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  • Cells, Cultured
  • American Association for the Advancement of Science (AAAS)  (33)
  • Elsevier
  • 1995-1999  (33)
  • 1980-1984
  • 1998  (33)
Collection
Keywords
Publisher
  • American Association for the Advancement of Science (AAAS)  (33)
  • Elsevier
Years
  • 1995-1999  (33)
  • 1980-1984
Year
  • 1
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    Induction of lens differentiation by activation of a bZIP transcription factor, L-Maf (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-04-29
    Description: After the vertebrate lens is induced from head ectoderm, lens-specific genes are expressed. Transcriptional regulation of the lens-specific alphaA-crystallin gene is controlled by an enhancer element, alphaCE2. A gene encoding an alphaCE2-binding protein, L-maf(lens-specific maf), was isolated. L-maf expression is initiated in the lens placode and is restricted to lens cells. The gene product L-Maf regulates the expression of multiple genes expressed in the lens, and ectopic expression of this transcription factor converts chick embryonic ectodermal cells and cultured cells into lens fibers. Thus, vertebrate lens induction and differentiation can be triggered by the activation of L-Maf.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ogino, H -- Yasuda, K -- New York, N.Y. -- Science. 1998 Apr 3;280(5360):115-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Graduate School of Biological Sciences, Nara Institute of Science and Technology, 8916-5 Takayama, Ikoma 630-0101, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9525857" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Basic-Leucine Zipper Transcription Factors ; Cell Differentiation ; Cells, Cultured ; Chick Embryo ; Crystallins/genetics ; DNA, Complementary ; DNA-Binding Proteins/chemistry/genetics ; Ectoderm ; Enhancer Elements, Genetic ; Eye Proteins/genetics ; G-Box Binding Factors ; *Gene Expression Regulation, Developmental ; Genes, Reporter ; Intermediate Filament Proteins/genetics ; Lens, Crystalline/*cytology/*embryology/metabolism ; Maf Transcription Factors ; Molecular Sequence Data ; Promoter Regions, Genetic ; Recombinant Fusion Proteins/metabolism ; Transcription Factors/chemistry/genetics/*metabolism ; *Transcription, Genetic ; Transcriptional Activation ; Transfection
    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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    Molecular basis of T cell inactivation by CTLA-4 (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-12-18
    Description: CTLA-4, a negative regulator of T cell function, was found to associate with the T cell receptor (TCR) complex zeta chain in primary T cells. The association of TCRzeta with CTLA-4, reconstituted in 293 transfectants, was enhanced by p56(lck)-induced tyrosine phosphorylation. Coexpression of the CTLA-4-associated tyrosine phosphatase, SHP-2, resulted in dephosphorylation of TCRzeta bound to CTLA-4 and abolished the p56(lck)-inducible TCRzeta-CTLA-4 interaction. Thus, CTLA-4 inhibits TCR signal transduction by binding to TCRzeta and inhibiting tyrosine phosphorylation after T cell activation. These findings have broad implications for the negative regulation of T cell function and T cell tolerance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, K M -- Chuang, E -- Griffin, M -- Khattri, R -- Hong, D K -- Zhang, W -- Straus, D -- Samelson, L E -- Thompson, C B -- Bluestone, J A -- P01 AI35294-6/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1998 Dec 18;282(5397):2263-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Ben May Institute for Cancer Research, and Committee on Immunology, University of Chicago, Chicago, IL 60637, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9856951" target="_blank"〉PubMed〈/a〉
    Keywords: Abatacept ; Animals ; Antigens, CD ; Antigens, Differentiation/*metabolism ; CTLA-4 Antigen ; Cell Line ; Cells, Cultured ; Humans ; *Immunoconjugates ; Intracellular Signaling Peptides and Proteins ; *Lymphocyte Activation ; Lymphocyte Specific Protein Tyrosine Kinase p56(lck)/genetics/metabolism ; Membrane Proteins/*metabolism ; Mice ; Mice, Inbred BALB C ; Models, Immunological ; Phosphorylation ; Phosphotyrosine/metabolism ; Protein Tyrosine Phosphatase, Non-Receptor Type 11 ; Protein Tyrosine Phosphatase, Non-Receptor Type 6 ; Protein Tyrosine Phosphatases/genetics/metabolism ; Receptors, Antigen, T-Cell/*metabolism ; Recombinant Fusion Proteins/metabolism ; SH2 Domain-Containing Protein Tyrosine Phosphatases ; *Signal Transduction ; T-Lymphocytes/*immunology ; Transfection ; src Homology Domains
    Print ISSN: 0036-8075
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  • 3
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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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  • 4
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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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  • 5
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    An essential role for ectodomain shedding in mammalian development (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-11-13
    Description: The ectodomains of numerous proteins are released from cells by proteolysis to yield soluble intercellular regulators. The responsible protease, tumor necrosis factor-alpha converting enzyme (TACE), has been identified only in the case when tumor necrosis factor-alpha (TNFalpha) is released. Analyses of cells lacking this metalloproteinase-disintegrin revealed an expanded role for TACE in the processing of other cell surface proteins, including a TNF receptor, the L-selectin adhesion molecule, and transforming growth factor-alpha (TGFalpha). The phenotype of mice lacking TACE suggests an essential role for soluble TGFalpha in normal development and emphasizes the importance of protein ectodomain shedding in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Peschon, J J -- Slack, J L -- Reddy, P -- Stocking, K L -- Sunnarborg, S W -- Lee, D C -- Russell, W E -- Castner, B J -- Johnson, R S -- Fitzner, J N -- Boyce, R W -- Nelson, N -- Kozlosky, C J -- Wolfson, M F -- Rauch, C T -- Cerretti, D P -- Paxton, R J -- March, C J -- Black, R A -- CA43793/CA/NCI NIH HHS/ -- DK53804/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1998 Nov 13;282(5392):1281-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immunex Corporation, Seattle, WA 98101, USA. peschon@immunex.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9812885" target="_blank"〉PubMed〈/a〉
