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  • Cell Line  (142)
  • American Association for the Advancement of Science (AAAS)  (142)
  • American Meteorological Society
  • Cell Press
  • 1995-1999  (142)
  • 1990-1994
  • 1998  (72)
  • 1996  (70)
Collection
Keywords
Publisher
  • American Association for the Advancement of Science (AAAS)  (142)
  • American Meteorological Society
  • Cell Press
Years
  • 1995-1999  (142)
  • 1990-1994
Year
  • 1
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    Identification of alpha-dystroglycan as a receptor for lymphocytic choriomeningitis virus and Lassa fever virus (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-12-16
    Description: A peripheral membrane protein that is interactive with lymphocytic choriomeningitis virus (LCMV) was purified from cells permissive to infection. Tryptic peptides from this protein were determined to be alpha-dystroglycan (alpha-DG). Several strains of LCMV and other arenaviruses, including Lassa fever virus (LFV), Oliveros, and Mobala, bound to purified alpha-DG protein. Soluble alpha-DG blocked both LCMV and LFV infection. Cells bearing a null mutation of the gene encoding DG were resistant to LCMV infection, and reconstitution of DG expression in null mutant cells restored susceptibility to LCMV infection. Thus, alpha-DG is a cellular receptor for both LCMV and LFV.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cao, W -- Henry, M D -- Borrow, P -- Yamada, H -- Elder, J H -- Ravkov, E V -- Nichol, S T -- Compans, R W -- Campbell, K P -- Oldstone, M B -- AG 00080/AG/NIA NIH HHS/ -- AI 09484/AI/NIAID NIH HHS/ -- DK09712/DK/NIDDK NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1998 Dec 11;282(5396):2079-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Virology, Department of Neuropharmacology, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9851928" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Arenavirus/metabolism ; Cell Line ; Cytoskeletal Proteins/chemistry/genetics/*metabolism ; Dystroglycans ; Lassa virus/*metabolism/physiology ; Lymphocytic choriomeningitis virus/*metabolism/physiology ; Membrane Glycoproteins/chemistry/genetics/*metabolism ; Mice ; Molecular Sequence Data ; Mutation ; Receptors, Virus/chemistry/*metabolism ; Recombinant Fusion Proteins/metabolism ; Virus Replication
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
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    Coupling of Ras and Rac guanosine triphosphatases through the Ras exchanger Sos (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-02-07
    Description: The Son of Sevenless (Sos) proteins control receptor-mediated activation of Ras by catalyzing the exchange of guanosine diphosphate for guanosine triphosphate on Ras. The NH2-terminal region of Sos contains a Dbl homology (DH) domain in tandem with a pleckstrin homology (PH) domain. In COS-1 cells, the DH domain of Sos stimulated guanine nucleotide exchange on Rac but not Cdc42 in vitro and in vivo. The tandem DH-PH domain of Sos (DH-PH-Sos) was defective in Rac activation but regained Rac stimulating activity when it was coexpressed with activated Ras. Ras-mediated activation of DH-PH-Sos did not require activation of mitogen-activated protein kinase but it was dependent on activation of phosphoinositide 3-kinase. These results reveal a potential mechanism for coupling of Ras and Rac signaling pathways.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nimnual, A S -- Yatsula, B A -- Bar-Sagi, D -- CA09176/CA/NCI NIH HHS/ -- CA28146/CA/NCI NIH HHS/ -- CA55360/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1998 Jan 23;279(5350):560-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics and Microbiology, State University of New York at Stony Brook, Stony Brook, NY 11794, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9438849" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/metabolism ; Animals ; COS Cells ; Calcium-Calmodulin-Dependent Protein Kinases/metabolism ; Cell Cycle Proteins/metabolism ; Cell Line ; Cell Membrane/ultrastructure ; Enzyme Activation ; GTP Phosphohydrolases/*metabolism ; GTP-Binding Proteins/*metabolism ; Guanine Nucleotide Exchange Factors ; Guanosine Diphosphate/metabolism ; Guanosine Triphosphate/metabolism ; Humans ; JNK Mitogen-Activated Protein Kinases ; Membrane Proteins/chemistry/*metabolism ; *Mitogen-Activated Protein Kinases ; Proteins/metabolism ; Proto-Oncogene Proteins ; Recombinant Fusion Proteins/metabolism ; Retroviridae Proteins, Oncogenic/chemistry ; Signal Transduction ; Son of Sevenless Proteins ; Transfection ; cdc42 GTP-Binding Protein ; rac GTP-Binding Proteins ; ras Guanine Nucleotide Exchange Factors ; ras Proteins/*metabolism
    Print ISSN: 0036-8075
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  • 3
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    Essential role of CED-4 oligomerization in CED-3 activation and apoptosis (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-08-28
    Description: Control of the activation of apoptosis is important both in development and in protection against cancer. In the classic genetic model Caenorhabditis elegans, the pro-apoptotic protein CED-4 activates the CED-3 caspase and is inhibited by the Bcl-2-like protein CED-9. Both processes are mediated by protein-protein interaction. Facilitating the proximity of CED-3 zymogen molecules was found to induce caspase activation and cell death. CED-4 protein oligomerized in cells and in vitro. This oligomerization induced CED-3 proximity and competed with CED-4:CED-9 interaction. Mutations that abolished CED-4 oligomerization inactivated its ability to activate CED-3. Thus, the mechanism of control is that CED-3 in CED-3:CED-4 complexes is activated by CED-4 oligomerization, which is inhibited by binding of CED-9 to CED-4.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yang, X -- Chang, H Y -- Baltimore, D -- CA51462/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1998 Aug 28;281(5381):1355-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9721101" target="_blank"〉PubMed〈/a〉
    Keywords: *Apoptosis ; Apoptosis Regulatory Proteins ; Biopolymers ; *Caenorhabditis elegans Proteins ; Calcium-Binding Proteins/*chemistry/genetics/*metabolism ; *Caspases ; Cell Line ; Chemistry, Physical ; Cysteine Endopeptidases/*metabolism ; Cysteine Proteinase Inhibitors/pharmacology ; Enzyme Activation ; Enzyme Precursors/metabolism ; HeLa Cells ; Helminth Proteins/*chemistry/genetics/*metabolism ; Humans ; Mutation ; Oligopeptides/pharmacology ; Physicochemical Phenomena ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins c-bcl-2/metabolism ; Recombinant Fusion Proteins/metabolism ; Tacrolimus/pharmacology ; Transfection ; bcl-X Protein
    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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    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
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  • 5
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    Differential use of CREB binding protein-coactivator complexes (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-02-21
    Description: CREB binding protein (CBP) functions as an essential coactivator of transcription factors that are inhibited by the adenovirus early gene product E1A. Transcriptional activation by the signal transducer and activator of transcription-1 (STAT1) protein requires the C/H3 domain in CBP, which is the primary target of E1A inhibition. Here it was found that the C/H3 domain is not required for retinoic acid receptor (RAR) function, nor is it involved in E1A inhibition. Instead, E1A inhibits RAR function by preventing the assembly of CBP-nuclear receptor coactivator complexes, revealing differences in required CBP domains for transcriptional activation by RAR and STAT1.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kurokawa, R -- Kalafus, D -- Ogliastro, M H -- Kioussi, C -- Xu, L -- Torchia, J -- Rosenfeld, M G -- Glass, C K -- New York, N.Y. -- Science. 1998 Jan 30;279(5351):700-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Cellular and Molecular Medicine, Department of Medicine, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0651, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9445474" target="_blank"〉PubMed〈/a〉
    Keywords: Adenovirus E1A Proteins/*metabolism/pharmacology ; Animals ; Binding Sites ; CREB-Binding Protein ; Cell Differentiation ; Cell Line ; DNA-Binding Proteins/metabolism ; Histone Acetyltransferases ; Humans ; Mutation ; Nuclear Proteins/chemistry/genetics/*metabolism ; Nuclear Receptor Coactivator 1 ; Nuclear Receptor Coactivator 3 ; Protein Binding ; Receptors, Retinoic Acid/metabolism ; Recombinant Fusion Proteins/metabolism ; STAT1 Transcription Factor ; Trans-Activators/metabolism ; Transcription Factors/chemistry/genetics/*metabolism ; *Transcription, Genetic ; Transcriptional Activation ; Tretinoin/pharmacology
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  • 6
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    Protein kinase B kinases that mediate phosphatidylinositol 3,4,5-trisphosphate-dependent activation of protein kinase B (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-02-21
    Description: Protein kinase B (PKB) is activated in response to phosphoinositide 3-kinases and their lipid products phosphatidylinositol 3,4, 5-trisphosphate [PtdIns(3,4,5)P3] and PtdIns(3,4)P2 in the signaling pathways used by a wide variety of growth factors, antigens, and inflammatory stimuli. PKB is a direct target of these lipids, but this regulation is complex. The lipids can bind to the pleckstrin homologous domain of PKB, causing its translocation to the membrane, and also enable upstream, Thr308-directed kinases to phosphorylate and activate PKB. Four isoforms of these PKB kinases were purified from sheep brain. They bound PtdIns(3,4,5)P3 and associated with lipid vesicles containing it. These kinases contain an NH2-terminal catalytic domain and a COOH-terminal pleckstrin homologous domain, and their heterologous expression augments receptor activation of PKB, which suggests they are the primary signal transducers that enable PtdIns(3,4,5)P3 or PtdIns- (3,4)P2 to activate PKB and hence to control signaling pathways regulating cell survival, glucose uptake, and glycogen metabolism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stephens, L -- Anderson, K -- Stokoe, D -- Erdjument-Bromage, H -- Painter, G F -- Holmes, A B -- Gaffney, P R -- Reese, C B -- McCormick, F -- Tempst, P -- Coadwell, J -- Hawkins, P T -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 1998 Jan 30;279(5351):710-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Inositide Laboratory, The Babraham Institute, Babraham, Cambridge CB2 4AT, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9445477" target="_blank"〉PubMed〈/a〉
    Keywords: 3-Phosphoinositide-Dependent Protein Kinases ; Alternative Splicing ; Amino Acid Sequence ; Animals ; Cell Line ; Cell Membrane/enzymology ; Cloning, Molecular ; DNA, Complementary ; Drosophila ; Drosophila Proteins ; Enzyme Activation ; Humans ; Liposomes/metabolism ; Molecular Sequence Data ; Open Reading Frames ; Phosphatidylinositol Phosphates/*metabolism ; Phosphorylation ; Platelet-Derived Growth Factor/pharmacology ; Protein-Serine-Threonine Kinases/chemistry/genetics/isolation & ; purification/*metabolism ; Proto-Oncogene Proteins/*metabolism ; Proto-Oncogene Proteins c-akt ; Rats ; Recombinant Proteins/metabolism ; Sheep ; *Signal Transduction
    Print ISSN: 0036-8075
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  • 7
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    Genetic dissection of a mammalian replicator in the human beta-globin locus (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-08-14
    Description: The timing and localization of DNA replication initiation in mammalian cells are heritable traits, but it is not known whether initiation requires specific DNA sequences. A site-specific recombination strategy was used to show that DNA sequences previously identified as replication initiation sites could initiate replication when transferred to new chromosomal locations. An 8-kilobase DNA sequence encompassing the origin of DNA replication in the human beta-globin locus initiated replication in the simian genome. Specific deletions within the globin origin did not initiate replication in these chromosomal sites. These data suggest that initiation of DNA replication in mammalian cells requires specific sequence information and extend the replicon hypothesis to higher eukaryotes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Aladjem, M I -- Rodewald, L W -- Kolman, J L -- Wahl, G M -- CA48405/CA/NCI NIH HHS/ -- GM51104/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1998 Aug 14;281(5379):1005-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Gene Expression Laboratory, The Salk Institute, San Diego, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9703500" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cercopithecus aethiops ; DNA/genetics ; DNA Nucleotidyltransferases/metabolism ; *DNA Replication ; Gene Targeting ; Globins/*genetics ; Humans ; Integrases/metabolism ; Polymerase Chain Reaction ; *Replication Origin ; S Phase ; Sequence Deletion ; *Viral Proteins
    Print ISSN: 0036-8075
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  • 8
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    Direct phosphorylation of IkappaB by IKKalpha and IKKbeta: discrimination between free and NF-kappaB-bound substrate (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-08-28
    Description: A large protein complex mediates the phosphorylation of the inhibitor of kappaB (IkappaB), which results in the activation of nuclear factor kappaB (NF-kappaB). Two subunits of this complex, IkappaB kinase alpha (IKKalpha) and IkappaB kinase beta (IKKbeta), are required for NF-kappaB activation. Purified recombinant IKKalpha and IKKbeta expressed in insect cells were used to demonstrate that each protein can directly phosphorylate IkappaB proteins. IKKalpha and IKKbeta were found to form both homodimers and heterodimers. Both IKKalpha and IKKbeta phosphorylated IkappaB bound to NF-kappaB more efficiently than they phosphorylated free IkappaB. This result explains how free IkappaB can accumulate in cells in which IKK is still active and thus can contribute to the termination of NF-kappaB activation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zandi, E -- Chen, Y -- Karin, M -- AI 43477/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1998 Aug 28;281(5381):1360-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Gene Regulation and Signal Transduction, Department of Pharmacology, University of California at San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9721103" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Dimerization ; Enzyme Activation ; HeLa Cells ; Helix-Loop-Helix Motifs ; Humans ; I-kappa B Kinase ; Leucine Zippers ; Mutation ; NF-kappa B/antagonists & inhibitors/*metabolism ; Phosphorylation ; Protein-Serine-Threonine Kinases/chemistry/genetics/*metabolism ; Proto-Oncogene Proteins/*metabolism ; Recombinant Fusion Proteins/metabolism ; Recombinant Proteins/metabolism ; Spodoptera ; Transcription Factor RelB ; *Transcription Factors
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  • 9
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    BRCA1 required for transcription-coupled repair of oxidative DNA damage (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-08-14
    Description: The breast and ovarian cancer susceptibility gene BRCA1 encodes a zinc finger protein of unknown function. Association of the BRCA1 protein with the DNA repair protein Rad51 and changes in the phosphorylation and cellular localization of the protein after exposure to DNA-damaging agents are consistent with a role for BRCA1 in DNA repair. Here, it is shown that mouse embryonic stem cells deficient in BRCA1 are defective in the ability to carry out transcription-coupled repair of oxidative DNA damage, and are hypersensitive to ionizing radiation and hydrogen peroxide. These results suggest that BRCA1 participates, directly or indirectly, in transcription-coupled repair of oxidative DNA damage.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gowen, L C -- Avrutskaya, A V -- Latour, A M -- Koller, B H -- Leadon, S A -- CA40453/CA/NCI NIH HHS/ -- CA70490/CA/NCI NIH HHS/ -- IP50CA58223/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1998 Aug 14;281(5379):1009-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Curriculum in Genetics and Molecular Biology and Department of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9703501" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; BRCA1 Protein/genetics/*physiology ; Cell Line ; DNA Damage ; *DNA Repair ; Hydrogen Peroxide ; Mice ; Oxidation-Reduction ; Stem Cells ; Thymine/analogs & derivatives/immunology/metabolism ; Transcription, Genetic ; Ultraviolet Rays
