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  • American Physical Society (APS)
  • American Association for the Advancement of Science (AAAS)
  • 1995-1999  (104)
  • 1
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    Friedreich's ataxia: autosomal recessive disease caused by an intronic GAA triplet repeat expansion (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-03-08
    Description: Friedreich's ataxia (FRDA) is an autosomal recessive, degenerative disease that involves the central and peripheral nervous systems and the heart. A gene, X25, was identified in the critical region for the FRDA locus on chromosome 9q13. This gene encodes a 210-amino acid protein, frataxin, that has homologs in distant species such as Caenorhabditis elegans and yeast. A few FRDA patients were found to have point mutations in X25, but the majority were homozygous for an unstable GAA trinucleotide expansion in the first X25 intron.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Campuzano, V -- Montermini, L -- Molto, M D -- Pianese, L -- Cossee, M -- Cavalcanti, F -- Monros, E -- Rodius, F -- Duclos, F -- Monticelli, A -- Zara, F -- Canizares, J -- Koutnikova, H -- Bidichandani, S I -- Gellera, C -- Brice, A -- Trouillas, P -- De Michele, G -- Filla, A -- De Frutos, R -- Palau, F -- Patel, P I -- Di Donato, S -- Mandel, J L -- Cocozza, S -- Koenig, M -- Pandolfo, M -- 722/Telethon/Italy -- NS34192/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1996 Mar 8;271(5254):1423-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department de Genetica, University of Valencia, Spain.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8596916" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Amino Acid Sequence ; Base Sequence ; Chromosomes, Human, Pair 9/*genetics ; DNA Primers ; Female ; Friedreich Ataxia/*genetics ; Genes, Recessive ; Heterozygote ; Humans ; *Introns ; *Iron-Binding Proteins ; Male ; Molecular Sequence Data ; Pedigree ; Point Mutation ; Polymerase Chain Reaction ; Proteins/chemistry/*genetics ; Sequence Alignment ; *Trinucleotide Repeats
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
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    T cell telomere length in HIV-1 infection: no evidence for increased CD4+ T cell turnover (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-11-29
    Description: Progression to acquired immunodeficiency syndrome (AIDS) has been related to exhaustion of the regenerative capacity of the immune system resulting from high T cell turnover. Analysis of telomeric terminal restriction fragment (TRF) length, a marker for cellular replicative history, showed that CD8(+) T cell TRF length decreased but CD4(+) T cell TRF length was stable during the course of human immunodeficiency virus type-1 (HIV-1) infection, which was not explained by differential telomerase activity. This observation provides evidence that turnover in the course of HIV-1 infection can be increased considerably in CD8(+) T cells, but not in CD4(+) T cells. These results are compatible with CD4(+) T cell decline in HIV-1 infection caused by interference with cell renewal.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wolthers, K C -- Bea, G -- Wisman, A -- Otto, S A -- de Roda Husman, A M -- Schaft, N -- de Wolf, F -- Goudsmit, J -- Coutinho, R A -- van der Zee, A G -- Meyaard, L -- Miedema, F -- New York, N.Y. -- Science. 1996 Nov 29;274(5292):1543-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Clinical Viro-Immunology, Central Laboratory of the Netherlands Red Cross Blood Transfusion Service, Amsterdam, The Netherlands. clbkvi@xs4all.nl〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8929418" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/*blood ; CD4 Lymphocyte Count ; CD4-Positive T-Lymphocytes/enzymology/immunology/*pathology/ultrastructure ; CD8-Positive T-Lymphocytes/enzymology/immunology/*pathology/ultrastructure ; Cell Death ; Cell Division ; Cross-Sectional Studies ; Disease Progression ; HIV Infections/blood/*immunology ; *Hiv-1 ; Humans ; Leukocytes, Mononuclear/enzymology/pathology/ultrastructure ; Lymphocyte Count ; Male ; Matched-Pair Analysis ; Telomerase/blood ; Telomere/*ultrastructure
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    Role of phosphorylation in regulation of the assembly of endocytic coat complexes (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-08-07