    Keywords: ADAM Proteins ; Amino Acid Sequence ; Animals ; Catalytic Domain ; Cell Membrane/*metabolism ; Cells, Cultured ; Crosses, Genetic ; *Embryonic and Fetal Development ; L-Selectin/metabolism ; Ligands ; Membrane Proteins/*metabolism ; Metalloendopeptidases/chemistry/genetics/*metabolism ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Mutation ; Phenotype ; Protein Processing, Post-Translational ; Receptors, Tumor Necrosis Factor/metabolism ; Transforming Growth Factor alpha/metabolism ; Tumor Necrosis Factor-alpha/*metabolism
    Print ISSN: 0036-8075
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  • 6
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    Biological action of leptin as an angiogenic factor (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-09-11
    Description: Leptin is a hormone that regulates food intake, and its receptor (OB-Rb) is expressed primarily in the hypothalamus. Here, it is shown that OB-Rb is also expressed in human vasculature and in primary cultures of human endothelial cells. In vitro and in vivo assays revealed that leptin has angiogenic activity. In vivo, leptin induced neovascularization in corneas from normal rats but not in corneas from fa/fa Zucker rats, which lack functional leptin receptors. These observations indicate that the vascular endothelium is a target for leptin and suggest a physiological mechanism whereby leptin-induced angiogenesis may facilitate increased energy expenditure.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sierra-Honigmann, M R -- Nath, A K -- Murakami, C -- Garcia-Cardena, G -- Papapetropoulos, A -- Sessa, W C -- Madge, L A -- Schechner, J S -- Schwabb, M B -- Polverini, P J -- Flores-Riveros, J R -- New York, N.Y. -- Science. 1998 Sep 11;281(5383):1683-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Boyer Center for Molecular Medicine, Yale University School of Medicine, New Haven, CT 06536, USA. rocio_sierra-honigmann@qm.yale.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9733517" target="_blank"〉PubMed〈/a〉
    Keywords: Adipocytes/metabolism ; Amino Acid Sequence ; Animals ; Carrier Proteins/analysis/*physiology ; Cells, Cultured ; Corneal Neovascularization ; DNA-Binding Proteins/metabolism ; Endothelial Growth Factors/pharmacology ; Endothelium, Vascular/chemistry/cytology/*physiology ; Energy Metabolism ; Humans ; Leptin ; Lipid Metabolism ; Lymphokines/pharmacology ; Molecular Sequence Data ; *Neovascularization, Physiologic ; Phosphorylation ; Proteins/pharmacology/*physiology ; Rats ; Rats, Zucker ; *Receptors, Cell Surface ; Receptors, Leptin ; STAT3 Transcription Factor ; Trans-Activators/metabolism ; Vascular Endothelial Growth Factor A ; Vascular Endothelial Growth Factors
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  • 7
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    Conversion of neuronal growth cone responses from repulsion to attraction by cyclic nucleotides (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-09-04
    Description: Nerve growth is regulated by attractive and repulsive factors in the nervous system. Microscopic gradients of Collapsin-1/Semaphorin III/D (Sema III) and myelin-associated glycoprotein trigger repulsive turning responses by growth cones of cultured Xenopus spinal neurons; the repulsion can be converted to attraction by pharmacological activation of the guanosine 3',5'-monophosphate (cGMP) and adenosine 3',5'-monophosphate signaling pathways, respectively. Sema III also causes the collapse of cultured rat sensory growth cones, which can be inhibited by activation of the cGMP pathway. Thus cyclic nucleotides can regulate growth cone behaviors and may be targets for designing treatments to alleviate the inhibition of nerve regeneration by repulsive factors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Song, H -- Ming, G -- He, Z -- Lehmann, M -- McKerracher, L -- Tessier-Lavigne, M -- Poo, M -- NS22764/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1998 Sep 4;281(5382):1515-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, University of California at San Diego, La Jolla, CA 92093-0357, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9727979" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/physiology ; Calcium/physiology ; Cells, Cultured ; Cyclic AMP/analogs & derivatives/pharmacology/*physiology ; Cyclic GMP/analogs & derivatives/pharmacology/*physiology ; Ganglia, Spinal/cytology ; Glycoproteins/*physiology ; Myelin-Associated Glycoprotein/physiology ; Nerve Growth Factors/*physiology ; Nerve Tissue Proteins/physiology ; Neurites/*physiology ; Neurons/cytology/*physiology ; Neuropilin-1 ; Rats ; Recombinant Proteins ; Semaphorin-3A ; Spinal Cord/cytology ; Thionucleotides/pharmacology ; Xenopus
    Print ISSN: 0036-8075
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  • 8
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    Regulation of nerve growth mediated by inositol 1,4,5-trisphosphate receptors in growth cones (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-11-30