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  • 10
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    Arabidopsis NPH1: a flavoprotein with the properties of a photoreceptor for phototropism (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-11-30
    Description: The NPH1 gene of Arabidopsis thaliana encodes a 120-kilodalton serine-threonine protein kinase hypothesized to function as a photoreceptor for phototropism. When expressed in insect cells, the NPH1 protein is phosphorylated in response to blue light irradiation. The biochemical and photochemical properties of the photosensitive protein reflect those of the native protein in microsomal membranes. Recombinant NPH1 noncovalently binds flavin mononucleotide, a likely chromophore for light-dependent autophosphorylation. The fluorescence excitation spectrum of the recombinant protein is similar to the action spectrum for phototropism, consistent with the conclusion that NPH1 is an autophosphorylating flavoprotein photoreceptor mediating phototropic responses in higher plants.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Christie, J M -- Reymond, P -- Powell, G K -- Bernasconi, P -- Raibekas, A A -- Liscum, E -- Briggs, W R -- New York, N.Y. -- Science. 1998 Nov 27;282(5394):1698-701.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Plant Biology, Carnegie Institution of Washington, 260 Panama Street, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9831559" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arabidopsis/genetics/*physiology ; *Arabidopsis Proteins ; Cell Line ; Cryptochromes ; *Drosophila Proteins ; *Eye Proteins ; Flavin Mononucleotide/metabolism ; Flavoproteins/physiology ; Genes, Plant ; Light ; Mutation ; Phosphoproteins/genetics/*metabolism ; Phosphorylation ; *Photoreceptor Cells, Invertebrate ; *Phototropism ; Protein-Serine-Threonine Kinases/genetics/*metabolism ; Receptors, G-Protein-Coupled ; Recombinant Proteins/metabolism ; Spectrometry, Fluorescence ; Spodoptera ; Transfection
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  • 11
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    Quantitation of transcription and clonal selection of single living cells with beta-lactamase as reporter (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-01-24
    Description: Gene expression was visualized in single living mammalian cells with beta-lactamase as a reporter that hydrolyzes a substrate loaded intracellularly as a membrane-permeant ester. Each enzyme molecule changed the fluorescence of many substrate molecules from green to blue by disrupting resonance energy transfer. This wavelength shift was detectable by eye or color film in individual cells containing less than 100 beta-lactamase molecules. The robust change in emission ratio reveals quantitative heterogeneity in real-time gene expression, enables clonal selection by flow cytometry, and forms a basis for high-throughput screening of pharmaceutical candidate drugs in living mammalian cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zlokarnik, G -- Negulescu, P A -- Knapp, T E -- Mere, L -- Burres, N -- Feng, L -- Whitney, M -- Roemer, K -- Tsien, R Y -- NS27177/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1998 Jan 2;279(5347):84-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Aurora Biosciences, 11010 Torreyana Road, San Diego, CA 92121, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9417030" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cell Separation/methods ; Clone Cells/*metabolism ; DNA-Binding Proteins/genetics/metabolism ; Drug Evaluation, Preclinical ; Energy Transfer ; Flow Cytometry ; Fluoresceins/metabolism ; Fluorescent Dyes/metabolism ; *Gene Expression ; *Genes, Reporter ; Half-Life ; Humans ; *Lactams ; Muscarinic Agonists/pharmacology ; Muscarinic Antagonists/pharmacology ; NFATC Transcription Factors ; *Nuclear Proteins ; Sensitivity and Specificity ; Spectrometry, Fluorescence ; Transcription Factors/genetics/metabolism ; *Transcription, Genetic ; Transfection ; Tumor Cells, Cultured ; Umbelliferones/metabolism ; beta-Lactamases/*genetics/metabolism ; beta-Lactams/metabolism
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  • 12
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    IEX-1L, an apoptosis inhibitor involved in NF-kappaB-mediated cell survival (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-08-14
    Description: Transcription factors of the nuclear factor-kappaB/rel (NF-kappaB) family may be important in cell survival by regulating unidentified, anti-apoptotic genes. One such gene that protects cells from apoptosis induced by Fas or tumor necrosis factor type alpha (TNF), IEX-1L, is described here. Its transcription induced by TNF was decreased in cells with defective NF-kappaB activation, rendering them sensitive to TNF-induced apoptosis, which was abolished by transfection with IEX-1L. In support, overexpression of antisense IEX-1L partially blocked TNF-induced expression of IEX-1L and sensitized normal cells to killing. This study demonstrates a key role of IEX-1L in cellular resistance to TNF-induced apoptosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wu, M X -- Ao, Z -- Prasad, K V -- Wu, R -- Schlossman, S F -- AI12069/AI/NIAID NIH HHS/ -- P30AI28691/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1998 Aug 14;281(5379):998-1001.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Tumor Immunology, Dana-Farber Cancer Institute, and the 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/9703517" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD95/physiology ; Apoptosis/genetics/*physiology ; Apoptosis Regulatory Proteins ; Cell Line ; Cell Survival ; Cloning, Molecular ; DNA, Antisense/genetics ; Gene Expression Regulation ; Genetic Vectors ; Humans ; Immediate-Early Proteins/genetics/*physiology ; Jurkat Cells ; Membrane Glycoproteins/genetics/*physiology ; Membrane Proteins ; Mice ; NF-kappa B/*physiology ; *Neoplasm Proteins ; Transfection ; Tumor Necrosis Factor-alpha/physiology
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  • 13
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    Membrane phospholipid control of nucleotide sensitivity of KATP channels (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-11-06
    Description: Adenosine triphosphate (ATP)-sensitive potassium (KATP) channels couple cell metabolism to electrical activity. Phosphatidylinositol phosphates (PIPs) profoundly antagonized ATP inhibition of KATP channels when applied to inside-out membrane patches. It is proposed that membrane-incorporated PIPs can bind to positive charges in the cytoplasmic region of the channel's Kir6.2 subunit, stabilizing the open state of the channel and antagonizing the inhibitory effect of ATP. The tremendous effect of PIPs on ATP sensitivity suggests that in vivo alterations of membrane PIP levels will have substantial effects on KATP channel activity and hence on the gain of metabolism-excitation coupling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shyng, S L -- Nichols, C G -- HL45742/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1998 Nov 6;282(5391):1138-41.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology and Physiology, Washington University School of Medicine, 660 South Euclid Avenue, St. Louis, MO 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9804554" target="_blank"〉PubMed〈/a〉
    Keywords: *ATP-Binding Cassette Transporters ; Adenosine Triphosphate/metabolism/*pharmacology ; Animals ; Binding Sites ; COS Cells ; Cell Line ; Islets of Langerhans/metabolism ; Mutation ; Myocardium/cytology/metabolism ; Patch-Clamp Techniques ; Phosphatidylinositol 4,5-Diphosphate/*metabolism/pharmacology ; Phosphatidylinositol Phosphates/*metabolism/pharmacology ; Potassium Channels/chemistry/genetics/*metabolism ; *Potassium Channels, Inwardly Rectifying ; Receptors, Drug/metabolism ; Recombinant Fusion Proteins/metabolism ; Sulfonylurea Receptors
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  • 14
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    Activation of the ATM kinase by ionizing radiation and phosphorylation of p53 (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-09-11
    Description: The p53 tumor suppressor protein is activated and phosphorylated on serine-15 in response to various DNA damaging agents. The gene product mutated in ataxia telangiectasia, ATM, acts upstream of p53 in a signal transduction pathway initiated by ionizing radiation. Immunoprecipitated ATM had intrinsic protein kinase activity and phosphorylated p53 on serine-15 in a manganese-dependent manner. Ionizing radiation, but not ultraviolet radiation, rapidly enhanced this p53-directed kinase activity of endogenous ATM. These observations, along with the fact that phosphorylation of p53 on serine-15 in response to ionizing radiation is reduced in ataxia telangiectasia cells, suggest that ATM is a protein kinase that phosphorylates p53 in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Canman, C E -- Lim, D S -- Cimprich, K A -- Taya, Y -- Tamai, K -- Sakaguchi, K -- Appella, E -- Kastan, M B -- Siliciano, J D -- CA71387/CA/NCI NIH HHS/ -- ES05777/ES/NIEHS NIH HHS/ -- New York, N.Y. -- Science. 1998 Sep 11;281(5383):1677-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Johns Hopkins School of Medicine, Oncology Center, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9733515" target="_blank"〉PubMed〈/a〉
    Keywords: Ataxia Telangiectasia Mutated Proteins ; Cell Cycle Proteins ; Cell Line ; DNA Damage ; DNA-Activated Protein Kinase ; *DNA-Binding Proteins ; Enzyme Activation ; Humans ; Lymphocytes/metabolism/radiation effects ; Mutation ; Nuclear Proteins ; Phosphatidylinositol 3-Kinases/metabolism ; Phosphorylation ; Phosphoserine/metabolism ; Protein Kinases/*metabolism ; Protein-Serine-Threonine Kinases/metabolism ; Proteins/genetics/*metabolism ; *Radiation, Ionizing ; Recombinant Fusion Proteins/metabolism ; Recombinant Proteins/metabolism ; Signal Transduction ; Transfection ; Tumor Suppressor Protein p53/*metabolism ; Tumor Suppressor Proteins ; Ultraviolet Rays
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  • 15
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    Uncoupling of nonreceptor tyrosine kinases from PLC-gamma1 in an SLP-76-deficient T cell (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-07-17
    Description: Activation of nonreceptor protein tyrosine kinases (PTKs) is essential for T cell receptor (TCR) responsiveness; however, the function of individual PTK substrates is often uncertain. A mutant T cell line was isolated that lacked expression of SLP-76 (SH2 domain-containing leukocyte protein of 76 kilodaltons), a hematopoietically expressed adaptor protein and PTK substrate. SLP-76 was not required for TCR-induced tyrosine phosphorylation of most proteins, but was required for optimal tyrosine phosphorylation and activation of phospholipase C-gamma1 (PLC-gamma1), as well as Ras pathway activation. TCR-inducible gene expression was dependent on SLP-76. Thus, coupling of TCR-regulated PTKs to downstream signaling pathways requires SLP-76.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yablonski, D -- Kuhne, M R -- Kadlecek, T -- Weiss, A -- CA72531/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1998 Jul 17;281(5375):413-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Howard Hughes Medical Institute, Box 0795, University of California, San Francisco, San Francisco, CA 94143-0795, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9665884" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptor Proteins, Signal Transducing ; Calcium/metabolism ; Calcium-Calmodulin-Dependent Protein Kinases/metabolism ; Carrier Proteins/metabolism ; Cell Line ; DNA-Binding Proteins/metabolism ; Enzyme Activation ; Gene Expression Regulation ; Humans ; Inositol Phosphates/metabolism ; Interleukin-2/genetics ; Isoenzymes/*metabolism ; Jurkat Cells ; *Membrane Proteins ; Mitogen-Activated Protein Kinase 1 ; NFATC Transcription Factors ; *Nuclear Proteins ; Phospholipase C gamma ; Phosphoproteins/metabolism/*physiology ; Phosphorylation ; Phosphotyrosine/metabolism ; Protein-Tyrosine Kinases/*metabolism ; Receptors, Antigen, T-Cell/*metabolism ; Signal Transduction ; T-Lymphocytes/enzymology/*metabolism ; Transcription Factors/metabolism ; Transcriptional Activation ; Transfection ; Type C Phospholipases/*metabolism ; ras Proteins/metabolism
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  • 16
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    Activation of apoptosis signal-regulating kinase 1 (ASK1) by the adapter protein Daxx (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-09-22
    Description: The Fas death receptor can activate the Jun NH2-terminal kinase (JNK) pathway through the receptor-associated protein Daxx. Daxx was found to activate the JNK kinase kinase ASK1, and overexpression of a kinase-deficient ASK1 mutant inhibited Fas- and Daxx-induced apoptosis and JNK activation. Fas activation induced Daxx to interact with ASK1, which consequently relieved an inhibitory intramolecular interaction between the amino- and carboxyl-termini of ASK1, activating its kinase activity. The Daxx-ASK1 connection completes a signaling pathway from a cell surface death receptor to kinase cascades that modulate nuclear transcription factors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chang, H Y -- Nishitoh, H -- Yang, X -- Ichijo, H -- Baltimore, D -- CA51462/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1998 Sep 18;281(5384):1860-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02138, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9743501" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; Alleles ; Amino Acid Sequence ; Animals ; Antigens, CD95/metabolism ; *Apoptosis ; Calcium-Calmodulin-Dependent Protein Kinases/metabolism ; Carrier Proteins/*metabolism ; Cell Line ; Enzyme Activation ; Humans ; *Intracellular Signaling Peptides and Proteins ; JNK Mitogen-Activated Protein Kinases ; MAP Kinase Kinase Kinases ; *Mitogen-Activated Protein Kinases ; Molecular Sequence Data ; *Nuclear Proteins ; Protein-Serine-Threonine Kinases/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Tumor Cells, Cultured
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 17
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    Role of MEKK1 in cell survival and activation of JNK and ERK pathways defined by targeted gene disruption (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-12-04
    Description: Targeted disruption of the gene encoding MEK kinase 1 (MEKK1), a mitogen-activated protein kinase (MAPK) kinase kinase, defined its function in the regulation of MAPK pathways and cell survival. MEKK1(-/-) embryonic stem cells from mice had lost or altered responses of the c-Jun amino-terminal kinase (JNK) to microtubule disruption and cold stress but activated JNK normally in response to heat shock, anisomycin, and ultraviolet irradiation. Activation of JNK was lost and that of extracellular signal-regulated protein kinase (ERK) was diminished in response to hyperosmolarity and serum factors in MEKK1(-/-) cells. Loss of MEKK1 expression resulted in a greater apoptotic response of cells to hyperosmolarity and microtubule disruption. When activated by specific stresses that alter cell shape and the cytoskeleton, MEKK1 signals to protect cells from apoptosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yujiri, T -- Sather, S -- Fanger, G R -- Johnson, G L -- DK37871/DK/NIDDK NIH HHS/ -- GM30324/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1998 Dec 4;282(5395):1911-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program in Molecular Signal Transduction, Division of Basic Sciences, National Jewish Medical and Research Center, Denver, CO 80206, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9836645" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anisomycin/pharmacology ; Apoptosis ; Calcium-Calmodulin-Dependent Protein Kinases/*metabolism ; Cell Line ; Cell Size ; *Cell Survival ; Enzyme Activation ; Gene Targeting ; JNK Mitogen-Activated Protein Kinases ; Lysophospholipids/pharmacology ; *MAP Kinase Kinase 4 ; *MAP Kinase Kinase Kinase 1 ; Mice ; *Mitogen-Activated Protein Kinase Kinases ; *Mitogen-Activated Protein Kinases ; Nocodazole/pharmacology ; Osmolar Concentration ; Phosphorylation ; Protein-Serine-Threonine Kinases/genetics/*metabolism ; Protein-Tyrosine Kinases/metabolism ; Recombinant Proteins/metabolism ; Stem Cells ; Temperature ; Transfection ; Ultraviolet Rays
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 18
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    Sphingosine-1-phosphate as a ligand for the G protein-coupled receptor EDG-1 (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-03-21
