AMD-associated alterations, both deletions and amino acid substitutions, were found in one allele of ABCR in 26 patients (16%). Identification of ABCR alterations will permit presymptomatic testing of high-risk individuals and may lead to earlier diagnosis of AMD and to new strategies for prevention and therapy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Allikmets, R -- Shroyer, N F -- Singh, N -- Seddon, J M -- Lewis, R A -- Bernstein, P S -- Peiffer, A -- Zabriskie, N A -- Li, Y -- Hutchinson, A -- Dean, M -- Lupski, J R -- Leppert, M -- New York, N.Y. -- Science. 1997 Sep 19;277(5333):1805-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Intramural Research Support Program, SAIC-Frederick, NCI-Frederick Cancer Research and Development Center, Frederick, MD 21702, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9295268" target="_blank"〉PubMed〈/a〉
    Keywords: ATP-Binding Cassette Transporters/*genetics/metabolism ; Adult ; Aged ; Aged, 80 and over ; Female ; Frameshift Mutation ; Heterozygote ; Humans ; Macula Lutea/pathology ; Macular Degeneration/*genetics/metabolism/pathology ; Male ; Middle Aged ; *Mutation ; Pedigree ; Pigment Epithelium of Eye/pathology ; Retinal Drusen/pathology ; Sequence Deletion
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    Modulating irrelevant motion perception by varying attentional load in an unrelated task (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-12-31
    Description: Lavie's theory of attention proposes that the processing load in a relevant task determines the extent to which irrelevant distractors are processed. This theory was tested by asking participants in a study to perform linguistic tasks of low or high load while ignoring irrelevant visual motion in the periphery of the display. Although task and distractor were unrelated, both functional imaging of motion-related activity in cortical area V5 and psychophysical measures of the motion aftereffect showed reduced motion processing during high load in the linguistic task. These findings fulfill the prediction that perception of irrelevant distractors depends on the relevant processing load.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rees, G -- Frith, C D -- Lavie, N -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 1997 Nov 28;278(5343):1616-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wellcome Department of Cognitive Neurology, Institute of Neurology, 12 Queen Square, London WC1N 3BG, UK. g.rees@fil.ion.ucl.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9374459" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Attention/*physiology ; Cerebral Cortex/*physiology ; Female ; Humans ; Magnetic Resonance Imaging ; Male ; *Motion Perception ; Psychomotor Performance ; Superior Colliculi/physiology
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    Preattentive filling-in of visual surfaces in parietal extinction (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-01-31
    Description: Unilateral brain damage frequently produces "extinction," in which patients can detect brief single visual stimuli on either side but are unaware of a contralesional stimulus if presented concurrently with an ipsilesional stimulus. Explanations for extinction have invoked deficits in initial processes that operate before the focusing of visual attention or in later attentive stages of vision. Preattentive vision was preserved in a parietally damaged patient, whose extinction was less severe when bilateral stimuli formed a common surface, even if this required visual filling-in to yield illusory Kanizsa figures or completion of partially occluded figures. These results show that parietal extinction arises only after substantial processing has generated visual surfaces, supporting recent claims that visual attention is surface-based.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mattingley, J B -- Davis, G -- Driver, J -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 1997 Jan 31;275(5300):671-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Experimental Psychology, University of Cambridge, Downing Street, Cambridge CB2 3EB, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9005854" target="_blank"〉PubMed〈/a〉
    Keywords: Aged ; *Attention ; Cerebrovascular Disorders/*physiopathology ; *Extinction, Psychological ; Female ; *Form Perception ; Humans ; Parietal Lobe/*physiopathology ; Psychomotor Performance ; Visual Pathways
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    Activation of beta-catenin-Tcf signaling in colon cancer by mutations in beta-catenin or APC (1997)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1997-03-21
    Description: Inactivation of the adenomatous polyposis coli (APC) tumor suppressor gene initiates colorectal neoplasia. One of the biochemical activities associated with the APC protein is down-regulation of transcriptional activation mediated by beta-catenin and T cell transcription factor 4 (Tcf-4). The protein products of mutant APC genes present in colorectal tumors were found to be defective in this activity. Furthermore, colorectal tumors with intact APC genes were found to contain activating mutations of beta-catenin that altered functionally significant phosphorylation sites. These results indicate that regulation of beta-catenin is critical to APC's tumor suppressive effect and that this regulation can be circumvented by mutations in either APC or beta-catenin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Morin, P J -- Sparks, A B -- Korinek, V -- Barker, N -- Clevers, H -- Vogelstein, B -- Kinzler, K W -- CA57345/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1997 Mar 21;275(5307):1787-90.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Johns Hopkins Oncology Center, 424 North Bond Street, Baltimore, MD 21231, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9065402" target="_blank"〉PubMed〈/a〉
    Keywords: Adenomatous Polyposis Coli Protein ; Colonic Neoplasms/*genetics/metabolism ; Cytoskeletal Proteins/*genetics/*metabolism ; Gene Expression Regulation, Neoplastic ; *Genes, APC ; Genes, Reporter ; Germ-Line Mutation ; Humans ; Mutation ; Phosphorylation ; Signal Transduction ; TCF Transcription Factors ; *Trans-Activators ; Transcription Factor 7-Like 2 Protein ; Transcription Factors/*metabolism ; *Transcription, Genetic ; Transfection ; Tumor Cells, Cultured ; beta Catenin
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    Evolutionary psychologists look for roots of cognition (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-01-03
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Williams, N -- New York, N.Y. -- Science. 1997 Jan 3;275(5296):29-30.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8999531" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Behavior, Animal ; *Biological Evolution ; Birds ; *Cognition ; Female ; Humans ; Macaca mulatta/psychology ; Male ; Memory ; Reward ; *Social Sciences
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    Targeting of HIV- and SIV-infected cells by CD4-chemokine receptor pseudotypes (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-12-31