    Description: The inositol 1,4,5-trisphosphate (IP3) receptor (IP3R) acts as a Ca2+ release channel on internal Ca2+ stores. Type 1 IP3R (IP3R1) is enriched in growth cones of neurons in chick dorsal root ganglia. Depletion of internal Ca2+ stores and inhibition of IP3 signaling with drugs inhibited neurite extension. Microinjection of heparin, a competitive IP3R blocker, induced neurite retraction. Acute localized loss of function of IP3R1 in the growth cone induced by chromophore-assisted laser inactivation resulted in growth arrest and neurite retraction. IP3-induced Ca2+ release in growth cones appears to have a crucial role in control of nerve growth.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Takei, K -- Shin, R M -- Inoue, T -- Kato, K -- Mikoshiba, K -- New York, N.Y. -- Science. 1998 Nov 27;282(5394):1705-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Calciosignal Net Project, Exploratory Research for Advanced Technology (ERATO), Japan Science and Technology Corporation (JST), Bunkyo-Ku, Tokyo 113-0021, Japan. kohtaro@ims.u-tokyo.ac.jp〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9831561" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/metabolism ; Calcium Channels/*metabolism ; Calcium Signaling ; Cells, Cultured ; Cerebellum/metabolism ; Chick Embryo ; Ganglia, Spinal/cytology ; Growth Cones/*metabolism ; Heparin/pharmacology ; Inositol 1,4,5-Trisphosphate/*metabolism ; Inositol 1,4,5-Trisphosphate Receptors ; Lasers ; Lithium Chloride/pharmacology ; Mice ; Microscopy, Video ; Microsomes/metabolism ; Microtubules/metabolism ; Neurites/drug effects/*physiology ; Pseudopodia/drug effects/physiology ; Receptors, Cytoplasmic and Nuclear/*metabolism ; Signal Transduction ; Thapsigargin/pharmacology
    Print ISSN: 0036-8075
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  • 9
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    Homing viruses (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-07-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sikorski, R -- Peters, R -- New York, N.Y. -- Science. 1998 Jun 19;280(5371):1956-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9669951" target="_blank"〉PubMed〈/a〉
    Keywords: Cells, Cultured ; Dependovirus/*genetics ; Drug Resistance/genetics ; *Gene Targeting ; *Genetic Vectors ; HeLa Cells ; Humans ; Hypoxanthine Phosphoribosyltransferase/genetics ; Neomycin/pharmacology ; *Recombination, Genetic ; *Transfection ; Virus Integration
    Print ISSN: 0036-8075
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  • 10
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    Entry of alphaherpesviruses mediated by poliovirus receptor-related protein 1 and poliovirus receptor (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-06-11
    Description: A human member of the immunoglobulin superfamily was shown to mediate entry of several alphaherpesviruses, including herpes simplex viruses (HSV) 1 and 2, porcine pseudorabies virus (PRV), and bovine herpesvirus 1 (BHV-1). This membrane glycoprotein is poliovirus receptor-related protein 1 (Prr1), designated here as HveC. Incubation of HSV-1 with a secreted form of HveC inhibited subsequent infection of a variety of cell lines, suggesting that HveC interacts directly with the virus. Poliovirus receptor (Pvr) itself mediated entry of PRV and BHV-1 but not of the HSV strains tested. HveC was expressed in human cells of epithelial and neuronal origin; it is the prime candidate for the coreceptor that allows both HSV-1 and HSV-2 to infect epithelial cells on mucosal surfaces and spread to cells of the nervous system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Geraghty, R J -- Krummenacher, C -- Cohen, G H -- Eisenberg, R J -- Spear, P G -- NS-30606/NS/NINDS NIH HHS/ -- NS-36731/NS/NINDS NIH HHS/ -- R01 AI 36293/AI/NIAID NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1998 Jun 5;280(5369):1618-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology-Immunology, Northwestern University Medical School, Chicago, IL 60611, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9616127" target="_blank"〉PubMed〈/a〉
    Keywords: Alphaherpesvirinae/*physiology ; Animals ; Base Sequence ; CHO Cells ; Cell Adhesion Molecules/genetics/*physiology ; Cells, Cultured ; Cricetinae ; Epithelial Cells/virology ; Gene Expression ; Herpesvirus 1, Bovine/physiology ; Herpesvirus 1, Human/*physiology ; Herpesvirus 1, Suid/physiology ; Herpesvirus 2, Human/*physiology ; Humans ; *Membrane Proteins ; Molecular Sequence Data ; Neurons/virology ; Polymerase Chain Reaction ; *Receptors, Virus ; Transfection ; Tumor Cells, Cultured ; Viral Envelope Proteins/metabolism
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  • 11
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    An antimicrobial activity of cytolytic T cells mediated by granulysin (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-10-02
    Description: Cytolytic T lymphocytes (CTLs) kill intracellular pathogens by a granule-dependent mechanism. Granulysin, a protein found in granules of CTLs, reduced the viability of a broad spectrum of pathogenic bacteria, fungi, and parasites in vitro. Granulysin directly killed extracellular Mycobacterium tuberculosis, altering the membrane integrity of the bacillus, and, in combination with perforin, decreased the viability of intracellular M. tuberculosis. The ability of CTLs to kill intracellular M. tuberculosis was dependent on the presence of granulysin in cytotoxic granules, defining a mechanism by which T cells directly contribute to immunity against intracellular pathogens.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stenger, S -- Hanson, D A -- Teitelbaum, R -- Dewan, P -- Niazi, K R -- Froelich, C J -- Ganz, T -- Thoma-Uszynski, S -- Melian, A -- Bogdan, C -- Porcelli, S A -- Bloom, B R -- Krensky, A M -- Modlin, R L -- New York, N.Y. -- Science. 1998 Oct 2;282(5386):121-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, UCLA School of Medicine, Los Angeles, CA 90095, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9756476" target="_blank"〉PubMed〈/a〉