    Description: The sphingolipid metabolite sphingosine-1-phosphate (SPP) has been implicated as a second messenger in cell proliferation and survival. However, many of its biological effects are due to binding to unidentified receptors on the cell surface. SPP activated the heterotrimeric guanine nucleotide binding protein (G protein)-coupled orphan receptor EDG-1, originally cloned as Endothelial Differentiation Gene-1. EDG-1 bound SPP with high affinity (dissociation constant = 8.1 nM) and high specificity. Overexpression of EDG-1 induced exaggerated cell-cell aggregation, enhanced expression of cadherins, and formation of well-developed adherens junctions in a manner dependent on SPP and the small guanine nucleotide binding protein Rho.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, M J -- Van Brocklyn, J R -- Thangada, S -- Liu, C H -- Hand, A R -- Menzeleev, R -- Spiegel, S -- Hla, T -- DK45659/DK/NIDDK NIH HHS/ -- GM43880/GM/NIGMS NIH HHS/ -- HL49094/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1998 Mar 6;279(5356):1552-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, University of Connecticut School of Medicine, Farmington, CT 06030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9488656" target="_blank"〉PubMed〈/a〉
    Keywords: Cadherins/*biosynthesis ; *Cell Aggregation ; Cell Differentiation ; Cell Line ; Cloning, Molecular ; GTP-Binding Proteins/metabolism ; Gene Expression ; Genes, Immediate-Early ; Humans ; Immediate-Early Proteins/genetics/*metabolism ; Intercellular Junctions/*ultrastructure ; Ligands ; *Lysophospholipids ; Mitogen-Activated Protein Kinase 1/metabolism ; Morphogenesis ; Receptors, Cell Surface/genetics/*metabolism ; *Receptors, G-Protein-Coupled ; Receptors, Lysophospholipid ; Signal Transduction ; Sphingosine/*analogs & derivatives/metabolism ; Transfection ; rho GTP-Binding Proteins
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  • 19
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    CBP: a signal-regulated transcriptional coactivator controlled by nuclear calcium and CaM kinase IV (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-09-04
    Description: Recruitment of the coactivator, CREB binding protein (CBP), by signal-regulated transcription factors, such as CREB [adenosine 3', 5'-monophosphate (cAMP) response element binding protein], is critical for stimulation of gene expression. The mouse pituitary cell line AtT20 was used to show that the CBP recruitment step (CREB phosphorylation on serine-133) can be uncoupled from CREB/CBP-activated transcription. CBP was found to contain a signal-regulated transcriptional activation domain that is controlled by nuclear calcium and calcium/calmodulin-dependent (CaM) protein kinase IV and by cAMP. Cytoplasmic calcium signals that stimulate the Ras mitogen-activated protein kinase signaling cascade or expression of the activated form of Ras provided the CBP recruitment signal but did not increase CBP activity and failed to activate CREB- and CBP-mediated transcription. These results identify CBP as a signal-regulated transcriptional coactivator and define a regulatory role for nuclear calcium and cAMP in CBP-dependent gene expression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chawla, S -- Hardingham, G E -- Quinn, D R -- Bading, H -- New York, N.Y. -- Science. 1998 Sep 4;281(5382):1505-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council, Laboratory of Molecular Biology, Hills Road, Cambridge CB2 2QH, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9727976" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CREB-Binding Protein ; Calcium/*metabolism ; Calcium Channels/metabolism ; Calcium-Calmodulin-Dependent Protein Kinase Type 2 ; Calcium-Calmodulin-Dependent Protein Kinase Type 4 ; Calcium-Calmodulin-Dependent Protein Kinases/antagonists & inhibitors/*metabolism ; Cell Line ; Cell Nucleus/*metabolism ; Cyclic AMP/metabolism ; Cyclic AMP Response Element-Binding Protein/metabolism ; Cytoplasm/metabolism ; Genes, Reporter ; Mice ; Models, Genetic ; Nuclear Proteins/*metabolism ; Phosphorylation ; Phosphoserine/metabolism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Trans-Activators/*metabolism ; Transcription, Genetic ; *Transcriptional Activation ; ras Proteins/metabolism
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  • 20
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    Recognition of stress-induced MHC molecules by intestinal epithelial gammadelta T cells (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-03-28
    Description: T cells with variable region Vdelta1 gammadelta T cell receptors (TCRs) are distributed throughout the human intestinal epithelium and may function as sentinels that respond to self antigens. The expression of a major histocompatibility complex (MHC) class I-related molecule, MICA, matches this localization. MICA and the closely related MICB were recognized by intestinal epithelial T cells expressing diverse Vdelta1 gammadelta TCRs. These interactions involved the alpha1alpha2 domains of MICA and MICB but were independent of antigen processing. With intestinal epithelial cell lines, the expression and recognition of MICA and MICB could be stress-induced. Thus, these molecules may broadly regulate protective responses by the Vdelta1 gammadelta T cells in the epithelium of the intestinal tract.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Groh, V -- Steinle, A -- Bauer, S -- Spies, T -- P01 CA18221/CA/NCI NIH HHS/ -- R01 AI30581/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1998 Mar 13;279(5357):1737-40.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Fred Hutchinson Cancer Research Center, Clinical Research Division, 1100 Fairview Avenue North, Seattle, WA 98109, USA. vgroh@fred.fhcrc.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9497295" target="_blank"〉PubMed〈/a〉
    Keywords: Antigen Presentation ; Carrier Proteins/analysis/*immunology ; Cell Line ; Cytotoxicity, Immunologic ; Heat-Shock Response ; Histocompatibility Antigens Class I/analysis/*immunology ; Hot Temperature ; Humans ; Immunophenotyping ; Intestinal Mucosa/cytology/*immunology ; Ligands ; Receptors, Antigen, T-Cell, gamma-delta/*immunology ; T-Lymphocyte Subsets/*immunology ; 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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  • 21
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    p53-independent role of MDM2 in TGF-beta1 resistance (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-12-18
    Description: Transforming growth factor-beta (TGF-beta) inhibits cell proliferation, and acquisition of TGF-beta resistance has been linked to tumorigenesis. A genetic screen was performed to identify complementary DNAs that abrogated TGF-beta sensitivity in mink lung epithelial cells. Ectopic expression of murine double minute 2 rescued TGF-beta-induced growth arrest in a p53-independent manner by interference with retinoblastoma susceptibility gene product (Rb)/E2F function. In human breast tumor cells, increased MDM2 expression levels correlated with TGF-beta resistance. Thus, MDM2 may confer TGF-beta resistance in a subset of tumors and may promote tumorigenesis by interference with two independent tumor suppressors, p53 and Rb.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sun, P -- Dong, P -- Dai, K -- Hannon, G J -- Beach, D -- New York, N.Y. -- Science. 1998 Dec 18;282(5397):2270-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cold Spring Harbor Laboratory, 1 Bungtown Road, Cold Spring Harbor, NY 11724, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9856953" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Breast Neoplasms/genetics/metabolism/pathology ; *Carrier Proteins ; *Cell Cycle Proteins ; *Cell Division ; Cell Line ; Cell Transformation, Neoplastic ; *DNA-Binding Proteins ; Drug Resistance, Neoplasm ; E2F Transcription Factors ; Gene Expression ; Genes, Retinoblastoma ; Genes, p53 ; Genetic Vectors ; Humans ; Mice ; Mink ; *Nuclear Proteins ; Phosphorylation ; Proto-Oncogene Proteins/genetics/*physiology ; Proto-Oncogene Proteins c-mdm2 ; Retinoblastoma Protein/metabolism ; Retinoblastoma-Binding Protein 1 ; Signal Transduction ; Transcription Factor DP1 ; Transcription Factors/genetics/metabolism ; Transcription, Genetic ; Transforming Growth Factor beta/*pharmacology/physiology ; Tumor Cells, Cultured ; Tumor Suppressor Protein p53/*physiology
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  • 22
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    Inhibition of cell migration, spreading, and focal adhesions by tumor suppressor PTEN (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-06-11
    Description: The tumor suppressor PTEN is a phosphatase with sequence similarity to the cytoskeletal protein tensin. Here the cellular roles of PTEN were investigated. Overexpression of PTEN inhibited cell migration, whereas antisense PTEN enhanced migration. Integrin-mediated cell spreading and the formation of focal adhesions were down-regulated by wild-type PTEN but not by PTEN with an inactive phosphatase domain. PTEN interacted with the focal adhesion kinase FAK and reduced its tyrosine phosphorylation. Overexpression of FAK partially antagonized the effects of PTEN. Thus, PTEN phosphatase may function as a tumor suppressor by negatively regulating cell interactions with the extracellular matrix.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tamura, M -- Gu, J -- Matsumoto, K -- Aota, S -- Parsons, R -- Yamada, K M -- New York, N.Y. -- Science. 1998 Jun 5;280(5369):1614-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Craniofacial Developmental Biology and Regeneration Branch, National Institute of Dental Research, National Institutes of Health, Bethesda, MD 20892-4370, USA. mtamura@yoda.nidr.nih.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9616126" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Animals ; *Cell Adhesion ; Cell Adhesion Molecules/metabolism ; Cell Line ; *Cell Movement ; Cell Size ; Concanavalin A ; Down-Regulation ; Ecdysone/pharmacology ; Fibronectins ; Focal Adhesion Kinase 1 ; Focal Adhesion Protein-Tyrosine Kinases ; Genes, Tumor Suppressor ; Humans ; Integrins/physiology ; Mice ; Mutation ; PTEN Phosphohydrolase ; *Phosphoric Monoester Hydrolases ; Phosphorylation ; Polylysine ; Protein Tyrosine Phosphatases/genetics/metabolism/pharmacology/*physiology ; Protein-Tyrosine Kinases/metabolism ; Recombinant Proteins/pharmacology ; Signal Transduction ; Transfection ; Tumor Cells, Cultured ; *Tumor Suppressor Proteins
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  • 23
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    Characterization of an avian influenza A (H5N1) virus isolated from a child with a fatal respiratory illness (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-02-07
    Description: An avian H5N1 influenza A virus (A/Hong Kong/156/97) was isolated from a tracheal aspirate obtained from a 3-year-old child in Hong Kong with a fatal illness consistent with influenza. Serologic analysis indicated the presence of an H5 hemagglutinin. All eight RNA segments were derived from an avian influenza A virus. The hemagglutinin contained multiple basic amino acids adjacent to the cleavage site, a feature characteristic of highly pathogenic avian influenza A viruses. The virus caused 87.5 to 100 percent mortality in experimentally inoculated White Plymouth Rock and White Leghorn chickens. These results may have implications for global influenza surveillance and planning for pandemic influenza.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Subbarao, K -- Klimov, A -- Katz, J -- Regnery, H -- Lim, W -- Hall, H -- Perdue, M -- Swayne, D -- Bender, C -- Huang, J -- Hemphill, M -- Rowe, T -- Shaw, M -- Xu, X -- Fukuda, K -- Cox, N -- New York, N.Y. -- Science. 1998 Jan 16;279(5349):393-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Influenza Branch, Centers for Disease Control and Prevention, Atlanta, GA 30333, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9430591" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cell Line ; Chickens ; Child, Preschool ; Disease Outbreaks ; Fatal Outcome ; Female ; Genes, Viral ; Hemagglutinin Glycoproteins, Influenza Virus/chemistry/*genetics ; Hong Kong/epidemiology ; Humans ; *Influenza A Virus, H5N1 Subtype ; Influenza A virus/*genetics/isolation & purification/*pathogenicity ; Influenza in Birds/virology ; Influenza, Human/epidemiology/*virology ; Male ; Molecular Sequence Data ; Neuraminidase/genetics ; Phylogeny ; Virulence ; Virus Replication
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    Feedback inhibition of macrophage tumor necrosis factor-alpha production by tristetraprolin (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-08-14
    Description: Tumor necrosis factor-alpha (TNF-alpha) is a major mediator of both acute and chronic inflammatory responses in many diseases. Tristetraprolin (TTP), the prototype of a class of Cys-Cys-Cys-His (CCCH) zinc finger proteins, inhibited TNF-alpha production from macrophages by destabilizing its messenger RNA. This effect appeared to result from direct TTP binding to the AU-rich element of the TNF-alpha messenger RNA. TTP is a cytosolic protein in these cells, and its biosynthesis was induced by the same agents that stimulate TNF-alpha production, including TNF-alpha itself. These findings identify TTP as a component of a negative feedback loop that interferes with TNF-alpha production by destabilizing its messenger RNA. This pathway represents a potential target for anti-TNF-alpha therapies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Carballo, E -- Lai, W S -- Blackshear, P J -- New York, N.Y. -- Science. 1998 Aug 14;281(5379):1001-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Office of Clinical Research and Laboratory of Signal Transduction, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9703499" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Animals ; Base Sequence ; Biological Transport ; Cell Line ; Cell Nucleus/metabolism ; Chick Embryo ; Cytosol/metabolism ; *DNA-Binding Proteins ; Feedback ; Gene Expression Regulation ; Humans ; *Immediate-Early Proteins ; Lipopolysaccharides/pharmacology ; Macrophages/*physiology ; Mice ; Mice, Knockout ; Proteins/*physiology ; RNA Probes ; RNA, Messenger/chemistry/genetics/metabolism ; Transfection ; Tristetraprolin ; Tumor Necrosis Factor-alpha/antagonists & inhibitors/*biosynthesis/genetics ; *Zinc Fingers
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    Regulation of cell death protease caspase-9 by phosphorylation (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-11-13
    Description: Caspases are intracellular proteases that function as initiators and effectors of apoptosis. The kinase Akt and p21-Ras, an Akt activator, induced phosphorylation of pro-caspase-9 (pro-Casp9) in cells. Cytochrome c-induced proteolytic processing of pro-Casp9 was defective in cytosolic extracts from cells expressing either active Ras or Akt. Akt phosphorylated recombinant Casp9 in vitro on serine-196 and inhibited its protease activity. Mutant pro-Casp9(Ser196Ala) was resistant to Akt-mediated phosphorylation and inhibition in vitro and in cells, resulting in Akt-resistant induction of apoptosis. Thus, caspases can be directly regulated by protein phosphorylation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cardone, M H -- Roy, N -- Stennicke, H R -- Salvesen, G S -- Franke, T F -- Stanbridge, E -- Frisch, S -- Reed, J C -- CA-69381/CA/NCI NIH HHS/ -- CA-69515/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1998 Nov 13;282(5392):1318-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program on Apoptosis and Cell Death Research, The Burnham Institute, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9812896" target="_blank"〉PubMed〈/a〉
    Keywords: *Apoptosis ; Caspase 9 ; Caspase Inhibitors ; Caspases/*metabolism ; Cell Line ; Cytochrome c Group/pharmacology ; Enzyme Precursors/metabolism ; Humans ; Mass Spectrometry ; Mutation ; Peptide Fragments/metabolism ; Phosphorylation ; Phosphoserine/metabolism ; Protein-Serine-Threonine Kinases/metabolism ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins c-akt ; Proto-Oncogene Proteins p21(ras)/metabolism ; Recombinant Fusion Proteins/metabolism ; Transfection
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    Partial hormone resistance in mice with disruption of the steroid receptor coactivator-1 (SRC-1) gene (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-04-16