    Description: Retroviral vectors containing CD4 and an appropriate chemokine receptor were evaluated for the ability to transduce cells infected with human immunodeficiency virus (HIV) and simian immunodeficiency virus (SIV). These CD4-chemokine receptor pseudotypes were able to target HIV- and SIV-infected cell lines and monocyte-derived macrophages in a manner that corresponded to the specificity of the viral envelope glycoprotein for its CD4-chemokine receptor complex. This approach could offer a way to deliver antiviral genes directly to HIV-infected cells in vivo and could provide an additional treatment strategy in conjunction with existing antiviral therapies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Endres, M J -- Jaffer, S -- Haggarty, B -- Turner, J D -- Doranz, B J -- O'Brien, P J -- Kolson, D L -- Hoxie, J A -- AI33854/AI/NIAID NIH HHS/ -- AI40880/AI/NIAID NIH HHS/ -- HL 07439/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1997 Nov 21;278(5342):1462-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Hematology-Oncology Division, University of Pennsylvania, Philadelphia, PA 19104, USA. endres@mail.med.upenn.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9367958" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD4/*genetics/metabolism ; Cell Line ; Gene Products, env/metabolism ; *Gene Transfer Techniques ; *Genetic Vectors ; HIV-1/*physiology ; Humans ; Macrophages/virology ; Plasmids ; Receptors, CCR5/genetics/metabolism ; Receptors, CXCR4/genetics/metabolism ; Receptors, Chemokine/*genetics/metabolism ; Simian Immunodeficiency Virus/*physiology ; Transfection
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    Getting the brain's attention (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-10-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wickelgren, I -- New York, N.Y. -- Science. 1997 Oct 3;278(5335):35-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9340756" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Attention/*physiology ; Brain/*physiology ; Dopamine/*physiology ; Emotions/*physiology ; Female ; Humans ; Learning/*physiology ; Male ; Memory/physiology ; Neurons/physiology ; Nucleus Accumbens/physiology ; Prefrontal Cortex/physiology ; *Reward ; Ventral Tegmental Area/physiology
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    Prevention of apoptosis by Bcl-2: release of cytochrome c from mitochondria blocked (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-02-21
    Description: Bcl-2 is an integral membrane protein located mainly on the outer membrane of mitochondria. Overexpression of Bcl-2 prevents cells from undergoing apoptosis in response to a variety of stimuli. Cytosolic cytochrome c is necessary for the initiation of the apoptotic program, suggesting a possible connection between Bcl-2 and cytochrome c, which is normally located in the mitochondrial intermembrane space. Cells undergoing apoptosis were found to have an elevation of cytochrome c in the cytosol and a corresponding decrease in the mitochondria. Overexpression of Bcl-2 prevented the efflux of cytochrome c from the mitochondria and the initiation of apoptosis. Thus, one possible role of Bcl-2 in prevention of apoptosis is to block cytochrome c release from mitochondria.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yang, J -- Liu, X -- Bhalla, K -- Kim, C N -- Ibrado, A M -- Cai, J -- Peng, T I -- Jones, D P -- Wang, X -- New York, N.Y. -- Science. 1997 Feb 21;275(5303):1129-32.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, Emory University School of Medicine, Atlanta, GA 30322, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9027314" target="_blank"〉PubMed〈/a〉
    Keywords: Apoproteins/metabolism ; *Apoptosis ; Caspase 3 ; *Caspases ; Cysteine Endopeptidases/metabolism ; Cytochrome c Group/*metabolism ; Cytochromes c ; Cytosol/metabolism ; DNA Fragmentation ; Enzyme Activation ; Etoposide/pharmacology ; HL-60 Cells ; HeLa Cells ; Humans ; Intracellular Membranes/metabolism ; Membrane Potentials/drug effects ; Mitochondria/*metabolism ; Poly(ADP-ribose) Polymerases/metabolism ; Proto-Oncogene Proteins c-bcl-2/genetics/*metabolism ; Staurosporine/pharmacology ; Transfection
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    Nuclear export of NF-ATc enhanced by glycogen synthase kinase-3 (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-03-28
    Description: The transcription factor NF-AT responds to Ca2+-calcineurin signals by translocating to the nucleus, where it participates in the activation of early immune response genes. Calcineurin dephosphorylates conserved serine residues in the amino terminus of NF-AT, resulting in nuclear import. Purification of the NF-AT kinase revealed that it is composed of a priming kinase activity and glycogen synthase kinase-3 (GSK-3). GSK-3 phosphorylates conserved serines necessary for nuclear export, promotes nuclear exit, and thereby opposes Ca2+-calcineurin signaling. Because GSK-3 responds to signals initiated by Wnt and other ligands, NF-AT family members could be effectors of these pathways.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Beals, C R -- Sheridan, C M -- Turck, C W -- Gardner, P -- Crabtree, G R -- New York, N.Y. -- Science. 1997 Mar 28;275(5308):1930-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Developmental Biology, Stanford University, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9072970" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Biological Transport ; Brain/enzymology ; COS Cells ; Calcineurin ; Calcium/metabolism ; Calcium-Calmodulin-Dependent Protein Kinases/*metabolism ; Calmodulin-Binding Proteins/metabolism ; Cell Nucleus/*metabolism ; Cloning, Molecular ; Cyclic AMP-Dependent Protein Kinases/metabolism ; DNA-Binding Proteins/genetics/*metabolism ; Glycogen Synthase Kinase 3 ; Glycogen Synthase Kinases ; Humans ; Molecular Sequence Data ; NFATC Transcription Factors ; *Nuclear Proteins ; Phosphoprotein Phosphatases/metabolism ; Phosphorylation ; Rats ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Transcription Factors/genetics/*metabolism ; Transfection
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    Activation of SAPK/JNK by TNF receptor 1 through a noncytotoxic TRAF2-dependent pathway (1997)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1997-01-10
    Description: Interaction of the p55 tumor necrosis factor receptor 1 (TNF-R1)-associated signal transducer TRADD with FADD signals apoptosis, whereas the TNF receptor-associated factor 2 protein (TRAF2) is required for activation of the nuclear transcription factor nuclear factor kappa B. TNF-induced activation of the stress-activated protein kinase (SAPK) was shown to occur through a noncytotoxic TRAF2-dependent pathway. TRAF2 was both sufficient and necessary for activation of SAPK by TNF-R1; conversely, expression of a dominant-negative FADD mutant, which blocks apoptosis, did not interfere with SAPK activation. Therefore, SAPK activation occurs through a pathway that is not required for TNF-R1-induced apoptosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Natoli, G -- Costanzo, A -- Ianni, A -- Templeton, D J -- Woodgett, J R -- Balsano, C -- Levrero, M -- New York, N.Y. -- Science. 1997 Jan 10;275(5297):200-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Fondazione Andrea Cesalpino and Istituto di I Clinica Medica, Policlinico Umberto I, Viale del Policlinico 155, 00161 Rome, Italy.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8985011" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcysteine/pharmacology ; *Adaptor Proteins, Signal Transducing ; Apoptosis ; Calcium-Calmodulin-Dependent Protein Kinases/*metabolism ; Carrier Proteins/metabolism ; Cell Line ; Dactinomycin/pharmacology ; Enzyme Activation ; Fas-Associated Death Domain Protein ; Free Radical Scavengers/pharmacology ; HeLa Cells ; Humans ; JNK Mitogen-Activated Protein Kinases ; *MAP Kinase Kinase Kinase 1 ; *Mitogen-Activated Protein Kinases ; NF-kappa B/metabolism ; Protein-Serine-Threonine Kinases/metabolism ; Proteins/*metabolism ; Reactive Oxygen Species/metabolism ; Receptors, Tumor Necrosis Factor/*metabolism ; Recombinant Proteins/pharmacology ; Signal Transduction ; TNF Receptor-Associated Factor 1 ; TNF Receptor-Associated Factor 2 ; Transfection ; Tumor Necrosis Factor-alpha/*pharmacology
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    Deciding advantageously before knowing the advantageous strategy (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-02-28