    Description: Clathrin-mediated endocytosis involves cycles of assembly and disassembly of clathrin coat components and their accessory proteins. Dephosphorylation of rat brain extract was shown to promote the assembly of dynamin 1, synaptojanin 1, and amphiphysin into complexes that also included clathrin and AP-2. Phosphorylation of dynamin 1 and synaptojanin 1 inhibited their binding to amphiphysin, whereas phosphorylation of amphiphysin inhibited its binding to AP-2 and clathrin. Thus, phosphorylation regulates the association and dissociation cycle of the clathrin-based endocytic machinery, and calcium-dependent dephosphorylation of endocytic proteins could prepare nerve terminals for a burst of endocytosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Slepnev, V I -- Ochoa, G C -- Butler, M H -- Grabs, D -- De Camilli, P -- CA46128/CA/NCI NIH HHS/ -- NS36251/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1998 Aug 7;281(5378):821-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Cell Biology, Yale University School of Medicine, 295 Congress Avenue, New Haven, CT 06510, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9694653" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Protein Complex alpha Subunits ; Adaptor Protein Complex beta Subunits ; Adaptor Proteins, Vesicular Transport ; Adenosine Triphosphate/metabolism ; Animals ; Binding Sites ; Carbazoles/pharmacology ; Chromatography, Affinity ; Clathrin/*metabolism ; Cyclosporine/pharmacology ; Dimerization ; Dynamin I ; Dynamins ; *Endocytosis ; Enzyme Inhibitors/pharmacology ; GTP Phosphohydrolases/*metabolism ; Indole Alkaloids ; Membrane Proteins/*metabolism ; Nerve Tissue Proteins/*metabolism ; Phosphoric Monoester Hydrolases/*metabolism ; Rats ; Recombinant Fusion Proteins/metabolism ; src Homology Domains
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    FADD: essential for embryo development and signaling from some, but not all, inducers of apoptosis (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-04-16
    Description: FADD (also known as Mort-1) is a signal transducer downstream of cell death receptor CD95 (also called Fas). CD95, tumor necrosis factor receptor type 1 (TNFR-1), and death receptor 3 (DR3) did not induce apoptosis in FADD-deficient embryonic fibroblasts, whereas DR4, oncogenes E1A and c-myc, and chemotherapeutic agent adriamycin did. Mice with a deletion in the FADD gene did not survive beyond day 11.5 of embryogenesis; these mice showed signs of cardiac failure and abdominal hemorrhage. Chimeric embryos showing a high contribution of FADD null mutant cells to the heart reproduce the phenotype of FADD-deficient mutants. Thus, not only death receptors, but also receptors that couple to developmental programs, may use FADD for signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yeh, W C -- de la Pompa, J L -- McCurrach, M E -- Shu, H B -- Elia, A J -- Shahinian, A -- Ng, M -- Wakeham, A -- Khoo, W -- Mitchell, K -- El-Deiry, W S -- Lowe, S W -- Goeddel, D V -- Mak, T W -- CA13106/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1998 Mar 20;279(5358):1954-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Amgen Institute, University of Toronto, Toronto, Ontario, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9506948" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptor Proteins, Signal Transducing ; Animals ; Antigens, CD95/genetics/physiology ; *Apoptosis ; Carrier Proteins/genetics/*physiology ; Cell Transformation, Neoplastic ; Cells, Cultured ; Doxorubicin/pharmacology ; *Embryonic and Fetal Development ; Endothelium, Vascular/embryology ; Fas-Associated Death Domain Protein ; Female ; Gene Expression ; Gene Targeting ; Heart/*embryology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Mutation ; Oncogenes ; Receptors, Tumor Necrosis Factor/genetics/physiology ; Signal Transduction ; Tumor Necrosis Factor-alpha/pharmacology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    Cloned transgenic calves produced from nonquiescent fetal fibroblasts (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-06-20