    Description: The in vivo biological function of a steroid receptor coactivator was assessed in mice in which the SRC-1 gene was inactivated by gene targeting. Although in both sexes the homozygous mutants were viable and fertile, target organs such as uterus, prostate, testis, and mammary gland exhibited decreased growth and development in response to steroid hormones. Expression of RNA encoding TIF2, a member of the SRC-1 family, was increased in the SRC-1 null mutant, perhaps compensating partially for the loss of SRC-1 function in target tissues. The results indicate that SRC-1 mediates steroid hormone responses in vivo and that loss of its coactivator function results in partial resistance to hormone.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Xu, J -- Qiu, Y -- DeMayo, F J -- Tsai, S Y -- Tsai, M J -- O'Malley, B W -- New York, N.Y. -- Science. 1998 Mar 20;279(5358):1922-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Baylor College of Medicine, Houston, TX 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9506940" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Drug Resistance ; Estradiol/blood/pharmacology ; Female ; Gene Targeting ; Genitalia, Male/drug effects/*growth & development ; Gonadal Steroid Hormones/*pharmacology ; Histone Acetyltransferases ; Male ; Mammary Glands, Animal/drug effects/*growth & development ; Mice ; Nuclear Receptor Coactivator 1 ; Nuclear Receptor Coactivator 2 ; Organ Size/drug effects ; Pregnancy ; Progesterone/blood/pharmacology ; Prostate/drug effects/growth & development ; Stem Cells ; Testis/drug effects/growth & development ; Testosterone/blood/pharmacology ; Transcription Factors/genetics/*physiology ; Uterus/drug effects/*growth & development
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    Distinct cellular interactions of secreted and transmembrane Ebola virus glycoproteins (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-03-07
    Description: The mechanisms by which Ebola virus evades detection and infects cells to cause hemorrhagic fever have not been defined, though its glycoprotein, synthesized in either a secreted or transmembrane form, is likely involved. Here the secreted glycoprotein was found to interact with neutrophils through CD16b, the neutrophil-specific form of the Fc gamma receptor III, whereas the transmembrane glycoprotein was found to interact with endothelial cells but not neutrophils. A murine retroviral vector pseudotyped with the transmembrane glycoprotein preferentially infected endothelial cells. Thus, the secreted glycoprotein inhibits early neutrophil activation, which likely affects the host response to infection, whereas binding of the transmembrane glycoprotein to endothelial cells may contribute to the hemorrhagic symptoms of this disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yang, Z -- Delgado, R -- Xu, L -- Todd, R F -- Nabel, E G -- Sanchez, A -- Nabel, G J -- New York, N.Y. -- Science. 1998 Feb 13;279(5353):1034-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Internal Medicine, University of Michigan, Ann Arbor, MI 48109, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9461435" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Ebolavirus/genetics/metabolism/*pathogenicity/physiology ; Endothelium, Vascular/cytology/*metabolism/virology ; Genes, Viral ; Genetic Vectors ; Glycoproteins/genetics/*metabolism/secretion ; Hemorrhagic Fever, Ebola/virology ; Humans ; L-Selectin/metabolism ; Membrane Glycoproteins/genetics/*metabolism ; Moloney murine leukemia virus/genetics/physiology ; Neutrophil Activation ; Neutrophils/immunology/*metabolism ; Receptors, IgG/metabolism ; Transfection ; Tumor Cells, Cultured ; Viral Matrix Proteins/genetics/*metabolism ; Viral Proteins/genetics/*metabolism/secretion
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    Identification of two distinct mechanisms of phagocytosis controlled by different Rho GTPases (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-11-30
    Description: The complement and immunoglobulin receptors are the major phagocytic receptors involved during infection. However, only immunoglobulin-dependent uptake results in a respiratory burst and an inflammatory response in macrophages. Rho guanosine triphosphatases (molecular switches that control the organization of the actin cytoskeleton) were found to be essential for both types of phagocytosis. Two distinct mechanisms of phagocytosis were identified: Type I, used by the immunoglobulin receptor, is mediated by Cdc42 and Rac, and type II, used by the complement receptor, is mediated by Rho. These results suggest a molecular basis for the different biological consequences that are associated with phagocytosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Caron, E -- Hall, A -- New York, N.Y. -- Science. 1998 Nov 27;282(5394):1717-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council Laboratory for Molecular Cell Biology, Cancer Research Campaign Oncogene and Signal Transduction Group, and Department of Biochemistry, University College London, Gower Street, London WC1E 6BT, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9831565" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Actins/metabolism ; Animals ; Antigens, CD/*immunology/metabolism ; *Bacterial Proteins ; Bacterial Toxins/pharmacology ; COS Cells ; Cell Cycle Proteins/metabolism ; Cell Line ; Enzyme Activation ; Erythrocytes/immunology ; GTP Phosphohydrolases/*metabolism ; GTP-Binding Proteins/metabolism ; Macrophage-1 Antigen/*immunology/metabolism ; Macrophages/immunology ; Mice ; Opsonin Proteins ; *Phagocytosis ; Phagosomes/enzymology ; Receptors, IgG/*immunology/metabolism ; Transfection ; cdc42 GTP-Binding Protein ; rac GTP-Binding Proteins
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    Protein kinase C isotypes controlled by phosphoinositide 3-kinase through the protein kinase PDK1 (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-09-25
    Description: Phosphorylation sites in members of the protein kinase A (PKA), PKG, and PKC kinase subfamily are conserved. Thus, the PKB kinase PDK1 may be responsible for the phosphorylation of PKC isotypes. PDK1 phosphorylated the activation loop sites of PKCzeta and PKCdelta in vitro and in a phosphoinositide 3-kinase (PI 3-kinase)-dependent manner in vivo in human embryonic kidney (293) cells. All members of the PKC family tested formed complexes with PDK1. PDK1-dependent phosphorylation of PKCdelta in vitro was stimulated by combined PKC and PDK1 activators. The activation loop phosphorylation of PKCdelta in response to serum stimulation of cells was PI 3-kinase-dependent and was enhanced by PDK1 coexpression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Le Good, J A -- Ziegler, W H -- Parekh, D B -- Alessi, D R -- Cohen, P -- Parker, P J -- New York, N.Y. -- Science. 1998 Sep 25;281(5385):2042-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Protein Phosphorylation Laboratory, Imperial Cancer Research Fund, 44 Lincoln's Inn Fields, London WC2A 3PX, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9748166" target="_blank"〉PubMed〈/a〉
    Keywords: 3-Phosphoinositide-Dependent Protein Kinases ; Binding Sites ; Cell Line ; Chromones/pharmacology ; Enzyme Activation ; Enzyme Inhibitors/pharmacology ; Humans ; Isoenzymes/*metabolism ; Morpholines/pharmacology ; Phosphatidylcholines/pharmacology ; Phosphatidylinositol 3-Kinases/*metabolism ; Phosphatidylinositol Phosphates ; Phosphatidylserines/pharmacology ; Phosphorylation ; Protein Kinase C/*metabolism ; Protein Kinase C beta ; Protein-Serine-Threonine Kinases/*metabolism ; Recombinant Proteins/metabolism ; Tetradecanoylphorbol Acetate/pharmacology
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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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  • 31
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    Role of substrates and products of PI 3-kinase in regulating activation of Rac-related guanosine triphosphatases by Vav (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-02-07
    Description: Mitogen stimulation of cytoskeletal changes and c-jun amino-terminal kinases is mediated by Rac small guanine nucleotide-binding proteins. Vav, a guanosine diphosphate (GDP)-guanosine triphosphate (GTP) exchange factor for Rac that stimulates the exchange of bound GDP for GTP, bound to and was directly controlled by substrates and products of phosphoinositide (PI) 3-kinase. The PI 3-kinase substrate phosphatidylinositol-4,5-bisphosphate inhibited activation of Vav by the tyrosine kinase Lck, whereas the product phosphatidylinositol-3,4,5-trisphosphate enhanced phosphorylation and activation of Vav by Lck. Control of Vav in response to mitogens by the products of PI 3-kinase suggests a mechanism for Ras-dependent activation of Rac.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Han, J -- Luby-Phelps, K -- Das, B -- Shu, X -- Xia, Y -- Mosteller, R D -- Krishna, U M -- Falck, J R -- White, M A -- Broek, D -- CA50261/CA/NCI NIH HHS/ -- CA71443/CA/NCI NIH HHS/ -- GM31278/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1998 Jan 23;279(5350):558-60.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Biology, Norris Comprehensive Cancer Center, University of Southern California, Los Angeles, CA 90033-0800, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9438848" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cell Line ; Enzyme Activation ; GTP Phosphohydrolases/*metabolism ; GTP-Binding Proteins/*metabolism ; Guanine Nucleotide Exchange Factors ; Guanosine Diphosphate/*metabolism ; Guanosine Triphosphate/metabolism ; Inositol 1,4,5-Trisphosphate/metabolism/pharmacology ; Lymphocyte Specific Protein Tyrosine Kinase p56(lck)/metabolism ; Mutagenesis, Site-Directed ; Oncogene Proteins/chemistry/*metabolism ; Phosphatidylinositol 3-Kinases/*metabolism ; Phosphatidylinositol 4,5-Diphosphate/metabolism/pharmacology ; Phosphatidylinositol Phosphates/metabolism/pharmacology ; Phosphatidylinositols/*metabolism/pharmacology ; Phosphorylation ; Proteins/metabolism ; Proto-Oncogene Proteins c-vav ; Rats ; rac GTP-Binding Proteins ; ras Guanine Nucleotide Exchange Factors
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    Structure of the amino-terminal protein interaction domain of STAT-4 (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-03-07
    Description: STATs (signal transducers and activators of transcription) are a family of transcription factors that are specifically activated to regulate gene transcription when cells encounter cytokines and growth factors. The crystal structure of an NH2-terminal conserved domain (N-domain) comprising the first 123 residues of STAT-4 was determined at 1.45 angstroms. The domain consists of eight helices that are assembled into a hook-like structure. The N-domain has been implicated in several protein-protein interactions affecting transcription, and it enables dimerized STAT molecules to polymerize and to bind DNA cooperatively. The structure shows that N-domains can interact through an extensive interface formed by polar interactions across one face of the hook. Mutagenesis of an invariant tryptophan residue at the heart of this interface abolished cooperative DNA binding by the full-length protein in vitro and reduced the transcriptional response after cytokine stimulation in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vinkemeier, U -- Moarefi, I -- Darnell, J E Jr -- Kuriyan, J -- AI32489/AI/NIAID NIH HHS/ -- AI34420/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1998 Feb 13;279(5353):1048-52.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Cell Biology and Laboratories of Molecular Biophysics, The Rockefeller University, New York, NY 10021, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9461439" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Binding Sites ; Cell Line ; Crystallography, X-Ray ; DNA/metabolism ; DNA-Binding Proteins/*chemistry/genetics/metabolism ; Humans ; Hydrogen Bonding ; Interferon-gamma/pharmacology ; Models, Molecular ; Molecular Sequence Data ; Oligodeoxyribonucleotides/metabolism ; *Protein Conformation ; Protein Structure, Tertiary ; STAT1 Transcription Factor ; STAT4 Transcription Factor ; Signal Transduction ; Trans-Activators/*chemistry/genetics/metabolism ; Transcription, Genetic ; Transfection ; src Homology Domains
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  • 33
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    Coupled gating between individual skeletal muscle Ca2+ release channels (ryanodine receptors) (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-08-07
    Description: Excitation-contraction coupling in skeletal muscle requires the release of intracellular calcium ions (Ca2+) through ryanodine receptor (RyR1) channels in the sarcoplasmic reticulum. Half of the RyR1 channels are activated by voltage-dependent Ca2+ channels in the plasma membrane. In planar lipid bilayers, RyR1 channels exhibited simultaneous openings and closings, termed "coupled gating." Addition of the channel accessory protein FKBP12 induced coupled gating, and removal of FKBP12 uncoupled channels. Coupled gating provides a mechanism by which RyR1 channels that are not associated with voltage-dependent Ca2+ channels can be regulated.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, S O -- Ondrias, K -- Marks, A R -- R01A139794/PHS HHS/ -- R01HL56180/HL/NHLBI NIH HHS/ -- R03TW00949/TW/FIC NIH HHS/ -- New York, N.Y. -- Science. 1998 Aug 7;281(5378):818-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Cardiology Program, Divisions of Cardiology and Circulatory Physiology, Department of Medicine, Columbia University College of Physicians and Surgeons, New York, NY 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9694652" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/*metabolism ; Calcium Channels/metabolism ; Carrier Proteins/metabolism ; Cell Line ; DNA-Binding Proteins/metabolism ; Heat-Shock Proteins/metabolism ; *Ion Channel Gating/drug effects ; Lipid Bilayers ; Muscle, Skeletal/metabolism ; Polyenes/pharmacology ; Probability ; Rabbits ; Recombinant Proteins/metabolism ; Ryanodine/metabolism ; Ryanodine Receptor Calcium Release Channel/*metabolism ; Sarcoplasmic Reticulum/*metabolism ; Sirolimus ; Spodoptera ; Tacrolimus Binding Proteins
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  • 34
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    Promotion of trophoblast stem cell proliferation by FGF4 (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-12-16
    Description: The trophoblast cell lineage is essential for the survival of the mammalian embryo in utero. This lineage is specified before implantation into the uterus and is restricted to form the fetal portion of the placenta. A culture of mouse blastocysts or early postimplantation trophoblasts in the presence of fibroblast growth factor 4 (FGF4) permitted the isolation of permanent trophoblast stem cell lines. These cell lines differentiated to other trophoblast subtypes in vitro in the absence of FGF4 and exclusively contributed to the trophoblast lineage in vivo in chimeras.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tanaka, S -- Kunath, T -- Hadjantonakis, A K -- Nagy, A -- Rossant, J -- New York, N.Y. -- Science. 1998 Dec 11;282(5396):2072-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, Ontario M5G 1X5, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9851926" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blastocyst/cytology ; Cell Differentiation ; Cell Division ; Cell Line ; Cell Lineage ; Chimera ; Culture Media, Conditioned ; Embryo, Mammalian/cytology ; Female ; Fibroblast Growth Factor 4 ; Fibroblast Growth Factors/*pharmacology/physiology ; Fibroblasts/cytology ; Gene Expression Regulation, Developmental ; Genetic Markers ; Karyotyping ; Male ; Mice ; Models, Biological ; Proto-Oncogene Proteins/*pharmacology/physiology ; Signal Transduction ; Stem Cells/*cytology/metabolism ; Trophoblasts/*cytology/metabolism
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    The tetrameric structure of a glutamate receptor channel (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-06-11
    Description: The subunit stoichiometry of several ligand-gated ion channel receptors is still unknown. A counting method was developed to determine the number of subunits in one family of brain glutamate receptors. Successful application of this method in an HEK cell line provides evidence that ionotropic glutamate receptors share a tetrameric structure with the voltage-gated potassium channels. The average conductance of these channels depends on how many subunits are occupied by an agonist.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rosenmund, C -- Stern-Bach, Y -- Stevens, C F -- NS 12961/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1998 Jun 5;280(5369):1596-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Workgroup Cellular Neurobiology, Max-Planck-Institute for Biophysical Chemistry, Gottingen, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9616121" target="_blank"〉PubMed〈/a〉