    Description: Deciding advantageously in a complex situation is thought to require overt reasoning on declarative knowledge, namely, on facts pertaining to premises, options for action, and outcomes of actions that embody the pertinent previous experience. An alternative possibility was investigated: that overt reasoning is preceded by a nonconscious biasing step that uses neural systems other than those that support declarative knowledge. Normal participants and patients with prefrontal damage and decision-making defects performed a gambling task in which behavioral, psychophysiological, and self-account measures were obtained in parallel. Normals began to choose advantageously before they realized which strategy worked best, whereas prefrontal patients continued to choose disadvantageously even after they knew the correct strategy. Moreover, normals began to generate anticipatory skin conductance responses (SCRs) whenever they pondered a choice that turned out to be risky, before they knew explicitly that it was a risky choice, whereas patients never developed anticipatory SCRs, although some eventually realized which choices were risky. The results suggest that, in normal individuals, nonconscious biases guide behavior before conscious knowledge does. Without the help of such biases, overt knowledge may be insufficient to ensure advantageous behavior.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bechara, A -- Damasio, H -- Tranel, D -- Damasio, A R -- P01 NS19632/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1997 Feb 28;275(5304):1293-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, Division of Behavioral Neurology and Cognitive Neuroscience, University of Iowa College of Medicine, Iowa City, IA 52242, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9036851" target="_blank"〉PubMed〈/a〉
    Keywords: Aged ; Brain Damage, Chronic/physiopathology/psychology ; *Decision Making ; Female ; Galvanic Skin Response ; Gambling/psychology ; Humans ; *Intuition ; Male ; Middle Aged ; Prefrontal Cortex/*physiology/physiopathology ; *Unconscious (Psychology)
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    Synergy paper questioned at toxicology meeting (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-03-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaiser, J -- New York, N.Y. -- Science. 1997 Mar 28;275(5308):1879.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9122688" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chlordan/metabolism/pharmacology ; Dieldrin/metabolism/pharmacology ; Drug Synergism ; Endosulfan/metabolism/pharmacology ; Estrogens, Non-Steroidal/metabolism/*pharmacology ; Female ; Humans ; Insecticides/metabolism/*pharmacology ; Receptors, Estrogen/*drug effects/metabolism ; Reproducibility of Results ; Tumor Cells, Cultured
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Forty-something breast screening (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-03-14
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sickles, E A -- New York, N.Y. -- Science. 1997 Mar 14;275(5306):1549.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9072815" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Age Factors ; Breast Neoplasms/*prevention & control ; Female ; Humans ; *Mammography ; *Mass Screening ; Middle Aged
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    The importance of a well-groomed child (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-10-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sapolsky, R M -- New York, N.Y. -- Science. 1997 Sep 12;277(5332):1620-1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Stanford University, Stanford, CA 94305, USA. sapolsky@leland.stanford.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9312858" target="_blank"〉PubMed〈/a〉
    Keywords: Aging ; Animals ; Animals, Newborn ; *Behavior, Animal ; Corticotropin-Releasing Hormone/metabolism ; Female ; Glucocorticoids/secretion ; *Grooming ; *Handling (Psychology) ; Hippocampus/physiology ; Humans ; *Maternal Behavior ; Rats ; Receptors, Glucocorticoid/metabolism
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    The inverse association between tuberculin responses and atopic disorder (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-01-03
    Description: Human immune responses are heterogeneous and may involve antagonism between T helper (TH) lymphocyte subsets and their cytokines. Atopy is characterized by immediate immunoglobulin E (IgE)-mediated hypersensitivity to agents such as dust mites and pollen, and it underlies the increasingly prevalent disorder asthma. Among Japanese schoolchildren, there was a strong inverse association between delayed hypersensitivity to Mycobacterium tuberculosis and atopy. Positive tuberculin responses predicted a lower incidence of asthma, lower serum IgE levels, and cytokine profiles biased toward TH1 type. Exposure and response to M. tuberculosis may, by modification of immune profiles, inhibit atopic disorder.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shirakawa, T -- Enomoto, T -- Shimazu, S -- Hopkin, J M -- New York, N.Y. -- Science. 1997 Jan 3;275(5296):77-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Lung Research Laboratory, Osler Chest Unit, Churchill Hospital, Oxford OX3 7LJ, UK. jhopkin@immsvr.jr2.ox.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8974396" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Asthma/epidemiology/etiology/immunology ; BCG Vaccine/immunology ; Child ; Confounding Factors (Epidemiology) ; Cytokines/blood ; Female ; Humans ; Hypersensitivity, Delayed/*immunology ; Hypersensitivity, Immediate/epidemiology/*etiology/immunology ; Immunoglobulin E/blood ; Interferon-gamma/blood ; Japan/epidemiology ; Male ; Th1 Cells/immunology ; Th2 Cells/immunology ; Tuberculin/*immunology ; Tuberculin Test ; Tuberculosis/*epidemiology/immunology
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    Bcl-2: prolonging life in a transgenic mouse model of familial amyotrophic lateral sclerosis (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-07-25
    Description: Mutations in the gene encoding copper/zinc superoxide dismutase enzyme produce an animal model of familial amyotrophic lateral sclerosis (FALS), a fatal disorder characterized by paralysis. Overexpression of the proto-oncogene bcl-2 delayed onset of motor neuron disease and prolonged survival in transgenic mice expressing the FALS-linked mutation in which glycine is substituted by alanine at position 93. It did not, however, alter the duration of the disease. Overexpression of bcl-2 also attenuated the magnitude of spinal cord motor neuron degeneration in the FALS-transgenic mice.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kostic, V -- Jackson-Lewis, V -- de Bilbao, F -- Dubois-Dauphin, M -- Przedborski, S -- NS01724/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1997 Jul 25;277(5325):559-62.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, Columbia University, 650 West 168 Street, BB-307, New York, NY 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9228005" target="_blank"〉PubMed〈/a〉
    Keywords: Amyotrophic Lateral Sclerosis/genetics/mortality/pathology/*therapy ; Animals ; Disease Models, Animal ; Female ; *Gene Expression ; *Genes, bcl-2 ; *Genetic Therapy ; Humans ; Male ; Mice ; Mice, Transgenic ; Motor Neurons/pathology ; Nerve Degeneration ; Proto-Oncogene Proteins c-bcl-2/*physiology ; Proto-Oncogene Proteins c-jun/analysis ; Spinal Cord/pathology ; Superoxide Dismutase/genetics/metabolism ; Survival Rate ; Ubiquitins/analysis
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    Breast-screening brawl (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-03-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kopans, D B -- New York, N.Y. -- Science. 1997 Mar 21;275(5307):1721-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9122674" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Breast Neoplasms/*mortality/prevention & control/radiography ; Female ; Humans ; Mammography/*statistics & numerical data ; Mass Screening/*statistics & numerical data ; Middle Aged ; Randomized Controlled Trials as Topic