    Keywords: Antigens, Differentiation, T-Lymphocyte/analysis/*immunology/pharmacology ; Cell Line ; Cell Membrane/ultrastructure ; Cells, Cultured ; Cytoplasmic Granules/immunology ; *Cytotoxicity, Immunologic ; Humans ; Macrophages/immunology/microbiology ; Membrane Glycoproteins/immunology/pharmacology ; Microscopy, Confocal ; Microscopy, Electron, Scanning ; Mycobacterium tuberculosis/*immunology/physiology/ultrastructure ; Perforin ; Pore Forming Cytotoxic Proteins ; Recombinant Proteins/pharmacology ; T-Lymphocytes, Cytotoxic/*immunology
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  • 12
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    Inhibitory function of p21Cip1/WAF1 in differentiation of primary mouse keratinocytes independent of cell cycle control (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-06-06
    Description: The cyclin-dependent kinase inhibitor p21(Cip1/WAF1) has been implicated as an inducer of differentiation. However, although expression of p21 is increased in postmitotic cells immediately adjacent to the proliferative compartment, its expression is decreased in cells further along the differentiation program. Expression of the p21 protein was decreased in terminally differentiated primary keratinocytes of mice, and this occurred by a proteasome-dependent pathway. Forced expression of p21 in these cells inhibited the expression of markers of terminal differentiation at both the protein and messenger RNA levels. These inhibitory effects on differentiation were not observed with a carboxyl-terminal truncation mutant or with the unrelated cyclin-dependent kinase inhibitor p16(INK4a), although all these molecules exerted similar inhibition of cell growth. These findings reveal an inhibitory role of p21 in the late stages of differentiation that does not result from the effects of p21 on the cell cycle.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Di Cunto, F -- Topley, G -- Calautti, E -- Hsiao, J -- Ong, L -- Seth, P K -- Dotto, G P -- AR39190/AR/NIAMS NIH HHS/ -- CA16038/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1998 May 15;280(5366):1069-72.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cutaneous Biology Research Center, Massachusetts General Hospital and Harvard Medical School, 13th Street, Charlestown, MA 02129, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9582119" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcysteine/analogs & derivatives/pharmacology ; Adenoviridae/genetics/physiology ; Animals ; Animals, Newborn ; *Cell Cycle ; *Cell Differentiation ; Cells, Cultured ; Cyclin-Dependent Kinase Inhibitor p21 ; Cyclin-Dependent Kinases/antagonists & inhibitors/metabolism ; Cyclins/genetics/*metabolism ; Enzyme Inhibitors/metabolism ; Gene Expression Regulation ; Keratinocytes/*cytology/metabolism/virology ; Leupeptins/pharmacology ; Membrane Proteins/biosynthesis/genetics ; Mice ; Mutation ; Promoter Regions, Genetic ; Protein Precursors/biosynthesis/genetics ; RNA, Messenger/genetics/metabolism ; Succinates/pharmacology ; Transfection
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  • 13
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    Is apoptosis key in Alzheimer's disease? (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-09-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1998 Aug 28;281(5381):1303-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9735049" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/metabolism/*pathology ; Amyloid beta-Peptides/biosynthesis/physiology ; *Apoptosis ; Brain/metabolism/*pathology ; Cells, Cultured ; Cysteine Endopeptidases/metabolism ; DNA Fragmentation ; Humans ; Membrane Proteins/genetics/physiology ; Mutation ; Neurons/metabolism/*pathology ; Presenilin-1 ; Presenilin-2
    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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  • 14
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    Positive selection through a motif in the alphabeta T cell receptor (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-08-07
    Description: The two lineages of T cells, alphabeta and gammadelta, differ in their developmental requirements: only alphabeta T cells require major histocompatibility complex recognition, a process known as positive selection. The alphabeta T cell receptor (TCR), but not its gammadelta counterpart, contains a motif within the alpha-chain connecting peptide domain (alpha-CPM) that has been conserved over the last 500 million years. In transgenic mice expressing an alphabeta TCR lacking the alpha-CPM, thymocytes were blocked in positive selection but could undergo negative selection. Thus, the alpha-CPM seems to participate in the generation of signals required for positive selection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Backstrom, B T -- Muller, U -- Hausmann, B -- Palmer, E -- New York, N.Y. -- Science. 1998 Aug 7;281(5378):835-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Basel Institute for Immunology, CH-4005 Basel, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9694657" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antigen-Presenting Cells/immunology ; Antigens, CD3/analysis ; CD4-Positive T-Lymphocytes/immunology ; Cell Lineage ; Cells, Cultured ; Histocompatibility Antigens Class II/immunology ; Ligands ; Lymphocyte Count ; Membrane Proteins/analysis ; Mice ; Mice, Inbred C57BL ; Mice, Nude ; Mice, Transgenic ; Molecular Sequence Data ; Mutation ; Receptor-CD3 Complex, Antigen, T-Cell/immunology/metabolism ; Receptors, Antigen, T-Cell/analysis ; Receptors, Antigen, T-Cell, alpha-beta/*chemistry/genetics/*immunology ; Signal Transduction ; T-Lymphocyte Subsets/*immunology ; Thymus Gland/immunology
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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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    Cell surface trafficking of Fas: a rapid mechanism of p53-mediated apoptosis (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-10-09