    Keywords: Binding Sites ; Cell Line ; Electric Conductivity ; Excitatory Amino Acid Agonists/metabolism ; Excitatory Amino Acid Antagonists/metabolism ; Humans ; Ligands ; Macromolecular Substances ; Models, Biological ; Patch-Clamp Techniques ; Quinoxalines/metabolism ; Quisqualic Acid/metabolism ; Receptors, AMPA/agonists/antagonists & inhibitors/*chemistry/*metabolism ; Receptors, Glutamate/chemistry/metabolism ; Receptors, Kainic Acid/agonists/antagonists & inhibitors/*chemistry/metabolism ; Recombinant Fusion Proteins/chemistry/metabolism
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    Role of vesicle-associated syntaxin 5 in the assembly of pre-Golgi intermediates (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-02-21
    Description: Syntaxins are thought to function during vesicular transport as receptors on the target membrane and to contribute to the specificity of membrane docking and fusion by interacting with vesicle-associated receptors. Here, syntaxin 5 (Syn5) was shown to be an integral component of endoplasmic reticulum-derived transport vesicles. This pool, but not the target, Golgi-associated Syn5 pool, was essential for the assembly of vesicular-tubular pre-Golgi intermediates and the delivery of cargo to the Golgi. The requirement for vesicle-associated Syn5 in transport suggests a reevaluation of the basis for operation of the early secretory pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rowe, T -- Dascher, C -- Bannykh, S -- Plutner, H -- Balch, W E -- CA58689/CA/NCI NIH HHS/ -- GM 42336/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1998 Jan 30;279(5351):696-700.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9445473" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Animals ; Antibodies ; Biological Transport ; Carrier Proteins/metabolism ; Cell Line ; Endoplasmic Reticulum/*metabolism ; Golgi Apparatus/*metabolism/ultrastructure ; Mannose-Binding Lectins ; Membrane Fusion ; *Membrane Glycoproteins ; Membrane Proteins/immunology/*metabolism ; N-Ethylmaleimide-Sensitive Proteins ; Organelles/metabolism ; Qa-SNARE Proteins ; Qb-SNARE Proteins ; Qc-SNARE Proteins ; R-SNARE Proteins ; Rats ; SNARE Proteins ; *Vesicular Transport Proteins ; Vesicular stomatitis Indiana virus/physiology ; Viral Envelope Proteins/metabolism
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    Attenuation of virulence by disruption of the Mycobacterium tuberculosis erp gene (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-10-23
    Description: The virulence of the mycobacteria that cause tuberculosis depends on their ability to multiply in mammalian hosts. Disruption of the bacterial erp gene, which encodes the exported repetitive protein, impaired multiplication of M. tuberculosis and M. bovis Bacille Calmette-Guerin in cultured macrophages and mice. Reintroduction of erp into the mutants restored their ability to multiply. These results indicate that erp contributes to the virulence of M. tuberculosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Berthet, F X -- Lagranderie, M -- Gounon, P -- Laurent-Winter, C -- Ensergueix, D -- Chavarot, P -- Thouron, F -- Maranghi, E -- Pelicic, V -- Portnoi, D -- Marchal, G -- Gicquel, B -- AI 35207/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1998 Oct 23;282(5389):759-62.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Unite de Genetique Mycobacterienne, Institut Pasteur, 25 rue du Docteur Roux, 75724 Paris Cedex 15, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9784137" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; BCG Vaccine ; Bacterial Proteins/analysis/genetics/*physiology ; Cell Line ; Genes, Bacterial ; Genetic Complementation Test ; Immunohistochemistry ; Lung/microbiology ; Macrophages/microbiology ; Membrane Proteins/analysis/genetics/*physiology ; Mice ; Mice, Inbred BALB C ; Mutation ; Mycobacterium bovis/genetics/growth & development ; Mycobacterium tuberculosis/genetics/growth & ; development/metabolism/*pathogenicity ; Phagosomes/microbiology ; Recombinant Fusion Proteins ; Tuberculosis/microbiology ; Vaccines, Attenuated ; Virulence/genetics
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  • 38
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    MP1: a MEK binding partner that enhances enzymatic activation of the MAP kinase cascade (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-09-11
    Description: Signal transduction is controlled both by regulation of enzyme activation and by organization of enzymatic complexes with nonenzymatic adapters, scaffolds, and anchor proteins. The extracellular signal-regulated kinase (ERK) cascade is one of several evolutionarily conserved mitogen-activated protein (MAP) kinase cascades important in the regulation of growth, apoptosis, and differentiation. A two-hybrid screen was conducted to identify nonenzymatic components of this signaling cascade that might be important in regulating its activity. A protein called MP1 (MEK Partner 1) was identified that bound specifically to MEK1 and ERK1 and facilitated their activation. When overexpressed in cultured cells, MP1 enhanced activation of ERK1 and activation of a reporter driven by the transcription factor Elk-1. Expression of MP1 in cells increased binding of ERK1 to MEK1. MP1 apparently functions as an adapter to enhance the efficiency of the MAP kinase cascade.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schaeffer, H J -- Catling, A D -- Eblen, S T -- Collier, L S -- Krauss, A -- Weber, M J -- CA39076/CA/NCI NIH HHS/ -- GM47332/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1998 Sep 11;281(5383):1668-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Cancer Center, University of Virginia Health Sciences Center, Charlottesville, VA 22908, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9733512" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium-Calmodulin-Dependent Protein Kinases/*metabolism ; Carrier Proteins/*metabolism ; Cell Line ; *DNA-Binding Proteins ; Enzyme Activation ; MAP Kinase Kinase 1 ; MAP Kinase Kinase 2 ; Mitogen-Activated Protein Kinase 1 ; Mitogen-Activated Protein Kinase 3 ; *Mitogen-Activated Protein Kinase Kinases ; *Mitogen-Activated Protein Kinases ; Molecular Sequence Data ; Phosphorylation ; Protein-Serine-Threonine Kinases/*metabolism ; Protein-Tyrosine Kinases/*metabolism ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins c-raf/metabolism ; Recombinant Fusion Proteins/metabolism ; *Signal Transduction ; *Transcription Factors ; Transcriptional Activation ; Transfection ; ets-Domain Protein Elk-1
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    Aspirin-like molecules that covalently inactivate cyclooxygenase-2 (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-06-20
    Description: Many of aspirin's therapeutic effects arise from its acetylation of cyclooxygenase-2 (COX-2), whereas its antithrombotic and ulcerogenic effects result from its acetylation of COX-1. Here, aspirin-like molecules were designed that preferentially acetylate and irreversibly inactivate COX-2. The most potent of these compounds was o-(acetoxyphenyl)hept-2-ynyl sulfide (APHS). Relative to aspirin, APHS was 60 times as reactive against COX-2 and 100 times as selective for its inhibition; it also inhibited COX-2 in cultured macrophages and colon cancer cells and in the rat air pouch in vivo. Such compounds may lead to the development of aspirin-like drugs for the treatment or prevention of immunological and proliferative diseases without gastrointestinal or hematologic side effects.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kalgutkar, A S -- Crews, B C -- Rowlinson, S W -- Garner, C -- Seibert, K -- Marnett, L J -- CA47479/CA/NCI NIH HHS/ -- CA68485/CA/NCI NIH HHS/ -- ES00267/ES/NIEHS NIH HHS/ -- New York, N.Y. -- Science. 1998 May 22;280(5367):1268-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉A.B. Hancock Jr. Memorial Laboratory for Cancer Research, Vanderbilt Cancer Center, Vanderbilt University School of Medicine, Nashville, TN 37232, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9596581" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Acetylene/*analogs & derivatives/chemical synthesis/chemistry/pharmacology ; Alkynes ; Animals ; Anti-Inflammatory Agents, Non-Steroidal/*chemical ; synthesis/chemistry/pharmacology ; Aspirin/chemistry/pharmacology ; Binding Sites ; Cell Division/drug effects ; Cell Line ; Colonic Neoplasms/enzymology/pathology ; Cyclooxygenase 2 ; Cyclooxygenase 2 Inhibitors ; Cyclooxygenase Inhibitors/*chemical synthesis/chemistry/pharmacology ; Dinoprostone/biosynthesis ; Drug Design ; Humans ; Indomethacin/pharmacology ; Isoenzymes/chemistry/genetics/*metabolism ; Macrophages/enzymology ; Membrane Proteins ; Mutagenesis, Site-Directed ; Prostaglandin D2/biosynthesis ; Prostaglandin-Endoperoxide Synthases/chemistry/genetics/*metabolism ; Rats ; Rats, Inbred Lew ; Sulfides/*chemical synthesis/chemistry/pharmacology ; Thromboxane B2/biosynthesis ; Tumor Cells, Cultured
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    Extension of life-span by introduction of telomerase into normal human cells (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-02-07
    Description: Normal human cells undergo a finite number of cell divisions and ultimately enter a nondividing state called replicative senescence. It has been proposed that telomere shortening is the molecular clock that triggers senescence. To test this hypothesis, two telomerase-negative normal human cell types, retinal pigment epithelial cells and foreskin fibroblasts, were transfected with vectors encoding the human telomerase catalytic subunit. In contrast to telomerase-negative control clones, which exhibited telomere shortening and senescence, telomerase-expressing clones had elongated telomeres, divided vigorously, and showed reduced straining for beta-galactosidase, a biomarker for senescence. Notably, the telomerase-expressing clones have a normal karyotype and have already exceeded their normal life-span by at least 20 doublings, thus establishing a causal relationship between telomere shortening and in vitro cellular senescence. The ability to maintain normal human cells in a phenotypically youthful state could have important applications in research and medicine.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bodnar, A G -- Ouellette, M -- Frolkis, M -- Holt, S E -- Chiu, C P -- Morin, G B -- Harley, C B -- Shay, J W -- Lichtsteiner, S -- Wright, W E -- AG05747/AG/NIA NIH HHS/ -- AG07992/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 1998 Jan 16;279(5349):349-52.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Geron Corporation, Menlo Park, CA 94025, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9454332" target="_blank"〉PubMed〈/a〉
    Keywords: Biomarkers ; Catalysis ; *Cell Aging ; *Cell Division ; Cell Line ; Cell Transformation, Neoplastic ; Cloning, Molecular ; DNA-Binding Proteins ; Fibroblasts/cytology ; Homeostasis ; Humans ; Karyotyping ; Phenotype ; Pigment Epithelium of Eye/cytology ; Proteins/genetics/*metabolism ; *Rna ; RNA-Directed DNA Polymerase/genetics/metabolism ; Stem Cells/cytology/enzymology ; Telomerase/genetics/*metabolism ; Telomere/metabolism/*physiology/ultrastructure ; Transfection ; Tumor Cells, Cultured ; beta-Galactosidase/metabolism
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    Disruption of splicing regulated by a CUG-binding protein in myotonic dystrophy (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-05-23
    Description: Myotonic dystrophy (DM) is caused by a CTG expansion in the 3' untranslated region of the DM gene. One model of DM pathogenesis suggests that RNAs from the expanded allele create a gain-of-function mutation by the inappropriate binding of proteins to the CUG repeats. Data presented here indicate that the conserved heterogeneous nuclear ribonucleoprotein, CUG-binding protein (CUG-BP), may mediate the trans-dominant effect of the RNA. CUG-BP was found to bind to the human cardiac troponin T (cTNT) pre-messenger RNA and regulate its alternative splicing. Splicing of cTNT was disrupted in DM striated muscle and in normal cells expressing transcripts that contain CUG repeats. Altered expression of genes regulated posttranscriptionally by CUG-BP therefore may contribute to DM pathogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Philips, A V -- Timchenko, L T -- Cooper, T A -- AR 44387/AR/NIAMS NIH HHS/ -- HL45565/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1998 May 1;280(5364):737-41.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Baylor College of Medicine, Houston, TX 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9563950" target="_blank"〉PubMed〈/a〉
    Keywords: *Alternative Splicing ; CELF1 Protein ; Cell Line ; Cell Nucleus/metabolism ; Exons ; Humans ; Introns ; Muscle, Skeletal/cytology/embryology/metabolism ; Mutation ; Myotonic Dystrophy/*genetics/metabolism ; Myotonin-Protein Kinase ; Phosphorylation ; Protein-Serine-Threonine Kinases/*genetics ; RNA Precursors/metabolism ; RNA, Messenger/*genetics/metabolism ; RNA-Binding Proteins/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Ribonucleoproteins/genetics/*metabolism ; Transcription, Genetic ; Transfection ; *Trinucleotide Repeats ; Troponin/genetics ; Troponin T
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    Segregation of transcription and replication sites into higher order domains (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-09-04
    Description: Microscopy shows that individual sites of DNA replication and transcription of mammalian nuclei segregate into sets of roughly 22 and 16 higher order domains, respectively. Each domain set displayed a distinct network-like appearance, including regions of individual domains and interdigitation of domains between the two networks. These data support a dynamic mosaic model for the higher order arrangement of genomic function inside the cell nuclei.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wei, X -- Samarabandu, J -- Devdhar, R S -- Siegel, A J -- Acharya, R -- Berezney, R -- GM 23922/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1998 Sep 4;281(5382):1502-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, State University of New York at Buffalo, Buffalo, NY 14260, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9727975" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Animals ; Cell Line ; Cell Nucleolus/metabolism/ultrastructure ; Cell Nucleus/*metabolism/ultrastructure ; *DNA Replication ; *Genome ; Genome, Human ; Humans ; Image Processing, Computer-Assisted ; Mice ; Microscopy, Confocal ; Models, Biological ; S Phase ; *Transcription, Genetic
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    Visualization of single RNA transcripts in situ (1998)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1998-05-09
    Description: Fluorescence in situ hybridization (FISH) and digital imaging microscopy were modified to allow detection of single RNA molecules. Oligodeoxynucleotide probes were synthesized with five fluorochromes per molecule, and the light emitted by a single probe was calibrated. Points of light in exhaustively deconvolved images of hybridized cells gave fluorescent intensities and distances between probes consistent with single messenger RNA molecules. Analysis of beta-actin transcription sites after serum induction revealed synchronous and cyclical transcription from single genes. The rates of transcription initiation and termination and messenger RNA processing could be determined by positioning probes along the transcription unit. This approach extends the power of FISH to yield quantitative molecular information on a single cell.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Femino, A M -- Fay, F S -- Fogarty, K -- Singer, R H -- GM 54887/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1998 Apr 24;280(5363):585-90.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy and Structural Biology and Cell Biology, Albert Einstein College of Medicine, Bronx, NY 10461, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9554849" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/genetics ; Animals ; Cell Line ; Fluorescein-5-isothiocyanate ; *In Situ Hybridization, Fluorescence ; Kinetics ; Oligonucleotide Probes ; RNA Processing, Post-Transcriptional ; RNA, Messenger/*analysis/*genetics/metabolism ; Rats ; *Transcription, Genetic
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    A family of cAMP-binding proteins that directly activate Rap1 (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-12-18