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    Regulation of human placental development by oxygen tension (1997)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1997-09-12
    Description: Cytotrophoblasts, specialized placental cells, proliferate early in pregnancy and then differentiate into tumor-like cells that establish blood flow to the placenta by invading the uterus and its vasculature. In this study, cytotrophoblasts cultured under hypoxic conditions (2 percent oxygen), mimicking the environment near the uterine surface before 10 weeks of gestation, continued proliferating and differentiated poorly. When cultured in 20 percent oxygen, mimicking the environment near uterine arterioles, the cells stopped proliferating and differentiated normally. Thus, oxygen tension determines whether cytotrophoblasts proliferate or invade, thereby regulating placental growth and cellular architecture.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Genbacev, O -- Zhou, Y -- Ludlow, J W -- Fisher, S J -- CA 56904/CA/NCI NIH HHS/ -- HD30367/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1997 Sep 12;277(5332):1669-72.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Stomatology, University of California, San Francisco, CA 94143-0512, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9287221" target="_blank"〉PubMed〈/a〉
    Keywords: Antigens, CD/biosynthesis ; Cell Differentiation ; Cell Division ; Cell Hypoxia ; Chorionic Villi/growth & development ; Cyclin-Dependent Kinase Inhibitor p21 ; Cyclins/biosynthesis ; Female ; Humans ; Integrin alpha1 ; Mitosis ; Organ Culture Techniques ; Oxygen/*physiology ; Placenta/blood supply/cytology ; Placental Lactogen/analysis ; *Placentation ; Pregnancy ; S Phase ; Trophoblasts/*cytology/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    An antagonist decoy receptor and a death domain-containing receptor for TRAIL (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-08-08
    Description: TRAIL, also called Apo2L, is a cytotoxic protein that induces apoptosis of many transformed cell lines but not of normal tissues, even though its death domain-containing receptor, DR4, is expressed on both cell types. An antagonist decoy receptor (designated as TRID for TRAIL receptor without an intracellular domain) that may explain the resistant phenotype of normal tissues was identified. TRID is a distinct gene product with an extracellular TRAIL-binding domain and a transmembrane domain but no intracellular signaling domain. TRID transcripts were detected in many normal human tissues but not in most cancer cell lines examined. Ectopic expression of TRID protected mammalian cells from TRAIL-induced apoptosis, which is consistent with a protective role. Another death domain-containing receptor for TRAIL (designated as death receptor-5), which preferentially engaged a FLICE (caspase-8)-related death protease, was also identified.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pan, G -- Ni, J -- Wei, Y F -- Yu, G -- Gentz, R -- Dixit, V M -- ES08111/ES/NIEHS NIH HHS/ -- New York, N.Y. -- Science. 1997 Aug 8;277(5327):815-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, University of Michigan Medical School, Ann Arbor, MI, 48109, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9242610" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; *Apoptosis ; Apoptosis Regulatory Proteins ; Caspase 10 ; Caspase 8 ; Caspase 9 ; *Caspases ; Cell Line, Transformed ; Cysteine Endopeptidases/metabolism ; GPI-Linked Proteins ; HeLa Cells ; Humans ; Ligands ; Membrane Glycoproteins/*metabolism ; Molecular Sequence Data ; Protein Sorting Signals ; Receptors, TNF-Related Apoptosis-Inducing Ligand ; Receptors, Tumor Necrosis Factor/chemistry/genetics/*metabolism ; Sequence Alignment ; Signal Transduction ; TNF-Related Apoptosis-Inducing Ligand ; Transfection ; Tumor Cells, Cultured ; Tumor Necrosis Factor Decoy Receptors ; Tumor Necrosis Factor-alpha/*metabolism
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    Induction of cell migration by matrix metalloprotease-2 cleavage of laminin-5 (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-07-11
    Description: Structural changes in the extracellular matrix are necessary for cell migration during tissue remodeling and tumor invasion. Specific cleavage of laminin-5 (Ln-5) by matrix metalloprotease-2 (MMP2) was shown to induce migration of breast epithelial cells. MMP2 cleaved the Ln-5 gamma2 subunit at residue 587, exposing a putative cryptic promigratory site on Ln-5 that triggers cell motility. This altered form of Ln-5 is found in tumors and in tissues undergoing remodeling, but not in quiescent tissues. Cleavage of Ln-5 by MMP2 and the resulting activation of the Ln-5 cryptic site may provide new targets for modulation of tumor cell invasion and tissue remodeling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Giannelli, G -- Falk-Marzillier, J -- Schiraldi, O -- Stetler-Stevenson, W G -- Quaranta, V -- CA47858/CA/NCI NIH HHS/ -- DE10063/DE/NIDCR NIH HHS/ -- New York, N.Y. -- Science. 1997 Jul 11;277(5323):225-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, 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/9211848" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Breast/*cytology/metabolism ; Cell Adhesion ; Cell Adhesion Molecules/*metabolism ; Cell Division ; Cell Line ; *Cell Movement ; Cell Size ; Collagenases/metabolism ; Epithelial Cells ; Epithelium/metabolism ; Extracellular Matrix/*metabolism ; Female ; Fibrinolysin/metabolism ; Gelatinases/antagonists & inhibitors/*metabolism ; Humans ; Matrix Metalloproteinase 2 ; Matrix Metalloproteinase 9 ; Metalloendopeptidases/antagonists & inhibitors/*metabolism ; Mice ; Phenylalanine/analogs & derivatives/pharmacology ; Protease Inhibitors/pharmacology ; Rats ; Recombinant Fusion Proteins/metabolism ; Skin Neoplasms/metabolism/pathology ; Thiophenes/pharmacology
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    Association of mutations in a lysosomal protein with classical late-infantile neuronal ceroid lipofuscinosis (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-09-20
    Description: Classical late-infantile neuronal ceroid lipofuscinosis (LINCL) is a fatal neurodegenerative disease whose defective gene has remained elusive. A molecular basis for LINCL was determined with an approach applicable to other lysosomal storage diseases. When the mannose 6-phosphate modification of newly synthesized lysosomal enzymes was used as an affinity marker, a single protein was identified that is absent in LINCL. Sequence comparisons suggest that this protein is a pepstatin-insensitive lysosomal peptidase, and a corresponding enzymatic activity was deficient in LINCL autopsy specimens. Mutations in the gene encoding this protein were identified in LINCL patients but not in normal controls.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sleat, D E -- Donnelly, R J -- Lackland, H -- Liu, C G -- Sohar, I -- Pullarkat, R K -- Lobel, P -- DK45992/DK/NIDDK NIH HHS/ -- NS30147/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1997 Sep 19;277(5333):1802-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Advanced Biotechnology and Medicine, Piscataway, NJ 08854, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9295267" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Aminopeptidases ; Chromosome Mapping ; Chromosomes, Human, Pair 11 ; Codon ; Dipeptidyl-Peptidases and Tripeptidyl-Peptidases ; Endopeptidases ; Female ; Glycosylation ; Humans ; Isoelectric Point ; Lysosomes/*enzymology ; Male ; Mannosephosphates/analysis ; Molecular Sequence Data ; Molecular Weight ; *Mutation ; Neuronal Ceroid-Lipofuscinoses/enzymology/*genetics ; Pepstatins/pharmacology ; Peptide Hydrolases/*chemistry/deficiency/*genetics ; Polymerase Chain Reaction ; Serine Proteases