    Description: An efficient system for genetic modification and large-scale cloning of cattle is of importance for agriculture, biotechnology, and human medicine. Here, actively dividing fetal fibroblasts were genetically modified with a marker gene, a clonal line was selected, and the cells were fused to enucleated mature oocytes. Out of 28 embryos transferred to 11 recipient cows, three healthy, identical, transgenic calves were generated. Furthermore, the life-span of near senescent fibroblasts could be extended by nuclear transfer, as indicated by population doublings in fibroblast lines derived from a 40-day-old fetal clone. With the ability to extend the life-span of these primary cultured cells, this system would be useful for inducing complex genetic modifications in cattle.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cibelli, J B -- Stice, S L -- Golueke, P J -- Kane, J J -- Jerry, J -- Blackwell, C -- Ponce de Leon, F A -- Robl, J M -- New York, N.Y. -- Science. 1998 May 22;280(5367):1256-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Veterinary and Animal Sciences, University of Massachusetts, Amherst, MA 01003, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9596577" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Animals, Genetically Modified ; Blastocyst ; Cattle/embryology/*genetics ; Cell Aging ; Cell Division ; Cell Nucleus/genetics ; Cells, Cultured ; Clone Cells ; *Cloning, Organism ; Embryo Transfer ; Female ; Fetus/cytology ; Fibroblasts/*cytology ; G1 Phase ; Male ; Nuclear Transfer Techniques ; Oocytes/cytology ; Transfection ; Transgenes
    Print ISSN: 0036-8075
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  • 6
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    Chlamydia infections and heart disease linked through antigenic mimicry (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-02-26
    Description: Chlamydia infections are epidemiologically linked to human heart disease. A peptide from the murine heart muscle-specific alpha myosin heavy chain that has sequence homology to the 60-kilodalton cysteine-rich outer membrane proteins of Chlamydia pneumoniae, C. psittaci, and C. trachomatis was shown to induce autoimmune inflammatory heart disease in mice. Injection of the homologous Chlamydia peptides into mice also induced perivascular inflammation, fibrotic changes, and blood vessel occlusion in the heart, as well as triggering T and B cell reactivity to the homologous endogenous heart muscle-specific peptide. Chlamydia DNA functioned as an adjuvant in the triggering of peptide-induced inflammatory heart disease. Infection with C. trachomatis led to the production of autoantibodies to heart muscle-specific epitopes. Thus, Chlamydia-mediated heart disease is induced by antigenic mimicry of a heart muscle-specific protein.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bachmaier, K -- Neu, N -- de la Maza, L M -- Pal, S -- Hessel, A -- Penninger, J M -- New York, N.Y. -- Science. 1999 Feb 26;283(5406):1335-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Amgen Institute, Ontario Cancer Institute, Departments of Medical Biophysics and 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/10037605" target="_blank"〉PubMed〈/a〉
    Keywords: Adoptive Transfer ; Amino Acid Sequence ; Animals ; Antigens, Bacterial/chemistry/immunology ; Autoantibodies/biosynthesis ; Autoimmune Diseases/immunology/*microbiology/pathology ; B-Lymphocytes/immunology ; Bacterial Outer Membrane Proteins/chemistry/*immunology ; CD4-Positive T-Lymphocytes/immunology ; Chlamydia/*immunology ; Chlamydia Infections/complications/*immunology ; Chlamydia trachomatis/immunology ; CpG Islands ; Humans ; Immunization ; Lymphocyte Activation ; Mice ; Mice, Inbred BALB C ; *Molecular Mimicry ; Molecular Sequence Data ; Myocarditis/immunology/*microbiology/pathology ; Myocardium/immunology/pathology ; Myosin Heavy Chains/chemistry/*immunology ; Oligodeoxyribonucleotides/immunology ; Sequence Homology, Amino Acid
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  • 7
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    AP-2 recruitment to synaptotagmin stimulated by tyrosine-based endocytic motifs (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-08-24
    Description: Clathrin-mediated endocytosis is initiated by the recruitment of the clathrin adaptor protein AP-2 to the plasma membrane where the membrane protein synaptotagmin is thought to act as a docking site. AP-2 also interacts with endocytic motifs present in other cargo proteins. Peptides with a tyrosine-based endocytic motif stimulated binding of AP-2 to synaptotagmin and enhanced AP-2 recruitment to the plasma membrane of neuronal and non-neuronal cells. This suggests a mechanism by which nucleation of clathrin-coated pits is stimulated by the loading of cargo proteins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Haucke, V -- De Camilli, P -- CA46128/CA/NCI NIH HHS/ -- NS36252/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1999 Aug 20;285(5431):1268-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology and Howard Hughes Medical Institute, Yale University School of Medicine, 295 Congress Avenue, New Haven, CT 