    Description: cAMP (3',5' cyclic adenosine monophosphate) is a second messenger that in eukaryotic cells induces physiological responses ranging from growth, differentiation, and gene expression to secretion and neurotransmission. Most of these effects have been attributed to the binding of cAMP to cAMP-dependent protein kinase A (PKA). Here, a family of cAMP-binding proteins that are differentially distributed in the mammalian brain and body organs and that exhibit both cAMP-binding and guanine nucleotide exchange factor (GEF) domains is reported. These cAMP-regulated GEFs (cAMP-GEFs) bind cAMP and selectively activate the Ras superfamily guanine nucleotide binding protein Rap1A in a cAMP-dependent but PKA-independent manner. Our findings suggest the need to reformulate concepts of cAMP-mediated signaling to include direct coupling to Ras superfamily signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kawasaki, H -- Springett, G M -- Mochizuki, N -- Toki, S -- Nakaya, M -- Matsuda, M -- Housman, D E -- Graybiel, A M -- P01 CA42063/CA/NCI NIH HHS/ -- P01 HL41484/HL/NHLBI NIH HHS/ -- R01 HD28341/HD/NICHD NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1998 Dec 18;282(5397):2275-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology (MIT), Cambridge, MA, 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9856955" target="_blank"〉PubMed〈/a〉
    Keywords: 1-Methyl-3-isobutylxanthine/pharmacology ; Adrenal Glands/metabolism ; Adult ; Amino Acid Sequence ; Animals ; Brain/metabolism ; Cell Line ; Colforsin/pharmacology ; Cyclic AMP/*metabolism ; Cyclic AMP-Dependent Protein Kinases/antagonists & inhibitors/metabolism ; Fetus/metabolism ; GTP-Binding Proteins/*metabolism ; Gene Expression ; Guanine Nucleotide Exchange Factors ; Humans ; In Situ Hybridization ; Molecular Sequence Data ; Phosphorylation ; Proteins/chemistry/genetics/*metabolism ; Rats ; Second Messenger Systems ; Sequence Deletion ; Signal Transduction ; rap GTP-Binding Proteins ; ras Guanine Nucleotide Exchange Factors
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  • 45
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    Mediation of Sonic hedgehog-induced expression of COUP-TFII by a protein phosphatase (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-01-07
    Description: A Sonic hedgehog (Shh) response element was identified in the chicken ovalbumin upstream promoter-transcription factor II (COUP-TFII) promoter that binds to a factor distinct from Gli, a gene known to mediate Shh signaling. Although this binding activity is specifically stimulated by Shh-N (amino-terminal signaling domain), it can also be unmasked with protein phosphatase treatment in the mouse cell line P19, and induction by Shh-N can be blocked by phosphatase inhibitors. Thus, Shh-N signaling may result in dephosphorylation of a target factor that is required for activation of COUP-TFII-, Islet1-, and Gli response element-dependent gene expression. This finding identifies another step in the Shh-N signaling pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Krishnan, V -- Pereira, F A -- Qiu, Y -- Chen, C H -- Beachy, P A -- Tsai, S Y -- Tsai, M J -- New York, N.Y. -- Science. 1997 Dec 12;278(5345):1947-50.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Baylor College of Medicine, 1 Baylor Plaza, Houston, TX 77030 USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9395397" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; COUP Transcription Factor II ; COUP Transcription Factors ; Cell Line ; DNA/metabolism ; DNA-Binding Proteins/*genetics/metabolism ; Enzyme Inhibitors/pharmacology ; *Gene Expression Regulation ; Hedgehog Proteins ; Mice ; Okadaic Acid/pharmacology ; Oxazoles/pharmacology ; Phosphoprotein Phosphatases/antagonists & inhibitors/*metabolism ; Phosphorylation ; Promoter Regions, Genetic ; Proteins/*genetics/*metabolism ; *Receptors, Steroid ; Signal Transduction ; *Trans-Activators ; Transcription Factors/*genetics/metabolism
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    Progression to AIDS (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-07-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Donfield, S M -- Lynn, H S -- Hilgartner, M W -- New York, N.Y. -- Science. 1998 Jun 19;280(5371):1819-20.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9669928" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/genetics/*immunology ; CD4 Lymphocyte Count ; Cell Line ; Cohort Studies ; Disease Progression ; Genotype ; HIV Infections/genetics/*immunology ; HIV Seropositivity ; Humans ; Mutation ; Receptors, CCR2 ; Receptors, Chemokine/*genetics
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    Inactivation of a serotonin-gated ion channel by a polypeptide toxin from marine snails (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-07-24
    Description: The venom of predatory marine snails is a rich source of natural products that act on specific receptors and ion channels within the mammalian nervous system. A 41-amino acid peptide, final sigma-conotoxin GVIIIA, was purified on the basis of its ability to inactivate the 5-HT3 receptor, an excitatory serotonin-gated ion channel. final sigma-Conotoxin contains a brominated tryptophan residue, which may be important for peptide activity because the endogenous ligand for the 5-HT3 receptor is a hydroxylated derivative of tryptophan. final sigma-Conotoxin inactivates the 5-HT3 receptor through competitive antagonism and is a highly selective inhibitor of this receptor. Serotonin receptors can now be included among the molecular targets of natural polypeptide neurotoxins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉England, L J -- Imperial, J -- Jacobsen, R -- Craig, A G -- Gulyas, J -- Akhtar, M -- Rivier, J -- Julius, D -- Olivera, B M -- GM44298/GM/NIGMS NIH HHS/ -- GM48677/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1998 Jul 24;281(5376):575-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cellular and Molecular Pharmacology, University of California, San Francisco, CA 94143-0450, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9677203" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Amino Acids/analysis ; Animals ; Benzamides/pharmacology ; Bicyclo Compounds, Heterocyclic/pharmacology ; Binding Sites ; Cell Line ; Cloning, Molecular ; *Conotoxins ; DNA, Complementary ; Ion Channel Gating ; Ion Channels/*antagonists & inhibitors ; Molecular Sequence Data ; Mollusk Venoms/chemistry/genetics/isolation & purification/*pharmacology ; Peptides, Cyclic/pharmacology ; Receptors, Serotonin/*metabolism ; Receptors, Serotonin, 5-HT3 ; Receptors, Serotonin, 5-HT4 ; Recombinant Fusion Proteins/antagonists & inhibitors/metabolism ; Recombinant Proteins/antagonists & inhibitors ; Serotonin/metabolism/pharmacology ; Serotonin Antagonists/chemistry/isolation & purification/*pharmacology ; Snails/*chemistry ; Tryptophan/analysis/metabolism
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    'Playing chicken' over gene markers (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-02-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marshall, E -- New York, N.Y. -- Science. 1997 Dec 19;278(5346):2046-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9432713" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; *Chromosome Mapping ; Confidentiality ; *Databases, Factual ; *Databases, Nucleic Acid ; Federal Government ; Genetic Privacy ; *Genetic Research ; Genetic Techniques ; Genetic Variation ; Genome, Human ; *Human Genome Project/economics ; Humans ; *Information Dissemination ; Informed Consent ; National Institutes of Health (U.S.) ; Patents as Topic ; *Polymorphism, Genetic ; Research Support as Topic ; United States
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  • 49
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    Linkage of ATM to cell cycle regulation by the Chk2 protein kinase (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-12-04
    Description: In response to DNA damage and replication blocks, cells prevent cell cycle progression through the control of critical cell cycle regulators. We identified Chk2, the mammalian homolog of the Saccharomyces cerevisiae Rad53 and Schizosaccharomyces pombe Cds1 protein kinases required for the DNA damage and replication checkpoints. Chk2 was rapidly phosphorylated and activated in response to replication blocks and DNA damage; the response to DNA damage occurred in an ataxia telangiectasia mutated (ATM)-dependent manner. In vitro, Chk2 phosphorylated Cdc25C on serine-216, a site known to be involved in negative regulation of Cdc25C. This is the same site phosphorylated by the protein kinase Chk1, which suggests that, in response to DNA damage and DNA replicational stress, Chk1 and Chk2 may phosphorylate Cdc25C to prevent entry into mitosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Matsuoka, S -- Huang, M -- Elledge, S J -- GM44664/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1998 Dec 4;282(5395):1893-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Verna and Marrs McLean Department of Biochemistry, 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/9836640" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Ataxia Telangiectasia Mutated Proteins ; *Cell Cycle ; Cell Cycle Proteins/metabolism ; Cell Line ; Checkpoint Kinase 2 ; *DNA Damage ; *DNA Replication ; DNA-Binding Proteins ; Enzyme Activation ; Gamma Rays ; HeLa Cells ; Humans ; Models, Biological ; Molecular Sequence Data ; Phosphorylation ; *Protein Kinases ; Protein-Serine-Threonine Kinases/chemistry/genetics/*metabolism ; Proteins/*metabolism ; Recombinant Fusion Proteins/metabolism ; Saccharomyces cerevisiae/cytology/genetics/growth & development ; Tumor Suppressor Proteins ; Ultraviolet Rays ; *cdc25 Phosphatases
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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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    Auxin-dependent cell expansion mediated by overexpressed auxin-binding protein 1 (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-11-06
    Description: To test the hypothesis that auxin-binding protein 1 (ABP1) is a receptor controlling auxin-mediated plant cell expansion, ABP1 complementary DNAs were expressed in a controllable fashion in tobacco plants and constitutively in maize cell lines. Induction of Arabidopsis ABP1 expression in tobacco leaf strips resulted in an increased capacity for auxin-mediated cell expansion, whereas induction of ABP1 in intact plants resulted in leaves with a normal morphology, but larger cells. Similarly, constitutive expression of maize ABP1 in maize cell lines conferred on them the capacity to respond to auxin by increasing cell size. These results support a role of ABP1 as an auxin receptor controlling plant growth.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jones, A M -- Im, K H -- Savka, M A -- Wu, M J -- DeWitt, N G -- Shillito, R -- Binns, A N -- GM7369-06/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1998 Nov 6;282(5391):1114-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, University of North Carolina, Chapel Hill, NC 27599-3280, USA. alan_jones@unc.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9804548" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Cell Size ; Gene Expression Regulation, Plant ; Genes, Plant ; Indoleacetic Acids/*metabolism/pharmacology ; Phenotype ; *Plant Growth Regulators ; Plant Leaves/*cytology/growth & development/metabolism ; *Plant Proteins ; Plants, Genetically Modified ; Plants, Toxic ; Receptors, Cell Surface/*genetics/*physiology ; Tetracyclines/pharmacology ; Tobacco/cytology/metabolism ; Transformation, Genetic ; Transgenes ; Zea mays/cytology/metabolism
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    Dependence of BSAP repressor and activator functions on BSAP concentration (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-04-16
    Description: During a B cell immune response, the transcription factor BSAP maintains its activator functions but is relieved of its repressor functions. This selective targeting of BSAP activities was shown to be regulated by a concentration-dependent mechanism whereby activator motifs for BSAP had a 20-fold higher binding affinity than repressor motifs. An exchange of activator and repressor motifs, however, showed that the context of the motif, rather than the affinity, determined whether BSAP operated as an activator or repressor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wallin, J J -- Gackstetter, E R -- Koshland, M E -- CA09179/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1998 Mar 20;279(5358):1961-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immunology Division, Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, CA 94720, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9506950" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD19/genetics ; B-Cell-Specific Activator Protein ; B-Lymphocytes/cytology/immunology/*metabolism ; Binding Sites ; Cell Line ; DNA-Binding Proteins/*genetics/*metabolism ; Gene Expression ; *Gene Expression Regulation ; Genes, Immunoglobulin ; Immunoglobulin Heavy Chains/genetics ; Immunoglobulin J-Chains/genetics ; Mice ; Nuclear Proteins/*genetics/*metabolism ; Phenotype ; Plasma Cells/immunology/metabolism ; Promoter Regions, Genetic ; *Regulatory Sequences, Nucleic Acid ; Repressor Proteins/genetics/metabolism ; Transcription Factors/*metabolism ; Transfection
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    Phosphorylation and activation of p70s6k by PDK1 (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-02-21
    Description: Activation of the protein p70s6k by mitogens leads to increased translation of a family of messenger RNAs that encode essential components of the protein synthetic apparatus. Activation of the kinase requires hierarchical phosphorylation at multiple sites, culminating in the phosphorylation of the threonine in position 229 (Thr229), in the catalytic domain. The homologous site in protein kinase B (PKB), Thr308, has been shown to be phosphorylated by the phosphoinositide-dependent protein kinase PDK1. A regulatory link between p70s6k and PKB was demonstrated, as PDK1 was found to selectively phosphorylate p70s6k at Thr229. More importantly, PDK1 activated p70s6k in vitro and in vivo, whereas the catalytically inactive PDK1 blocked insulin-induced activation of p70s6k.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pullen, N -- Dennis, P B -- Andjelkovic, M -- Dufner, A -- Kozma, S C -- Hemmings, B A -- Thomas, G -- New York, N.Y. -- Science. 1998 Jan 30;279(5351):707-10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Friedrich Miescher Institute, Maulbeerstrasse 66, CH-4058, Basel, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9445476" target="_blank"〉PubMed〈/a〉
    Keywords: 3-Phosphoinositide-Dependent Protein Kinases ; Amino Acid Sequence ; Androstadienes/pharmacology ; Animals ; Binding Sites ; Calcium-Calmodulin-Dependent Protein Kinase Type 4 ; Calcium-Calmodulin-Dependent Protein Kinases/metabolism ; Catalysis ; Cell Line ; Enzyme Activation ; Insulin/pharmacology ; Insulin Antagonists/pharmacology ; Molecular Sequence Data ; Phosphorylation ; Phosphothreonine/metabolism ; Polyenes/pharmacology ; Protein-Serine-Threonine Kinases/*metabolism ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins c-akt ; Recombinant Proteins/metabolism ; Ribosomal Protein S6 Kinases/*metabolism ; Sirolimus
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  • 54
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    Enhanced phosphorylation of p53 by ATM in response to DNA damage (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-09-11
    Description: The ATM protein, encoded by the gene responsible for the human genetic disorder ataxia telangiectasia (A-T), regulates several cellular responses to DNA breaks. ATM shares a phosphoinositide 3-kinase-related domain with several proteins, some of them protein kinases. A wortmannin-sensitive protein kinase activity was associated with endogenous or recombinant ATM and was abolished by structural ATM mutations. In vitro substrates included the translation repressor PHAS-I and the p53 protein. ATM phosphorylated p53 in vitro on a single residue, serine-15, which is phosphorylated in vivo in response to DNA damage. This activity was markedly enhanced within minutes after treatment of cells with a radiomimetic drug; the total amount of ATM remained unchanged. Various damage-induced responses may be activated by enhancement of the protein kinase activity of ATM.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Banin, S -- Moyal, L -- Shieh, S -- Taya, Y -- Anderson, C W -- Chessa, L -- Smorodinsky, N I -- Prives, C -- Reiss, Y -- Shiloh, Y -- Ziv, Y -- NS31763/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1998 Sep 11;281(5383):1674-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Human Genetics and Molecular Medicine, Sackler School of Medicine, Tel Aviv University, Ramat Aviv 69978, Israel.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9733514" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; Androstadienes/pharmacology ; Ataxia Telangiectasia/metabolism ; Ataxia Telangiectasia Mutated Proteins ; *Carrier Proteins ; Cell Cycle Proteins ; Cell Line ; *DNA Damage ; DNA-Binding Proteins ; Enzyme Inhibitors/pharmacology ; Humans ; Mutation ; Phosphatidylinositol 3-Kinases/chemistry ; Phosphoproteins/metabolism ; Phosphorylation ; Protein Kinase Inhibitors ; Protein Kinases/chemistry/*metabolism ; *Protein-Serine-Threonine Kinases ; Proteins/antagonists & inhibitors/chemistry/genetics/*metabolism ; Recombinant Proteins/metabolism ; Tumor Cells, Cultured ; Tumor Suppressor Protein p53/*metabolism ; Tumor Suppressor Proteins ; Zinostatin/pharmacology