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    The receptor for the cytotoxic ligand TRAIL (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-04-04
    Description: TRAIL (also known as Apo-2L) is a member of the tumor necrosis factor (TNF) ligand family that rapidly induces apoptosis in a variety of transformed cell lines. The human receptor for TRAIL was found to be an undescribed member of the TNF-receptor family (designated death receptor-4, DR4) that contains a cytoplasmic "death domain" capable of engaging the cell suicide apparatus but not the nuclear factor kappa B pathway in the system studied. Unlike Fas, TNFR-1, and DR3, DR4 could not use FADD to transmit the death signal, suggesting the use of distinct proximal signaling machinery. Thus, the DR4-TRAIL axis defines another receptor-ligand pair involved in regulating cell suicide and tissue homeostasis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pan, G -- O'Rourke, K -- Chinnaiyan, A M -- Gentz, R -- Ebner, R -- Ni, J -- Dixit, V M -- DAMD17-96-1-6085/DA/NIDA NIH HHS/ -- ES08111/ES/NIEHS NIH HHS/ -- New York, N.Y. -- Science. 1997 Apr 4;276(5309):111-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, University of Michigan Medical School, Ann Arbor, MI 48109, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9082980" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptor Proteins, Signal Transducing ; Amino Acid Sequence ; *Apoptosis ; Apoptosis Regulatory Proteins ; Carrier Proteins/metabolism ; Cell Line ; Fas-Associated Death Domain Protein ; Humans ; Ligands ; Membrane Glycoproteins/*metabolism ; Molecular Sequence Data ; NF-kappa B/metabolism ; Proteins/metabolism ; RNA, Messenger/genetics/metabolism ; Receptor-Interacting Protein Serine-Threonine Kinases ; Receptors, TNF-Related Apoptosis-Inducing Ligand ; Receptors, Tumor Necrosis Factor/chemistry/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; TNF Receptor-Associated Factor 1 ; TNF-Related Apoptosis-Inducing Ligand ; Transfection ; Tumor Cells, Cultured ; Tumor Necrosis Factor-alpha/*metabolism
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    Maintenance of human T cell anergy: blocking of IL-2 gene transcription by activated Rap1 (1997)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1997-10-06
    Description: In the absence of costimulation, T cells activated through their antigen receptor become unresponsive (anergic) and do not transcribe the gene encoding interleukin-2 (IL-2) when restimulated with antigen. Anergic alloantigen-specific human T cells contained phosphorylated Cbl that coimmunoprecipitated with Fyn. The adapter protein CrkL was associated with both phosphorylated Cbl and the guanidine nucleotide-releasing factor C3G, which catalyzes guanosine triphosphate (GTP) exchange on Rap1. Active Rap1 (GTP-bound form) was present in anergic cells. Forced expression of low amounts of Rap1-GTP in Jurkat T cells recapitulated the anergic defect and blocked T cell antigen receptor (TCR)- and CD28-mediated IL-2 gene transcription. Therefore, Rap1 functions as a negative regulator of TCR-mediated IL-2 gene transcription and may be responsible for the specific defect in IL-2 production in T cell anergy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Boussiotis, V A -- Freeman, G J -- Berezovskaya, A -- Barber, D L -- Nadler, L M -- AI 35225/AI/NIAID NIH HHS/ -- AI39671/AI/NIAID NIH HHS/ -- HL 54785/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1997 Oct 3;278(5335):124-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Adult Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA. vassiliki_boussiotis@macmailgw.dfci.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9311917" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptor Proteins, Signal Transducing ; Antigens, CD28/immunology ; *Clonal Anergy ; GTP-Binding Proteins/*metabolism ; Gene Expression Regulation ; Guanine Nucleotide Exchange Factors ; Guanosine Triphosphate/metabolism ; Humans ; Interleukin-2/*genetics ; Jurkat Cells ; Nuclear Proteins/metabolism ; Phosphorylation ; Protein-Tyrosine Kinases/metabolism ; Proteins/metabolism ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins c-cbl ; Proto-Oncogene Proteins c-fyn ; Receptors, Antigen, T-Cell/immunology ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; T-Lymphocytes/*immunology/metabolism ; *Transcription, Genetic ; Transfection ; *Ubiquitin-Protein Ligases ; rap GTP-Binding Proteins ; ras Guanine Nucleotide Exchange Factors ; ras Proteins/metabolism ; src Homology Domains
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    Bone sizes trace the decline of man (and woman) (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-05-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gibbons, A -- New York, N.Y. -- Science. 1997 May 9;276(5314):896-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9163034" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Evolution ; *Body Constitution ; Body Weight ; Brain/*anatomy & histology ; Female ; Femur Head/*anatomy & histology ; *Fossils ; Hominidae/*anatomy & histology ; Humans ; Male
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    Ideas on human origins evolve at anthropology gathering (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-04-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gibbons, A -- New York, N.Y. -- Science. 1997 Apr 25;276(5312):535-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9148414" target="_blank"〉PubMed〈/a〉
    Keywords: Africa ; Animals ; Asia ; Biological Evolution ; Europe ; *Family ; Female ; Fossils ; *Haplotypes ; Hominidae/*genetics ; Humans ; *Longevity ; Male ; *Postmenopause
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    Defective TNF-alpha-induced apoptosis in STAT1-null cells due to low constitutive levels of caspases (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-12-31
    Description: Signal transducers and activators of transcription (STATs) enhance transcription of specific genes in response to cytokines and growth factors. STAT1 is also required for efficient constitutive expression of the caspases Ice, Cpp32, and Ich-1 in human fibroblasts. As a consequence, STAT1-null cells are resistant to apoptosis by tumor necrosis factor alpha (TNF-alpha). Reintroduction of STAT1alpha restored both TNF-alpha-induced apoptosis and the expression of Ice, Cpp32, and Ich-1. Variant STAT1 proteins carrying point mutations that inactivate domains required for STAT dimer formation nevertheless restored protease expression and sensitivity to apoptosis, indicating that the functions of STAT1 required for these activities are different from those that mediate induced gene expression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kumar, A -- Commane, M -- Flickinger, T W -- Horvath, C M -- Stark, G R -- P01 CA62220/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1997 Nov 28;278(5343):1630-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Lerner Research Institute, The Cleveland Clinic Foundation, Cleveland, OH 44195, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9374464" target="_blank"〉PubMed〈/a〉
    Keywords: *Apoptosis ; Caspase 1 ; Caspase 2 ; Caspase 3 ; *Caspases ; Cell Line ; Cysteine Endopeptidases/genetics/*metabolism ; DNA-Binding Proteins/chemistry/genetics/*metabolism ; Dactinomycin/pharmacology ; Dimerization ; Gene Expression Regulation, Enzymologic ; Humans ; Interferon-gamma/pharmacology ; Phosphorylation ; Point Mutation ; Proteins/genetics/*metabolism ; STAT1 Transcription Factor ; Signal Transduction ; Trans-Activators/chemistry/genetics/*metabolism ; Transfection ; Tumor Necrosis Factor-alpha/*pharmacology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 86
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    Transgenic knockout mice with exclusively human sickle hemoglobin and sickle cell disease (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-11-05