06510, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10455054" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Protein Complex alpha Subunits ; Adaptor Proteins, Vesicular Transport ; Animals ; Binding Sites ; CHO Cells ; *Calcium-Binding Proteins ; Cattle ; Cell Membrane/metabolism ; Clathrin/*metabolism ; Coated Pits, Cell-Membrane/*metabolism ; Cricetinae ; *Endocytosis ; Membrane Glycoproteins/chemistry/*metabolism ; Membrane Proteins/*metabolism ; Nerve Tissue Proteins/chemistry/*metabolism ; Neurons/metabolism ; Oligopeptides/chemistry/metabolism/*pharmacology ; Phospholipase D/metabolism ; Protein Binding ; Rats ; Recombinant Fusion Proteins/metabolism ; Synaptic Membranes/*metabolism ; Synaptotagmins ; Tyrosine/chemistry
    Print ISSN: 0036-8075
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  • 8
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    Switchable tackiness and wettability of a liquid crystalline polymer (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-08-24
    Description: The spreading velocity of liquids on the surface of a liquid crystalline polymer can be tremendously affected by a slight temperature change. Indeed, a bulk transition between a highly ordered smectic and an isotropic phase induces a sharp change from a rigid to a soft behavior, with consequent effects on the tack properties of the liquid crystalline polymer and on the dewetting dynamics of a liquid on its surface.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉de Crevoisier G -- Fabre -- Corpart -- Leibler -- New York, N.Y. -- Science. 1999 Aug 20;285(5431):1246-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Unite Mixte de Recherche 167 CNRS/Elf Atochem, Service Agents d'Interfaces, Elf Atochem, 95 rue Danton, 92303 Levallois-Perret, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10455047" target="_blank"〉PubMed〈/a〉
    Print ISSN: 0036-8075
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  • 9
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    Unlimited mileage from telomerase? (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-03-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉de Lange, T -- DePinho, R A -- CA76027/CA/NCI NIH HHS/ -- HD 348880/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1999 Feb 12;283(5404):947-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory for Cell Biology and Genetics, Rockefeller University, New York, NY 10021, USA. delange@rockvax.rockefeller.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10075559" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Aging ; *Cell Division ; *Cell Transformation, Neoplastic ; Cyclin-Dependent Kinase Inhibitor p16/metabolism ; Humans ; Neoplasms/enzymology/metabolism/pathology ; Proto-Oncogene Proteins c-myc/metabolism ; Retinoblastoma Protein/metabolism ; Signal Transduction ; Telomerase/genetics/*metabolism ; Telomere/*metabolism ; ras Proteins/metabolism
    Print ISSN: 0036-8075
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  • 10
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    Environment and behavior of 2.5-million-year-old Bouri hominids (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-24
    Description: The Hata Member of the Bouri Formation is defined for Pliocene sedimentary outcrops in the Middle Awash Valley, Ethiopia. The Hata Member is dated to 2.5 million years ago and has produced a new species of Australopithecus and hominid postcranial remains not currently assigned to species. Spatially associated zooarchaeological remains show that hominids acquired meat and marrow by 2.5 million years ago and that they are the near contemporary of Oldowan artifacts at nearby Gona. The combined evidence suggests that behavioral changes associated with lithic technology and enhanced carnivory may have been coincident with the emergence of the Homo clade from Australopithecus afarensis in eastern Africa.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉de Heinzelin, J -- Clark, J D -- White, T -- Hart, W -- Renne, P -- WoldeGabriel, G -- Beyene, Y -- Vrba, E -- New York, N.Y. -- Science. 1999 Apr 23;284(5414):625-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut Royal des Sciences Naturelles de Belgique, Rue Vautier 29, B-1000 Bruxelles, Belgium.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10213682" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Diet ; Ethiopia ; *Fossils ; *Geologic Sediments ; History, Ancient ; *Hominidae ; Humans
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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