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    RasGRP, a Ras guanyl nucleotide- releasing protein with calcium- and diacylglycerol-binding motifs (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-06-06
    Description: RasGRP, a guanyl nucleotide-releasing protein for the small guanosine triphosphatase Ras, was characterized. Besides the catalytic domain, RasGRP has an atypical pair of "EF hands" that bind calcium and a diacylglycerol (DAG)-binding domain. RasGRP activated Ras and caused transformation in fibroblasts. A DAG analog caused sustained activation of Ras-Erk signaling and changes in cell morphology. Signaling was associated with partitioning of RasGRP protein into the membrane fraction. Sustained ligand-induced signaling and membrane partitioning were absent when the DAG-binding domain was deleted. RasGRP is expressed in the nervous system, where it may couple changes in DAG and possibly calcium concentrations to Ras activation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ebinu, J O -- Bottorff, D A -- Chan, E Y -- Stang, S L -- Dunn, R J -- Stone, J C -- New York, N.Y. -- Science. 1998 May 15;280(5366):1082-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, University of Alberta, Edmonton, Alberta, Canada T6G 2H7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9582122" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Brain/*metabolism ; Calcium/metabolism ; Calcium-Calmodulin-Dependent Protein Kinases/metabolism ; Catalysis ; Cell Cycle Proteins/genetics/metabolism ; Cell Line ; Cell Membrane/metabolism ; Cell Size ; Cell Transformation, Neoplastic ; Cloning, Molecular ; DNA, Complementary ; DNA-Binding Proteins/*chemistry/genetics/*metabolism ; Diglycerides/metabolism ; Genes, ras ; *Guanine Nucleotide Exchange Factors ; Guanosine Diphosphate/metabolism ; Guanosine Triphosphate/metabolism ; Molecular Sequence Data ; Neurons/metabolism ; Phosphoprotein Phosphatases/genetics/metabolism ; Rats ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; ras Proteins/*metabolism ; ras-GRF1
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    Conservation of T cell receptor conformation in epidermal gammadelta cells with disrupted primary Vgamma gene usage (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-03-28
    Description: A feature that distinguishes gammadelta T cell subsets from most alphabeta T cells and B cells is the association of expression of single T cell receptor (TCR) gamma and delta variable (V) region gene segments with specific anatomic sites. Mice lacking the TCR Vgamma5 chain normally expressed by most dendritic epidermal T cells were shown to retain a conformational determinant (idiotype) ordinarily expressed exclusively by such Vgamma5+ cells. Conservation by shuffled gammadelta TCR chains of an idiotype associated with a specific anatomic site indicates that for TCRgammadelta, as for immunoglobulin, conformation is associated to a greater extent with the function or development of lymphocyte repertoires than is the use of particular gene segments.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mallick-Wood, C A -- Lewis, J M -- Richie, L I -- Owen, M J -- Tigelaar, R E -- Hayday, A C -- AI27404/AI/NIAID NIH HHS/ -- AI27855/AI/NIAID NIH HHS/ -- GM37759/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1998 Mar 13;279(5357):1729-33.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular, Cell, and Developmental Biology and Section of Immunobiology, Yale University, New Haven, CT 06520, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9497293" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Dendritic Cells/*immunology ; Epidermis/cytology/*immunology ; Epitopes/analysis ; Female ; Gene Rearrangement ; Hybridomas ; Male ; Mice ; Mice, Inbred C57BL ; Polymerase Chain Reaction ; Polymorphism, Restriction Fragment Length ; Protein Conformation ; Receptors, Antigen, T-Cell, gamma-delta/chemistry/*genetics/*immunology ; T-Lymphocyte Subsets/*immunology
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    Identification of c-MYC as a target of the APC pathway (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-09-04
    Description: The adenomatous polyposis coli gene (APC) is a tumor suppressor gene that is inactivated in most colorectal cancers. Mutations of APC cause aberrant accumulation of beta-catenin, which then binds T cell factor-4 (Tcf-4), causing increased transcriptional activation of unknown genes. Here, the c-MYC oncogene is identified as a target gene in this signaling pathway. Expression of c-MYC was shown to be repressed by wild-type APC and activated by beta-catenin, and these effects were mediated through Tcf-4 binding sites in the c-MYC promoter. These results provide a molecular framework for understanding the previously enigmatic overexpression of c-MYC in colorectal cancers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉He, T C -- Sparks, A B -- Rago, C -- Hermeking, H -- Zawel, L -- da Costa, L T -- Morin, P J -- Vogelstein, B -- Kinzler, K W -- CA57345/CA/NCI NIH HHS/ -- CA62924/CA/NCI NIH HHS/ -- GM07309/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1998 Sep 4;281(5382):1509-12.〈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/9727977" target="_blank"〉PubMed〈/a〉
    Keywords: Adenomatous Polyposis Coli Protein ; Binding Sites ; Cell Line ; Colorectal Neoplasms/*genetics ; Cytoskeletal Proteins/genetics/metabolism ; *Gene Expression Regulation, Neoplastic ; *Genes, APC ; Genes, Reporter ; *Genes, myc ; HT29 Cells ; Humans ; Mutation ; Promoter Regions, Genetic ; Proto-Oncogene Proteins c-myc/metabolism ; Signal Transduction ; TCF Transcription Factors ; *Trans-Activators ; Transcription Factor 7-Like 2 Protein ; Transcription Factors/metabolism ; Transcription, Genetic ; beta Catenin
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    Closing the circadian loop: CLOCK-induced transcription of its own inhibitors per and tim (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-06-11
    Description: The circadian oscillator generates a rhythmic output with a period of about 24 hours. Despite extensive studies in several model systems, the biochemical mode of action has not yet been demonstrated for any of its components. Here, the Drosophila CLOCK protein was shown to induce transcription of the circadian rhythm genes period and timeless. dCLOCK functioned as a heterodimer with a Drosophila homolog of BMAL1. These proteins acted through an E-box sequence in the period promoter. The timeless promoter contains an 18-base pair element encompassing an E-box, which was sufficient to confer dCLOCK responsiveness to a reporter gene. PERIOD and TIMELESS proteins blocked dCLOCK's ability to transactivate their promoters via the E-box. Thus, dCLOCK drives expression of period and timeless, which in turn inhibit dCLOCK's activity and close the circadian loop.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Darlington, T K -- Wager-Smith, K -- Ceriani, M F -- Staknis, D -- Gekakis, N -- Steeves, T D -- Weitz, C J -- Takahashi, J S -- Kay, S A -- MH-51573/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1998 Jun 5;280(5369):1599-603.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology and NSF Center for Biological Timing, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9616122" target="_blank"〉PubMed〈/a〉
    Keywords: ARNTL Transcription Factors ; Animals ; Basic Helix-Loop-Helix Transcription Factors ; Biological Clocks ; CLOCK Proteins ; Cell Line ; Cell Nucleus/metabolism ; Circadian Rhythm/genetics/*physiology ; Dimerization ; Drosophila ; *Drosophila Proteins ; Feedback ; Gene Expression ; Helix-Loop-Helix Motifs ; Insect Proteins/*genetics/metabolism ; Nuclear Proteins/*genetics/metabolism ; Period Circadian Proteins ; Promoter Regions, Genetic ; RNA, Messenger/genetics/metabolism ; Trans-Activators/genetics/*metabolism ; Transcription Factors/genetics/*metabolism ; *Transcriptional Activation ; Transfection
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    Telomeres and senescence: ending the debate (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-02-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉de Lange, T -- New York, N.Y. -- Science. 1998 Jan 16;279(5349):334-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory for Cell Biology and Genetics, The 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/9454329" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antineoplastic Agents/pharmacology ; *Cell Aging ; *Cell Division ; Cell Line ; Cell Transformation, Neoplastic ; DNA-Binding Proteins ; Enzyme Activation ; Genes, Tumor Suppressor ; Humans ; Mice ; Neoplasms/drug therapy/enzymology/pathology ; Proteins/genetics/*metabolism ; *Rna ; RNA-Directed DNA Polymerase/genetics/metabolism ; Telomerase/antagonists & inhibitors/genetics/*metabolism ; Telomere/metabolism/*physiology/ultrastructure ; Transfection
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Patterning of cortical efferent projections by semaphorin-neuropilin interactions (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-12-04
    Description: Cortical neurons communicate with various cortical and subcortical targets by way of stereotyped axon projections through the white matter. Slice overlay experiments indicate that the initial growth of cortical axons toward the white matter is regulated by a diffusible chemorepulsive signal localized near the marginal zone. Semaphorin III is a major component of this diffusible signal, and cortical neurons transduce this signal by way of the neuropilin-1 receptor. These observations indicate that semaphorin-neuropilin interactions play a critical role in the initial patterning of projections in the developing cortex.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Polleux, F -- Giger, R J -- Ginty, D D -- Kolodkin, A L -- Ghosh, A -- NS35165/NS/NINDS NIH HHS/ -- NS36176/NS/NINDS NIH HHS/ -- NS534814/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1998 Dec 4;282(5395):1904-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, Johns Hopkins University School of Medicine, 725 North Wolfe Street, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9836643" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/*physiology ; Cell Line ; Cerebral Cortex/*cytology/embryology ; Coculture Techniques ; Gene Targeting ; Glycoproteins/genetics/*physiology ; Humans ; Mice ; Nerve Growth Factors/*metabolism ; Nerve Tissue Proteins/*physiology ; Neurons, Efferent/cytology/*physiology ; Neuropilin-1 ; Rats ; Recombinant Proteins/metabolism ; Semaphorin-3A ; Signal Transduction
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    Ultraviolet-induced cell death blocked by a selenoprotein from a human dermatotropic poxvirus (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-01-24
    Description: Selenium, an essential trace element, is a component of prokaryotic and eukaryotic antioxidant proteins. A candidate selenoprotein homologous to glutathione peroxidase was deduced from the sequence of molluscum contagiosum, a poxvirus that causes persistent skin neoplasms in children and acquired immunodeficiency syndrome (AIDS) patients. Selenium was incorporated into this protein during biosynthesis, and a characteristic stem-loop structure near the end of the messenger RNA was required for alternative selenocysteine decoding of a potential UGA stop codon within the open reading frame. The selenoprotein protected human keratinocytes against cytotoxic effects of ultraviolet irradiation and hydrogen peroxide, providing a mechanism for a virus to defend itself against environmental stress.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shisler, J L -- Senkevich, T G -- Berry, M J -- Moss, B -- DK47320/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1998 Jan 2;279(5347):102-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 4 Center Drive, MSC 0445, Bethesda, MD 20892-0445, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9417017" target="_blank"〉PubMed〈/a〉
    Keywords: *Apoptosis ; Base Sequence ; Cell Line ; Codon ; Glutathione Peroxidase/genetics/*metabolism ; HeLa Cells ; Humans ; Hydrogen Peroxide/pharmacology ; Keratinocytes/*cytology/drug effects ; Molecular Sequence Data ; Molluscum contagiosum virus/genetics/*physiology ; Open Reading Frames ; Point Mutation ; Proteins/genetics/*metabolism ; Selenium/metabolism ; Selenocysteine/genetics ; Selenoproteins ; Transfection ; Ultraviolet Rays ; Viral Proteins/genetics/*metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Binding of hepatitis C virus to CD81 (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-10-30
    Description: Chronic hepatitis C virus (HCV) infection occurs in about 3 percent of the world's population and is a major cause of liver disease. HCV infection is also associated with cryoglobulinemia, a B lymphocyte proliferative disorder. Virus tropism is controversial, and the mechanisms of cell entry remain unknown. The HCV envelope protein E2 binds human CD81, a tetraspanin expressed on various cell types including hepatocytes and B lymphocytes. Binding of E2 was mapped to the major extracellular loop of CD81. Recombinant molecules containing this loop bound HCV and antibodies that neutralize HCV infection in vivo inhibited virus binding to CD81 in vitro.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pileri, P -- Uematsu, Y -- Campagnoli, S -- Galli, G -- Falugi, F -- Petracca, R -- Weiner, A J -- Houghton, M -- Rosa, D -- Grandi, G -- Abrignani, S -- New York, N.Y. -- Science. 1998 Oct 30;282(5390):938-41.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉IRIS, Chiron, Siena 53100, Italy.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9794763" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antibodies/immunology ; Antibodies, Viral/immunology ; Antigens, CD/chemistry/genetics/immunology/*metabolism ; Antigens, CD81 ; Cell Line ; DNA, Complementary ; Gene Library ; Hepacivirus/immunology/*metabolism ; Hepatitis C/immunology ; Humans ; Liver/cytology/immunology/virology ; Lymphocytes/immunology/virology ; Membrane Proteins/chemistry/genetics/immunology/*metabolism ; Mice ; Molecular Sequence Data ; Pan troglodytes ; Recombinant Fusion Proteins/metabolism ; Recombinant Proteins/metabolism/pharmacology ; Sequence Alignment ; Tumor Cells, Cultured ; Viral Envelope Proteins/genetics/immunology/*metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    A small, nonpeptidyl mimic of granulocyte-colony-stimulating factor [see commetns] (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-07-10
    Description: A nonpeptidyl small molecule SB 247464, capable of activating granulocyte-colony-stimulating factor (G-CSF) signal transduction pathways, was identified in a high-throughput assay in cultured cells. Like G-CSF, SB 247464 induced tyrosine phosphorylation of multiple signaling proteins and stimulated primary murine bone marrow cells to form granulocytic colonies in vitro. It also elevated peripheral blood neutrophil counts in mice. The extracellular domain of the murine G-CSF receptor was required for the activity of SB 247464, suggesting that the compound acts by oligomerizing receptor chains. The results indicate that a small molecule can activate a receptor that normally binds a relatively large protein ligand.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tian, S S -- Lamb, P -- King, A G -- Miller, S G -- Kessler, L -- Luengo, J I -- Averill, L -- Johnson, R K -- Gleason, J G -- Pelus, L M -- Dillon, S B -- Rosen, J -- New York, N.Y. -- Science. 1998 Jul 10;281(5374):257-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Transcription Research, Ligand Pharmaceuticals, San Diego, CA 92121, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9657720" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Benzimidazoles/chemistry/metabolism/*pharmacology ; Cell Line ; Colony-Forming Units Assay ; DNA-Binding Proteins/metabolism ; Dimerization ; Female ; Granulocyte Colony-Stimulating Factor/metabolism/pharmacology ; Granulocytes/cytology ; Guanidines/chemistry/metabolism/*pharmacology ; Humans ; Janus Kinase 1 ; Janus Kinase 2 ; Leukocyte Count ; Leukopoiesis ; Mice ; Mice, Inbred C57BL ; *Milk Proteins ; Neutrophils/cytology ; Phosphorylation ; Phosphotyrosine/metabolism ; Protein-Tyrosine Kinases/metabolism ; *Proto-Oncogene Proteins ; Receptors, Granulocyte Colony-Stimulating Factor/chemistry/*metabolism ; Recombinant Fusion Proteins/chemistry/metabolism ; STAT3 Transcription Factor ; STAT5 Transcription Factor ; Signal Transduction/drug effects ; Species Specificity ; Trans-Activators/metabolism ; 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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    Molecular basis for interactions of G protein betagamma subunits with effectors (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-06-20