    Description: To create mice expressing exclusively human sickle hemoglobin (HbS), transgenic mice expressing human alpha-, gamma-, and betaS-globin were generated and bred with knockout mice that had deletions of the murine alpha- and beta-globin genes. These sickle cell mice have the major features (irreversibly sickled red cells, anemia, multiorgan pathology) found in humans with sickle cell disease and, as such, represent a useful in vivo system to accelerate the development of improved therapies for this common genetic disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Paszty, C -- Brion, C M -- Manci, E -- Witkowska, H E -- Stevens, M E -- Mohandas, N -- Rubin, E M -- HL20985/HL/NHLBI NIH HHS/ -- HL31579/HL/NHLBI NIH HHS/ -- N01-HB-07086/HB/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1997 Oct 31;278(5339):876-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Human Genome Center and Department of Subcellular Structure, Lawrence Berkeley National Laboratory, 1 Cyclotron Road (MS 74-157), University of California, Berkeley, CA 94720, USA. c_paszty@csa2.lbl.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9346488" target="_blank"〉PubMed〈/a〉
    Keywords: Anemia, Sickle Cell/*genetics/pathology ; Animals ; Disease Models, Animal ; Female ; Globins/genetics ; Hemoglobin, Sickle/genetics ; Humans ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Transgenic
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  • 87
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    LKLF: A transcriptional regulator of single-positive T cell quiescence and survival (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-09-26
    Description: Mature single-positive (SP) T lymphocytes enter a "resting" state in which they are proliferatively quiescent and relatively resistant to apoptosis. The molecular mechanisms regulating this quiescent phenotype were unknown. Here it was found that the expression of a Kruppel-like zinc finger transcription factor, lung Kruppel-like factor (LKLF), is developmentally induced during the maturation of SP quiescent T cells and rapidly extinguished after SP T cell activation. LKLF-deficient T cells produced by gene targeting had a spontaneously activated phenotype and died in the spleen and lymph nodes from Fas ligand-induced apoptosis. Thus, LKLF is required to program the quiescent state of SP T cells and to maintain their viability in the peripheral lymphoid organs and blood.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kuo, C T -- Veselits, M L -- Leiden, J M -- AI29637/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1997 Sep 26;277(5334):1986-90.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of Chicago, Chicago, IL 60637, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9302292" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD95/biosynthesis ; Apoptosis ; B-Lymphocytes/metabolism ; Cell Survival ; Chimera ; Fas Ligand Protein ; Gene Deletion ; Gene Targeting ; *Interphase ; Kruppel-Like Transcription Factors ; Lymph Nodes/cytology ; Lymphocyte Activation ; Membrane Glycoproteins/biosynthesis ; Mice ; Mice, Inbred C57BL ; Spleen/cytology ; T-Lymphocyte Subsets/metabolism ; T-Lymphocytes/*cytology/*immunology/metabolism ; Trans-Activators/biosynthesis/genetics/*physiology ; Transfection ; *Zinc Fingers
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  • 88
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    A TEL-JAK2 fusion protein with constitutive kinase activity in human leukemia (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-11-21
    Description: The Janus family of tyrosine kinases (JAK) plays an essential role in development and in coupling cytokine receptors to downstream intracellular signaling events. A t(9;12)(p24;p13) chromosomal translocation in a T cell childhood acute lymphoblastic leukemia patient was characterized and shown to fuse the 3' portion of JAK2 to the 5' region of TEL, a gene encoding a member of the ETS transcription factor family. The TEL-JAK2 fusion protein includes the catalytic domain of JAK2 and the TEL-specific oligomerization domain. TEL-induced oligomerization of TEL-JAK2 resulted in the constitutive activation of its tyrosine kinase activity and conferred cytokine-independent proliferation to the interleukin-3-dependent Ba/F3 hematopoietic cell line.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lacronique, V -- Boureux, A -- Valle, V D -- Poirel, H -- Quang, C T -- Mauchauffe, M -- Berthou, C -- Lessard, M -- Berger, R -- Ghysdael, J -- Bernard, O A -- New York, N.Y. -- Science. 1997 Nov 14;278(5341):1309-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉U 301 de l'Institut National de la Sante et de la Recherche Medicale and SD 401 No. 301 CNRS, Institut de Genetique Moleculaire, 27 rue Juliette Dodu, 75010 Paris, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9360930" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Biopolymers ; Cell Division ; Cell Line ; Child, Preschool ; DNA-Binding Proteins/chemistry/genetics/metabolism ; Enzyme Activation ; Humans ; Interleukin-3/physiology ; Janus Kinase 2 ; Leukemia-Lymphoma, Adult T-Cell/genetics/*metabolism ; Male ; Mice ; *Milk Proteins ; Molecular Sequence Data ; Oncogene Proteins, Fusion/chemistry/genetics/*metabolism ; Phosphorylation ; Protein-Tyrosine Kinases/chemistry/genetics/*metabolism ; *Proto-Oncogene Proteins ; Proto-Oncogene Proteins c-ets ; *Repressor Proteins ; STAT5 Transcription Factor ; Signal Transduction ; Trans-Activators/metabolism ; Transcription Factors/chemistry/genetics/metabolism ; Transfection ; Translocation, Genetic
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 89
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    Breast-screening brawl (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-03-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sowinski, J -- New York, N.Y. -- Science. 1997 Mar 21;275(5307):1721.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9122673" target="_blank"〉PubMed〈/a〉
    Keywords: Breast Neoplasms/*mortality/prevention & control/radiography ; Canada ; Female ; Humans ; Mammography/*statistics & numerical data ; Mass Screening/*statistics & numerical data ; Randomized Controlled Trials as Topic
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  • 90
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    Prevention of mucosal Escherichia coli infection by FimH-adhesin-based systemic vaccination (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-04-25
    Description: Virtually all uropathogenic strains of Escherichia coli, the primary cause of cystitis, assemble adhesive surface organelles called type 1 pili that contain the FimH adhesin. Sera from animals vaccinated with candidate FimH vaccines inhibited uropathogenic E. coli from binding to human bladder cells in vitro. Immunization with FimH reduced in vivo colonization of the bladder mucosa by more than 99 percent in a murine cystitis model, and immunoglobulin G to FimH was detected in urinary samples from protected mice. Furthermore, passive systemic administration of immune sera to FimH also resulted in reduced bladder colonization by uropathogenic E. coli. This approach may represent a means of preventing recurrent and acute infections of the urogenital mucosa.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Langermann, S -- Palaszynski, S -- Barnhart, M -- Auguste, G -- Pinkner, J S -- Burlein, J -- Barren, P -- Koenig, S -- Leath, S -- Jones, C H -- Hultgren, S J -- R01DK51406/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1997 Apr 25;276(5312):607-11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉MedImmune, Inc., Gaithersburg, MD 20878, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9110982" target="_blank"〉PubMed〈/a〉