    Description: p53 acts as a tumor suppressor by inducing both growth arrest and apoptosis. p53-induced apoptosis can occur without new RNA synthesis through an unknown mechanism. In human vascular smooth muscle cells, p53 activation transiently increased surface Fas (CD95) expression by transport from the Golgi complex. Golgi disruption blocked both p53-induced surface Fas expression and apoptosis. p53 also induced Fas-FADD binding and transiently sensitized cells to Fas-induced apoptosis. In contrast, lpr and gld fibroblasts were resistant to p53-induced apoptosis. Thus, p53 can mediate apoptosis through Fas transport from cytoplasmic stores.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bennett, M -- Macdonald, K -- Chan, S W -- Luzio, J P -- Simari, R -- Weissberg, P -- HL34073/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1998 Oct 9;282(5387):290-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of Cambridge, Addenbrooke's Hospital, Cambridge CB2 2QQ, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9765154" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptor Proteins, Signal Transducing ; Animals ; Antigens, CD95/genetics/*metabolism ; *Apoptosis/drug effects ; Brefeldin A/pharmacology ; Carrier Proteins/metabolism ; Cell Membrane/*metabolism ; Cells, Cultured ; Enzyme Inhibitors/pharmacology ; Etoposide/pharmacology ; Fas Ligand Protein ; Fas-Associated Death Domain Protein ; Golgi Apparatus/metabolism ; Humans ; Membrane Glycoproteins/genetics/metabolism ; Mice ; Muscle, Smooth, Vascular/cytology ; Mutation ; Protein Synthesis Inhibitors/pharmacology ; Rats ; Topoisomerase II Inhibitors ; Tumor Suppressor Protein p53/*physiology
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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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    Eight calves cloned from somatic cells of a single adult (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-12-16
    Description: Eight calves were derived from differentiated cells of a single adult cow, five from cumulus cells and three from oviductal cells out of 10 embryos transferred to surrogate cows (80 percent success). All calves were visibly normal, but four died at or soon after birth from environmental causes, and postmortem analysis revealed no abnormality. These results show that bovine cumulus and oviductal epithelial cells of the adult have the genetic content to direct the development of newborn calves.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kato, Y -- Tani, T -- Sotomaru, Y -- Kurokawa, K -- Kato, J -- Doguchi, H -- Yasue, H -- Tsunoda, Y -- New York, N.Y. -- Science. 1998 Dec 11;282(5396):2095-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Animal Reproduction, College of Agriculture and Research Institute for Animal Developmental Biotechnology, Kinki University, 3327-204, Nakamachi, Nara, 631-8505, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9851933" target="_blank"〉PubMed〈/a〉
    Keywords: Animal Husbandry ; Animals ; Blastocyst/cytology ; Cattle/embryology/*genetics ; Cell Fusion ; Cells, Cultured ; Cloning, Organism/*methods ; Cytoplasm/physiology ; Embryo Transfer/veterinary ; Epithelial Cells/cytology ; Fallopian Tubes/*cytology ; Female ; Microsatellite Repeats ; *Nuclear Transfer Techniques ; Oocytes/*cytology ; Ovarian Follicle/*cytology ; Pregnancy ; Pregnancy, Multiple
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  • 17
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    A viral mechanism for inhibition of the cellular phosphatase calcineurin (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-07-24
    Description: The transcription factor NFAT (nuclear factor of activated T cells) controls the expression of many immunomodulatory proteins. African swine fever virus inhibits proinflammatory cytokine expression in infected macrophages, and a viral protein A238L was found to display the activity of the immunosuppressive drug cyclosporin A by inhibiting NFAT-regulated gene transcription in vivo. This it does by binding the catalytic subunit of calcineurin and inhibiting calcineurin phosphatase activity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miskin, J E -- Abrams, C C -- Goatley, L C -- Dixon, L K -- New York, N.Y. -- Science. 1998 Jul 24;281(5376):562-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Animal Health, Pirbright Laboratory, Pirbright, Surrey, GU24 0NF, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9677199" target="_blank"〉PubMed〈/a〉
    Keywords: African Swine Fever Virus/*physiology ; Amino Acid Sequence ; Animals ; Binding Sites ; Calcineurin/metabolism ; *Calcineurin Inhibitors ; Cell Nucleus/metabolism ; Cells, Cultured ; Cercopithecus aethiops ; Cyclosporine/pharmacology ; DNA-Binding Proteins/genetics/*metabolism ; Genes, Reporter ; Macrophages, Alveolar/*virology ; Molecular Sequence Data ; NF-kappa B/metabolism ; NFATC Transcription Factors ; *Nuclear Proteins ; Recombinant Proteins/metabolism ; Swine ; Transcription Factors/genetics/*metabolism ; *Transcription, Genetic ; Vero Cells ; Viral Proteins/genetics/*metabolism
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  • 18
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    RNA-splicing machinery revealed (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-10-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ferber, D -- New York, N.Y. -- Science. 1998 Sep 11;281(5383):1581-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9767017" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; Cells, Cultured ; DNA, Complementary ; Databases, Factual ; Gene Expression ; Humans ; Mass Spectrometry ; Proteins/*chemistry/genetics/isolation & purification ; *RNA Splicing ; Spliceosomes/*chemistry