    Keywords: Adhesins, Bacterial/*immunology/metabolism ; *Adhesins, Escherichia coli ; Animals ; Antibodies, Bacterial/analysis/immunology ; Bacterial Adhesion ; *Bacterial Vaccines/administration & dosage/immunology ; Child ; Cystitis/immunology/*prevention & control ; Epithelium/microbiology ; Escherichia coli/immunology/metabolism/pathogenicity ; Escherichia coli Infections/immunology/*prevention & control ; Female ; *Fimbriae Proteins ; Fimbriae, Bacterial/immunology ; Humans ; Immunity, Mucosal ; Mice ; Mice, Inbred C3H ; Neutrophils/immunology ; Rabbits ; Urinary Bladder/microbiology ; Vaccination ; *Vaccines, Synthetic/administration & dosage/immunology
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  • 91
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    The endocrinology of aging (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-10-23
    Description: Most aging individuals die from atherosclerosis, cancer, or dementia; but in the oldest old, loss of muscle strength resulting in frailty is the limiting factor for an individual's chances of living an independent life until death. Three hormonal systems show decreasing circulating hormone concentrations during normal aging: (i) estrogen (in menopause) and testosterone (in andropause), (ii) dehydroepiandrosterone and its sulphate (in adrenopause), and (iii) the growth hormone/insulin-like growth factor I axis (in somatopause). Physical changes during aging have been considered physiologic, but there is evidence that some of these changes are related to this decline in hormonal activity. Hormone replacement strategies have been developed, but many of their aspects remain controversial, and increasing blood hormone levels in aging individuals to those found during mid-adult life has not been uniformly proven to be safe and of benefit.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lamberts, S W -- van den Beld, A W -- van der Lely, A J -- New York, N.Y. -- Science. 1997 Oct 17;278(5337):419-24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Erasmus University, Rotterdam, Netherlands. lamberts@inw3.azr.nl〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9334293" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenal Glands/physiology ; Aged ; Aged, 80 and over ; Aging/*physiology ; Animals ; Climacteric/physiology ; Dehydroepiandrosterone/blood/therapeutic use ; Endocrine Glands/*physiology ; Estrogen Replacement Therapy ; Female ; Frail Elderly ; Human Growth Hormone/secretion/therapeutic use ; Humans ; Male ; Menopause/physiology ; Pituitary Gland/physiology ; Testosterone/blood/therapeutic use
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  • 92
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    Controlling cell death (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-02-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Golstein, P -- New York, N.Y. -- Science. 1997 Feb 21;275(5303):1081-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre d'Immunologie INSERM-CNRS de Marseille-Luminy, France. golstein@ciml.univ-mrs.fr〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9054009" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Apoptosis Regulatory Proteins ; Caenorhabditis elegans/cytology/metabolism ; *Caenorhabditis elegans Proteins ; Calcium-Binding Proteins/metabolism ; Caspase 1 ; *Caspases ; Cysteine Endopeptidases/metabolism ; Cytochrome c Group/metabolism ; Cytosol/metabolism ; Helminth Proteins/metabolism ; Membrane Glycoproteins/metabolism ; Mitochondria/metabolism ; Perforin ; Pore Forming Cytotoxic Proteins ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins c-bcl-2/metabolism ; Signal Transduction ; Transfection ; bcl-X Protein
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  • 93
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    The architecture of hearing (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-12-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennisi, E -- New York, N.Y. -- Science. 1997 Nov 14;278(5341):1223-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9411747" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptor Proteins, Signal Transducing ; Animals ; Carrier Proteins/*genetics/physiology ; Chromosome Mapping ; Cilia/ultrastructure ; Cochlea/metabolism ; Connexins/*genetics ; Deafness/*genetics/pathology ; Dyneins ; Female ; Gap Junctions/physiology/ultrastructure ; Genes, Recessive ; Hair Cells, Auditory/physiology/ultrastructure ; Humans ; Male ; Mice ; Mice, Neurologic Mutants ; Mutation ; Myosins/*genetics ; Pedigree
    Print ISSN: 0036-8075
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  • 94
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    Tyrosine phosphorylation of transmembrane ligands for Eph receptors (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-03-14
    Description: Axonal pathfinding in the nervous system is mediated in part by cell-to-cell signaling events involving members of the Eph receptor tyrosine kinase (RTK) family and their membrane-bound ligands. Genetic evidence suggests that transmembrane ligands may transduce signals in the developing embryo. The cytoplasmic domain of the transmembrane ligand Lerk2 became phosphorylated on tyrosine residues after contact with the Nuk/Cek5 receptor ectodomain, which suggests that Lerk2 has receptorlike intrinsic signaling potential. Moreover, Lerk2 is an in vivo substrate for the platelet-derived growth factor receptor, which suggests crosstalk between Lerk2 signaling and signaling cascades activated by tyrosine kinases. It is proposed that transmembrane ligands of Eph receptors act not only as conventional RTK ligands but also as receptorlike signaling molecules.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bruckner, K -- Pasquale, E B -- Klein, R -- EY10576/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 1997 Mar 14;275(5306):1640-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉European Molecular Biology Laboratory, Meyerhofstrasse 1, 69117 Heidelberg, Germany. USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9054357" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Animals ; Axons/physiology ; Brain-Derived Neurotrophic Factor/metabolism ; Cell Membrane/*metabolism ; Embryo, Mammalian/metabolism ; Ephrin-B1 ; Ligands ; Mice ; Phosphorylation ; Phosphotyrosine/*metabolism ; Platelet-Derived Growth Factor/pharmacology ; Proteins/*metabolism/pharmacology ; Receptor Protein-Tyrosine Kinases/*metabolism ; Receptor, Ciliary Neurotrophic Factor ; Receptor, EphB2 ; Receptors, Nerve Growth Factor/metabolism ; Receptors, Platelet-Derived Growth Factor/metabolism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Transfection
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  • 95
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    Phosphorylation of the translational repressor PHAS-I by the mammalian target of rapamycin (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-07-04
    Description: The immunosuppressant rapamycin interferes with G1-phase progression in lymphoid and other cell types by inhibiting the function of the mammalian target of rapamycin (mTOR). mTOR was determined to be a terminal kinase in a signaling pathway that couples mitogenic stimulation to the phosphorylation of the eukaryotic initiation factor (eIF)-4E-binding protein, PHAS-I. The rapamycin-sensitive protein kinase activity of mTOR was required for phosphorylation of PHAS-I in insulin-stimulated human embryonic kidney cells. mTOR phosphorylated PHAS-I on serine and threonine residues in vitro, and these modifications inhibited the binding of PHAS-I to eIF-4E. These studies define a role for mTOR in translational control and offer further insights into the mechanism whereby rapamycin inhibits G1-phase progression in mammalian cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brunn, G J -- Hudson, C C -- Sekulic, A -- Williams, J M -- Hosoi, H -- Houghton, P J -- Lawrence, J C Jr -- Abraham, R T -- AR41189/AR/NIAMS NIH HHS/ -- DK28312/DK/NIDDK NIH HHS/ -- DK50628/DK/NIDDK NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1997 Jul 4;277(5322):99-101.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of Virginia School of Medicine, Charlottesville, VA 22908, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9204908" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; Androstadienes/pharmacology ; Animals ; Carrier Proteins/pharmacology ; Cell Line ; DNA-Binding Proteins/pharmacology ; Eukaryotic Initiation Factor-4E ; G1 Phase ; Heat-Shock Proteins/pharmacology ; Humans ; Insulin/pharmacology ; Peptide Initiation Factors/metabolism ; Phosphoproteins/genetics/*metabolism ; Phosphorylation ; Phosphotransferases (Alcohol Group Acceptor)/antagonists & inhibitors/*metabolism ; Polyenes/*pharmacology ; *Protein Kinases ; Rats ; Recombinant Proteins/metabolism ; Repressor Proteins/genetics/*metabolism ; Signal Transduction ; Sirolimus ; TOR Serine-Threonine Kinases ; Tacrolimus Binding Proteins ; Transfection ; Tumor Cells, Cultured