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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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    The importance of telomerase (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-02-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kelner, K L -- New York, N.Y. -- Science. 1997 Oct 24;278(5338):600.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9381167" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Transformation, Neoplastic ; Cells, Cultured ; Mice ; Mice, Transgenic ; Telomerase/genetics/*metabolism ; Telomere/*metabolism
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  • 20
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    Role of alpha-dystroglycan as a Schwann cell receptor for Mycobacterium leprae (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-12-16
    Description: alpha-Dystroglycan (alpha-DG) is a component of the dystroglycan complex, which is involved in early development and morphogenesis and in the pathogenesis of muscular dystrophies. Here, alpha-DG was shown to serve as a Schwann cell receptor for Mycobacterium leprae, the causative organism of leprosy. Mycobacterium leprae specifically bound to alpha-DG only in the presence of the G domain of the alpha2 chain of laminin-2. Native alpha-DG competitively inhibited the laminin-2-mediated M. leprae binding to primary Schwann cells. Thus, M. leprae may use linkage between the extracellular matrix and cytoskeleton through laminin-2 and alpha-DG for its interaction with Schwann cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rambukkana, A -- Yamada, H -- Zanazzi, G -- Mathus, T -- Salzer, J L -- Yurchenco, P D -- Campbell, K P -- Fischetti, V A -- New York, N.Y. -- Science. 1998 Dec 11;282(5396):2076-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Bacterial Pathogenesis and Immunology, Rockefeller University, New York, NY 10021, USA. rambuka@rockvax.rockefeller.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9851927" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Bacterial Adhesion ; Binding Sites ; Calcium/physiology ; Cell Line, Transformed ; Cells, Cultured ; Cytoskeletal Proteins/*metabolism/pharmacology ; Dystroglycans ; Edetic Acid/pharmacology ; Glycosylation ; Humans ; Laminin/chemistry/*metabolism ; Membrane Glycoproteins/*metabolism/pharmacology ; Mycobacterium leprae/*metabolism ; Peripheral Nerves/chemistry ; Rats ; Receptors, Laminin/metabolism ; Recombinant Fusion Proteins/metabolism ; Recombinant Proteins/chemistry/metabolism ; Schwann Cells/metabolism/*microbiology
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  • 21
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    Reaction to stem cells: a tale of the ticker (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-12-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Malakoff, D -- New York, N.Y. -- Science. 1998 Nov 13;282(5392):1239.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9867624" target="_blank"〉PubMed〈/a〉
    Keywords: Biotechnology/*economics ; *Cell Culture Techniques ; Cells, Cultured ; Humans ; *Investments ; Stem Cells/*cytology ; United States
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 22
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    Differentiation of monocytes into dendritic cells in a model of transendothelial trafficking (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-10-17
    Description: Essential to the dendritic cell system of antigen-presenting cells are the veiled dendritic cells that traverse afferent lymph to enter lymph nodes, where they initiate immune responses. The origin of veiled cells, which were discovered 20 years ago, is unclear. Monocytes cultured with endothelium differentiated into dendritic cells within 2 days, particularly after phagocytosing particles in subendothelial collagen. These nascent dendritic cells migrated across the endothelium in the ablumenal-to-lumenal direction, as would occur during entry into lymphatics. Monocytes that remained in the subendothelial matrix became macrophages. Therefore, monocytes have two potential fates associated with distinct patterns of migration.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Randolph, G J -- Beaulieu, S -- Lebecque, S -- Steinman, R M -- Muller, W A -- AI13013/AI/NIAID NIH HHS/ -- AI40045/AI/NIAID NIH HHS/ -- HL46849/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1998 Oct 16;282(5388):480-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Cornell University Medical College, 1300 York Avenue, Room C-420, New York, NY 10021, USA. GJRandol@mail.med.cornell.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9774276" target="_blank"〉PubMed〈/a〉
    Keywords: Antigens, CD/analysis ; Carrier Proteins/analysis ; Cell Count ; Cell Differentiation ; Cell Movement ; Cells, Cultured ; Collagen ; Dendritic Cells/cytology/immunology/*physiology ; Endothelium, Vascular/cytology/*physiology ; HLA-DR Antigens/analysis ; Humans ; Lymphocyte Activation ; Lymphocyte Culture Test, Mixed ; Macrophages/cytology/immunology/physiology ; Microfilament Proteins/analysis ; Monocytes/cytology/immunology/*physiology ; Phagocytosis ; T-Lymphocytes/immunology
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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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    Signaling path may lead to better heart-failure therapies (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-05-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1998 Apr 17;280(5362):383.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9575084" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcineurin/metabolism ; *Calcineurin Inhibitors ; Calcium/metabolism ; Cardiomegaly/etiology/metabolism ; Cells, Cultured ; Cyclosporine/*pharmacology/therapeutic use ; DNA-Binding Proteins/metabolism ; Enzyme Inhibitors/pharmacology ; GATA4 Transcription Factor ; Heart Failure/*drug therapy/etiology/metabolism ; Humans ; Mice ; Myocardium/*metabolism ; NFATC Transcription Factors ; *Nuclear Proteins ; Signal Transduction ; Tacrolimus/pharmacology ; Transcription Factors/metabolism
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  • 24