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 96
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    Bison study marks radical shift for research council (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-06-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lawler, A -- New York, N.Y. -- Science. 1997 Jun 20;276(5320):1786-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9206837" target="_blank"〉PubMed〈/a〉
    Keywords: Abortion, Veterinary/microbiology ; Animals ; *Bison ; *Brucella abortus ; Brucellosis/epidemiology/transmission/*veterinary ; Brucellosis, Bovine/*transmission ; Cattle ; Female ; Montana/epidemiology ; *National Academy of Sciences (U.S.) ; Pregnancy ; Risk Factors ; United States
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  • 97
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    Newfound gene holds key to cell's cholesterol traffic (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-07-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennisi, E -- New York, N.Y. -- Science. 1997 Jul 11;277(5323):180-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9235630" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Carrier Proteins ; Child ; Cholesterol/*metabolism ; Chromosome Mapping ; *Chromosomes, Human, Pair 18 ; Disease Models, Animal ; Female ; Humans ; Male ; *Membrane Glycoproteins ; Mice ; Mice, Mutant Strains ; Niemann-Pick Diseases/*genetics/metabolism ; Proteins/chemistry/*genetics/physiology
    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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  • 98
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    New tumor suppressor found--twice (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-03-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennisi, E -- New York, N.Y. -- Science. 1997 Mar 28;275(5308):1876-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9122687" target="_blank"〉PubMed〈/a〉
    Keywords: Brain Neoplasms/genetics ; Breast Neoplasms/genetics ; Chromosome Mapping ; *Chromosomes, Human, Pair 10 ; Female ; Gene Deletion ; *Genes, Tumor Suppressor ; Glioma/genetics ; Humans ; Male ; Microfilament Proteins/chemistry/metabolism ; Neoplasms/*genetics ; Patents as Topic ; Prostatic Neoplasms/genetics ; Protein Tyrosine Phosphatases/chemistry/*genetics/metabolism/physiology ; Publishing ; Tumor Cells, Cultured
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 99
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    Identification of a gene that causes primary open angle glaucoma (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-01-31
    Description: Glaucoma is a major cause of blindness and is characterized by progressive degeneration of the optic nerve and is usually associated with elevated intraocular pressure. Analyses of sequence tagged site (STS) content and haplotype sharing between families affected with chromosome 1q-linked open angle glaucoma (GLC1A) were used to prioritize candidate genes for mutation screening. A gene encoding a trabecular meshwork protein (TIGR) mapped to the narrowest disease interval by STS content and radiation hybrid mapping. Thirteen glaucoma patients were found to have one of three mutations in this gene (3.9 percent of the population studied). One of these mutations was also found in a control individual (0.2 percent). Identification of these mutations will aid in early diagnosis, which is essential for optimal application of existing therapies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stone, E M -- Fingert, J H -- Alward, W L -- Nguyen, T D -- Polansky, J R -- Sunden, S L -- Nishimura, D -- Clark, A F -- Nystuen, A -- Nichols, B E -- Mackey, D A -- Ritch, R -- Kalenak, J W -- Craven, E R -- Sheffield, V C -- EY02477/EY/NEI NIH HHS/ -- EY08905/EY/NEI NIH HHS/ -- EY10564/EY/NEI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1997 Jan 31;275(5300):668-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Ophthalmology, University of Iowa College of Medicine, Iowa City, IA 52242, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9005853" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Chromosome Mapping ; Chromosomes, Artificial, Yeast ; *Chromosomes, Human, Pair 1 ; Cytoskeletal Proteins ; Eye Proteins/*genetics ; Female ; Genetic Linkage ; Glaucoma, Open-Angle/*genetics ; *Glycoproteins ; Haplotypes ; Humans ; Male ; Molecular Sequence Data ; Mutation ; Pedigree ; Polymerase Chain Reaction ; Polymorphism, Single-Stranded Conformational ; Sequence Tagged Sites ; Trabecular Meshwork/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 100
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    PTEN, a putative protein tyrosine phosphatase gene mutated in human brain, breast, and prostate cancer (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-03-28
    Description: Mapping of homozygous deletions on human chromosome 10q23 has led to the isolation of a candidate tumor suppressor gene, PTEN, that appears to be mutated at considerable frequency in human cancers. In preliminary screens, mutations of PTEN were detected in 31% (13/42) of glioblastoma cell lines and xenografts, 100% (4/4) of prostate cancer cell lines, 6% (4/65) of breast cancer cell lines and xenografts, and 17% (3/18) of primary glioblastomas. The predicted PTEN product has a protein tyrosine phosphatase domain and extensive homology to tensin, a protein that interacts with actin filaments at focal adhesions. These homologies suggest that PTEN may suppress tumor cell growth by antagonizing protein tyrosine kinases and may regulate tumor cell invasion and metastasis through interactions at focal adhesions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, J -- Yen, C -- Liaw, D -- Podsypanina, K -- Bose, S -- Wang, S I -- Puc, J -- Miliaresis, C -- Rodgers, L -- McCombie, R -- Bigner, S H -- Giovanella, B C -- Ittmann, M -- Tycko, B -- Hibshoosh, H -- Wigler, M H -- Parsons, R -- 5R35 CA39829/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1997 Mar 28;275(5308):1943-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, College of Physicians & Surgeons, 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/9072974" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Brain Neoplasms/genetics ; Breast Neoplasms/genetics ; Chromosome Mapping ; *Chromosomes, Human, Pair 10 ; Female ; Frameshift Mutation ; *Genes, Tumor Suppressor ; Glioblastoma/genetics ; Humans ; Male ; Microfilament Proteins/chemistry ; Molecular Sequence Data ; *Mutation ; Neoplasm Transplantation ; Neoplasms/*genetics ; PTEN Phosphohydrolase ; *Phosphoric Monoester Hydrolases ; Phosphotyrosine/metabolism ; Prostatic Neoplasms/genetics ; Protein Tyrosine Phosphatases/chemistry/*genetics/physiology ; Protein-Tyrosine Kinases/antagonists & inhibitors ; Sequence Deletion ; Sequence Homology, Amino Acid ; Transplantation, Heterologous ; Tumor Cells, Cultured ; *Tumor Suppressor Proteins
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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