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    Rapid identification of subtype-selective agonists of the somatostatin receptor through combinatorial chemistry (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-10-23
    Description: Nonpeptide agonists of each of the five somatostatin receptors were identified in combinatorial libraries constructed on the basis of molecular modeling of known peptide agonists. In vitro experiments using these selective compounds demonstrated the role of the somatostatin subtype-2 receptor in inhibition of glucagon release from mouse pancreatic alpha cells and the somatostatin subtype-5 receptor as a mediator of insulin secretion from pancreatic beta cells. Both receptors regulated growth hormone release from the rat anterior pituitary gland. The availability of high-affinity, subtype-selective agonists for each of the somatostatin receptors provides a direct approach to defining their physiological functions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rohrer, S P -- Birzin, E T -- Mosley, R T -- Berk, S C -- Hutchins, S M -- Shen, D M -- Xiong, Y -- Hayes, E C -- Parmar, R M -- Foor, F -- Mitra, S W -- Degrado, S J -- Shu, M -- Klopp, J M -- Cai, S J -- Blake, A -- Chan, W W -- Pasternak, A -- Yang, L -- Patchett, A A -- Smith, R G -- Chapman, K T -- Schaeffer, J M -- New York, N.Y. -- Science. 1998 Oct 23;282(5389):737-40.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biochemistry and Physiology, Merck Research Laboratories, Post Office Box 2000, Rahway, NJ 07065, USA. susanvrohrer@merck.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9784130" target="_blank"〉PubMed〈/a〉
    Keywords: Amides/metabolism/*pharmacology ; Amino Acid Sequence ; Animals ; Cell Line ; Cells, Cultured ; Cricetinae ; Drug Design ; Glucagon/secretion ; Growth Hormone/secretion ; Insulin/secretion ; Islets of Langerhans/drug effects/secretion ; Ligands ; Membrane Proteins ; Mice ; Models, Chemical ; Molecular Sequence Data ; Pituitary Gland, Anterior/drug effects/metabolism ; Rats ; Receptors, Somatostatin/*agonists/physiology
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  • 25
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    Molecular plumbing (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-03-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Peters, R -- Sikorski, R -- New York, N.Y. -- Science. 1998 Feb 20;279(5354):1230-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9508694" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biomedical Engineering ; *Blood Vessel Prosthesis ; Blood Vessel Prosthesis Implantation ; Cells, Cultured ; Culture Techniques ; Dogs ; Endothelium, Vascular/cytology ; Fibroblasts/cytology ; Humans ; Muscle, Smooth, Vascular/cytology ; Transplantation, Heterologous
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  • 26
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    Role of PML in cell growth and the retinoic acid pathway (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-03-21
    Description: The PML gene is fused to the retinoic acid receptor alpha (RARalpha) gene in chromosomal translocations associated with acute promyelocytic leukemia (APL). Ablation of murine PML protein by homologous recombination revealed that PML regulates hemopoietic differentiation and controls cell growth and tumorigenesis. PML function was essential for the tumor-growth-suppressive activity of retinoic acid (RA) and for its ability to induce terminal myeloid differentiation of precursor cells. PML was needed for the RA-dependent transactivation of the p21WAF1/CIP1 gene, which regulates cell cycle progression and cellular differentiation. These results indicate that PML is a critical component of the RA pathway and that disruption of its activity by the PML-RARalpha fusion protein may be important in APL pathogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Z G -- Delva, L -- Gaboli, M -- Rivi, R -- Giorgio, M -- Cordon-Cardo, C -- Grosveld, F -- Pandolfi, P P -- CA 71692/CA/NCI NIH HHS/ -- CA-08748/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1998 Mar 6;279(5356):1547-51.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Human Genetics and Molecular Biology Program, Memorial Sloan-Kettering Cancer Center, Sloan-Kettering Division, Graduate School of Medical Sciences, Cornell University, New York, NY 10021, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9488655" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Cell Differentiation/drug effects ; *Cell Division ; Cell Transformation, Neoplastic ; Cells, Cultured ; Cyclin-Dependent Kinase Inhibitor p21 ; Cyclins/genetics ; Female ; Fibroblasts/cytology ; Gene Targeting ; Granulocytes/cytology ; Hematopoiesis ; Hematopoietic Stem Cells/cytology ; Leukemia, Promyelocytic, Acute/pathology ; Male ; Mice ; Monocytes/cytology ; Neoplasm Proteins/genetics/*physiology ; Neoplasms, Experimental/etiology ; *Nuclear Proteins ; Oncogene Proteins, Fusion/physiology ; Transcription Factors/genetics/*physiology ; Transcriptional Activation ; Tretinoin/pharmacology/*physiology ; Tumor Suppressor Proteins
    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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  • 27
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    Role of dynamin in the formation of transport vesicles from the trans-Golgi network (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-02-07
    Description: Dynamin guanosine triphosphatases support the scission of clathrin-coated vesicles from the plasmalemma during endocytosis. By fluorescence microscopy of cultured rat hepatocytes, a green fluorescent protein-dynamin II fusion protein localized with clathrin-coated vesicles at the Golgi complex. A cell-free assay was utilized to demonstrate the role of dynamin in vesicle formation at the trans-Golgi. Addition of peptide-specific anti-dynamin antibodies to the assay mixture inhibited both constitutive exocytic and clathrin-coated vesicle formation. Immunodepletion of dynamin proteins also inhibited vesicle formation, and budding efficiency was restored upon readdition of purified dynamin. These data suggest that dynamin participates in the formation of distinct transport vesicles from the trans-Golgi network.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jones, S M -- Howell, K E -- Henley, J R -- Cao, H -- McNiven, M A -- P30 CA-46934/CA/NCI NIH HHS/ -- P30 DK-34914/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1998 Jan 23;279(5350):573-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Basic Research in Digestive Diseases, Mayo Clinic and Foundation, Rochester, MN 55905, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9438853" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Animals ; Biological Transport ; Cell Membrane/chemistry ; Cells, Cultured ; Clathrin/analysis ; Coated Vesicles/chemistry/*metabolism/ultrastructure ; Cytosol/metabolism ; Dynamins ; GTP Phosphohydrolases/analysis/immunology/*metabolism ; Golgi Apparatus/chemistry/*metabolism ; Green Fluorescent Proteins ; Guanosine 5'-O-(3-Thiotriphosphate)/metabolism ; Liver/ultrastructure ; Luminescent Proteins ; Microscopy, Fluorescence ; Organelles/chemistry/*metabolism/ultrastructure ; Rats ; Recombinant Fusion Proteins/analysis
    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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  • 28
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    Nota bene: triplet repeat diseases. Innocent inclusions (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-12-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kelner, K L -- New York, N.Y. -- Science. 1998 Oct 23;282(5389):643.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9841418" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Death ; Cells, Cultured ; Huntington Disease/*genetics/pathology ; Inclusion Bodies/*physiology ; Mice ; Neurons/*pathology ; Spinocerebellar Degenerations/*genetics/pathology ; *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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  • 29
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    A method in Ebola's madness (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-03-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wickelgren, I -- New York, N.Y. -- Science. 1998 Feb 13;279(5353):983-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9490485" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Ebolavirus/metabolism/*pathogenicity ; Endothelium, Vascular/metabolism/virology ; Genetic Therapy ; Genetic Vectors ; Glycoproteins/*metabolism/secretion ; Hemorrhagic Fever, Ebola/*virology ; Humans ; Membrane Glycoproteins/*metabolism/secretion ; Neutrophils/metabolism ; Retroviridae/physiology ; Viral Matrix Proteins/*metabolism/secretion ; Viral Proteins/*metabolism/secretion
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 30
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    Quiescence in nuclear transfer (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-10-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wilmut, I -- Campbell, K H -- New York, N.Y. -- Science. 1998 Sep 11;281(5383):1611.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9767023" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cattle/embryology/*genetics ; Cells, Cultured ; *Cloning, Organism ; Fetus ; Fibroblasts/*cytology ; *G0 Phase ; G1 Phase ; *Nuclear Transfer Techniques
    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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  • 31
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    Claim of human-cow embryo greeted with skepticism (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-12-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marshall, E -- New York, N.Y. -- Science. 1998 Nov 20;282(5393):1390-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9867634" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bioethics ; Cattle ; Cell Culture Techniques ; Cells, Cultured ; Dna ; Embryo Research ; Embryo, Mammalian/*cytology ; *Genetic Research ; Humans ; Hybrid Cells/*cytology ; *Nuclear Transfer Techniques ; Stem Cells/*cytology ; *Transplantation, Heterologous
    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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  • 32
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    Developmental options (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-12-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shortman, K -- Maraskovsky, E -- New York, N.Y. -- Science. 1998 Oct 16;282(5388):424-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Walter and Eliza Hall Institute of Medical Research, Melbourne, Australia. van_es@wehi.edu.au〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9841399" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cell Lineage ; Cell Movement ; Cells, Cultured ; Cytokines/pharmacology ; Dendritic Cells/cytology/immunology/*physiology ; Endothelium, Vascular/cytology/*physiology ; Humans ; Macrophages/cytology/physiology ; Mice ; Monocytes/cytology/*physiology ; Phagocytosis
    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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  • 33
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    Can IL-2 smoke out HIV reservoirs? (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-12-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉WIlliams, N -- New York, N.Y. -- Science. 1998 Nov 20;282(5393):1394-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9867636" target="_blank"〉PubMed〈/a〉
    Keywords: Anti-HIV Agents/*therapeutic use ; Cells, Cultured ; Controlled Clinical Trials as Topic ; Drug Therapy, Combination ; HIV/drug effects/*physiology ; HIV Infections/*drug therapy/virology ; Humans ; Interleukin-2/*therapeutic use ; T-Lymphocytes/*virology ; Viremia/drug therapy
    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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