    Description: Both the alpha and betagamma subunits of heterotrimeric guanine nucleotide-binding proteins (G proteins) communicate signals from receptors to effectors. Gbetagamma subunits can regulate a diverse array of effectors, including ion channels and enzymes. Galpha subunits bound to guanine diphosphate (Galpha-GDP) inhibit signal transduction through Gbetagamma subunits, suggesting a common interface on Gbetagamma subunits for Galpha binding and effector interaction. The molecular basis for interaction of Gbetagamma with effectors was characterized by mutational analysis of Gbeta residues that make contact with Galpha-GDP. Analysis of the ability of these mutants to regulate the activity of calcium and potassium channels, adenylyl cyclase 2, phospholipase C-beta2, and beta-adrenergic receptor kinase revealed the Gbeta residues required for activation of each effector and provides evidence for partially overlapping domains on Gbeta for regulation of these effectors. This organization of interaction regions on Gbeta for different effectors and Galpha explains why subunit dissociation is crucial for signal transmission through Gbetagamma subunits.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ford, C E -- Skiba, N P -- Bae, H -- Daaka, Y -- Reuveny, E -- Shekter, L R -- Rosal, R -- Weng, G -- Yang, C S -- Iyengar, R -- Miller, R J -- Jan, L Y -- Lefkowitz, R J -- Hamm, H E -- DA02121/DA/NIDA NIH HHS/ -- DA02575/DA/NIDA NIH HHS/ -- MH40165/MH/NIMH NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1998 May 22;280(5367):1271-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Neuroscience and Department of Molecular Pharmacology and Biological Chemistry, Northwestern University, Chicago, IL 60611, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9596582" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Diphosphate Ribose/metabolism ; Adenylyl Cyclases/metabolism ; Binding Sites ; Calcium Channels/metabolism ; Cell Line ; Cyclic AMP-Dependent Protein Kinases/metabolism ; G Protein-Coupled Inwardly-Rectifying Potassium Channels ; GTP-Binding Proteins/*chemistry/*metabolism ; Guanosine Diphosphate/metabolism ; *Heterotrimeric GTP-Binding Proteins ; Humans ; Isoenzymes/metabolism ; Models, Molecular ; Mutation ; Phospholipase C beta ; Potassium Channels/metabolism ; *Potassium Channels, Inwardly Rectifying ; Protein Conformation ; Rhodopsin/pharmacology ; *Signal Transduction ; Transducin/metabolism ; Type C Phospholipases/metabolism ; beta-Adrenergic Receptor Kinases
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    Requirement for p53 and p21 to sustain G2 arrest after DNA damage (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-11-20
    Description: After DNA damage, many cells appear to enter a sustained arrest in the G2 phase of the cell cycle. It is shown here that this arrest could be sustained only when p53 was present in the cell and capable of transcriptionally activating the cyclin-dependent kinase inhibitor p21. After disruption of either the p53 or the p21 gene, gamma radiated cells progressed into mitosis and exhibited a G2 DNA content only because of a failure of cytokinesis. Thus, p53 and p21 appear to be essential for maintaining the G2 checkpoint in human cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bunz, F -- Dutriaux, A -- Lengauer, C -- Waldman, T -- Zhou, S -- Brown, J P -- Sedivy, J M -- Kinzler, K W -- Vogelstein, B -- CA 43460/CA/NCI NIH HHS/ -- CA 57345/CA/NCI NIH HHS/ -- CA 62924/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1998 Nov 20;282(5393):1497-501.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Howard Hughes Medical Institute and The 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/9822382" target="_blank"〉PubMed〈/a〉
    Keywords: Apoptosis ; CDC2 Protein Kinase/antagonists & inhibitors/metabolism ; Cell Line ; Cyclin B/metabolism ; Cyclin B1 ; Cyclin-Dependent Kinase Inhibitor p21 ; Cyclins/genetics/*physiology ; DNA/analysis ; *DNA Damage ; *G2 Phase/drug effects ; Gamma Rays ; Gene Expression Regulation ; Genes, p53 ; Humans ; Mitosis ; Mutation ; Nocodazole/pharmacology ; Tumor Cells, Cultured ; Tumor Suppressor Protein p53/*physiology
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    Gain-of-function mutations of c-kit in human gastrointestinal stromal tumors (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-02-07
    Description: Gastrointestinal stromal tumors (GISTs) are the most common mesenchymal tumors in the human digestive tract, but their molecular etiology and cellular origin are unknown. Sequencing of c-kit complementary DNA, which encodes a proto-oncogenic receptor tyrosine kinase (KIT), from five GISTs revealed mutations in the region between the transmembrane and tyrosine kinase domains. All of the corresponding mutant KIT proteins were constitutively activated without the KIT ligand, stem cell factor (SCF). Stable transfection of the mutant c-kit complementary DNAs induced malignant transformation of Ba/F3 murine lymphoid cells, suggesting that the mutations contribute to tumor development. GISTs may originate from the interstitial cells of Cajal (ICCs) because the development of ICCs is dependent on the SCF-KIT interaction and because, like GISTs, these cells express both KIT and CD34.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hirota, S -- Isozaki, K -- Moriyama, Y -- Hashimoto, K -- Nishida, T -- Ishiguro, S -- Kawano, K -- Hanada, M -- Kurata, A -- Takeda, M -- Muhammad Tunio, G -- Matsuzawa, Y -- Kanakura, Y -- Shinomura, Y -- Kitamura, Y -- New York, N.Y. -- Science. 1998 Jan 23;279(5350):577-80.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Osaka University Medical School, Yamada-oka 2-2, Suita 565, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9438854" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antigens, CD34/analysis ; Cell Line ; Cell Transformation, Neoplastic ; DNA, Complementary ; Digestive System/cytology ; Esophageal Neoplasms/genetics/metabolism/pathology ; Gastrointestinal Neoplasms/chemistry/*genetics/pathology ; Humans ; Intestinal Neoplasms/chemistry/genetics/pathology ; Ligands ; Mice ; Mice, Nude ; Molecular Sequence Data ; *Mutation ; Phosphorylation ; Phosphotyrosine/metabolism ; Proto-Oncogene Proteins c-kit/analysis/chemistry/*genetics/metabolism ; Recombinant Proteins/pharmacology ; Sequence Deletion ; Stem Cell Factor/pharmacology ; Stomach Neoplasms/genetics/metabolism/pathology ; Transfection
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    The minor histocompatibility antigen HA-1: a diallelic gene with a single amino acid polymorphism (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-03-07
    Description: The minor histocompatibility antigen (mHag) HA-1 is the only known mHag for which mismatching is correlated with the development of severe graft versus host disease (GvHD) after human leukocyte antigen-identical bone marrow transplantation. HA-1 was found to be a nonapeptide derived from an allele of the KIAA0223 gene. The HA-1-negative allelic counterpart encoded by KIAA0223 had one amino acid difference from HA-1. Family analysis with HA-1 allele-specific polymerase chain reaction showed an exact correlation between this allelic polymorphism and the HA-1 phenotype. HA-1 allele typing of donor and recipient should improve donor selection and allow the determination of bone marrow transplantation recipients with high risk for HA-1-induced GvHD development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉den Haan, J M -- Meadows, L M -- Wang, W -- Pool, J -- Blokland, E -- Bishop, T L -- Reinhardus, C -- Shabanowitz, J -- Offringa, R -- Hunt, D F -- Engelhard, V H -- Goulmy, E -- AI07496/AI/NIAID NIH HHS/ -- AI21393/AI/NIAID NIH HHS/ -- AI3393/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1998 Feb 13;279(5353):1054-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunohematology and Bloodbank, Leiden University Medical Center, Albinusdreef 2, 2333 ZA Leiden, The Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9461441" target="_blank"〉PubMed〈/a〉
    Keywords: *Alleles ; Amino Acid Sequence ; Bone Marrow Transplantation/adverse effects ; Cell Line ; Cell Line, Transformed ; Female ; Graft vs Host Disease/immunology ; HLA-A Antigens/*immunology ; Histocompatibility Testing ; Humans ; Male ; Mass Spectrometry ; Minor Histocompatibility Antigens/chemistry/*genetics/*immunology ; *Minor Histocompatibility Loci ; Oligopeptides/chemistry/*genetics/*immunology ; Phenotype ; Polymerase Chain Reaction ; *Polymorphism, Genetic ; T-Lymphocytes, Cytotoxic/immunology
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    A mammalian scaffold complex that selectively mediates MAP kinase activation (1998)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1998-09-11
    Description: The c-Jun NH2-terminal kinase (JNK) group of mitogen-activated protein (MAP) kinases is activated by the exposure of cells to multiple forms of stress. A putative scaffold protein was identified that interacts with multiple components of the JNK signaling pathway, including the mixed-lineage group of MAP kinase kinase kinases (MLK), the MAP kinase kinase MKK7, and the MAP kinase JNK. This scaffold protein selectively enhanced JNK activation by the MLK signaling pathway. These data establish that a mammalian scaffold protein can mediate activation of a MAP kinase signaling pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Whitmarsh, A J -- Cavanagh, J -- Tournier, C -- Yasuda, J -- Davis, R J -- New York, N.Y. -- Science. 1998 Sep 11;281(5383):1671-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program in Molecular Medicine, Department of Biochemistry and Molecular Biology, University of Massachusetts Medical School and Howard Hughes Medical Institute, Worcester, MA 01605, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9733513" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; COS Cells ; Calcium-Calmodulin-Dependent Protein Kinases/*metabolism ; Carrier Proteins/*metabolism ; Cell Line ; Cercopithecus aethiops ; Enzyme Activation ; Interleukin-1/metabolism ; JNK Mitogen-Activated Protein Kinases ; MAP Kinase Kinase 7 ; *MAP Kinase Kinase Kinases ; *Mitogen-Activated Protein Kinase Kinases ; *Mitogen-Activated Protein Kinases ; Molecular Sequence Data ; Protein Kinases/*metabolism ; Protein-Serine-Threonine Kinases/*metabolism ; Recombinant Fusion Proteins/metabolism ; *Signal Transduction
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    Inhibition of xenoreactive natural antibody production by retroviral gene therapy (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-09-22
    Description: The major barrier to transplantation across discordant species, such as from pig to human, is rejection mediated by xenoreactive natural antibodies (XNA) that bind the carbohydrate epitope Galalpha1-3Galbeta1-4GlcNAc-R (alphaGal) on donor tissues. This epitope is synthesized by the enzyme glucosyltransferase uridine 5'-diphosphate galactose:beta-D-galactosyl-1, 4-N-acetyl-D-glucosaminide alpha(1-3)galactosyltransferase (E.C. 2.4.1.151), or simply alphaGT. When a functional alphaGT gene was introduced by retroviral gene transfer into bone marrow cells, alphaGal XNA production in a murine model ceased. Thus, genetic engineering of bone marrow may overcome humoral rejection of discordant xenografts and may be useful for inducing B cell tolerance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bracy, J L -- Sachs, D H -- Iacomini, J -- New York, N.Y. -- Science. 1998 Sep 18;281(5384):1845-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cellular and Molecular Biology Program, Allegheny University of the Health Sciences, 2900 Queen Lane, Philadelphia, PA 19129, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9743496" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antibody Formation ; B-Lymphocytes/immunology ; Bone Marrow Cells/*enzymology ; Bone Marrow Transplantation ; Cell Line ; Cloning, Molecular ; Enzyme-Linked Immunosorbent Assay ; Epitopes/biosynthesis/*immunology ; Galactosyltransferases/biosynthesis/*genetics/*immunology ; Gene Targeting ; Gene Transfer Techniques ; *Genetic Therapy ; Genetic Vectors ; Graft Rejection/*prevention & control ; Graft vs Host Disease/prevention & control ; Humans ; Immune Tolerance ; Mice ; Mice, Knockout ; Retroviridae/genetics ; Swine ; *Transplantation, Heterologous
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    Role of Rac1 and oxygen radicals in collagenase-1 expression induced by cell shape change (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-05-23
    Description: Integrin-mediated reorganization of cell shape leads to an altered cellular phenotype. Disruption of the actin cytoskeleton, initiated by binding of soluble antibody to alpha5beta1 integrin, led to increased expression of the collagenase-1 gene in rabbit synovial fibroblasts. Activation of the guanosine triphosphate-binding protein Rac1, which was downstream of the integrin, was necessary for this process, and expression of activated Rac1 was sufficient to increase expression of collagenase-1. Rac1 activation generated reactive oxygen species that were essential for nuclear factor kappa B-dependent transcriptional regulation of interleukin-1alpha, which, in an autocrine manner, induced collagenase-1 gene expression. Remodeling of the extracellular matrix and consequent alterations of integrin-mediated adhesion and cytoarchitecture are central to development, wound healing, inflammation, and malignant disease. The resulting activation of Rac1 may lead to altered gene regulation and alterations in cellular morphogenesis, migration, and invasion.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kheradmand, F -- Werner, E -- Tremble, P -- Symons, M -- Werb, Z -- AR20684/AR/NIAMS NIH HHS/ -- DE10306/DE/NIDCR NIH HHS/ -- HL03732/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1998 May 8;280(5365):898-902.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of California, San Francisco, CA, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9572733" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; *Cell Size ; Collagenases/*genetics ; Cytochalasin D/pharmacology ; Enzyme Activation ; Fibroblasts ; Free Radicals ; GTP Phosphohydrolases/genetics/*metabolism ; GTP-Binding Proteins/genetics/*metabolism ; *Gene Expression Regulation, Enzymologic ; Genes, Reporter ; Hydrogen Peroxide ; Interleukin-1/genetics/metabolism ; Matrix Metalloproteinase 1 ; NF-kappa B/metabolism ; Rabbits ; Reactive Oxygen Species/*metabolism ; Receptors, Fibronectin/physiology ; Transcription, Genetic ; rac GTP-Binding Proteins
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  • 71
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    In situ visualization of DNA double-strand break repair in human fibroblasts (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-05-09
    Description: A method was developed to examine DNA repair within the intact cell. Ultrasoft x-rays were used to induce DNA double-strand breaks (DSBs) in defined subnuclear volumes of human fibroblasts and DNA repair was visualized at those sites. The DSBs remained in a fixed position during the initial stages of DNA repair, and the DSB repair protein hMre11 migrated to the sites of damage within 30 minutes. In contrast, hRad51, a human RecA homolog, did not localize at sites of DNA damage, a finding consistent with the distinct roles of these proteins in DNA repair.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nelms, B E -- Maser, R S -- MacKay, J F -- Lagally, M G -- Petrini, J H -- 5T32GM07133/GM/NIGMS NIH HHS/ -- 5T32GM08349/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1998 Apr 24;280(5363):590-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Genetics and Department of Medical Physics, University of Wisconsin Medical School, Madison, WI 53706, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9554850" target="_blank"〉PubMed〈/a〉
    Keywords: Bromodeoxyuridine/immunology/metabolism ; Cell Line ; Cell Nucleus/*metabolism ; DNA/*metabolism/radiation effects ; *DNA Damage ; *DNA Repair ; DNA-Binding Proteins/metabolism ; Fibroblasts ; Fluorescein-5-isothiocyanate ; Fluorescent Antibody Technique ; Humans ; Microscopy, Confocal ; Rad51 Recombinase
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 72
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    The secreted product of Xenopus gene lunatic Fringe, a vertebrate signaling molecule (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-07-19
    Description: Signaling molecules are essential for vertebrate embryonic development. Here, two Xenopus homologs of the Drosophila gene fringe, lunatic Fringe (lFng) and radical Fringe (rFng), were identified and the protein product of lFng further characterized. The messenger RNA of lFng is supplied as a maternal message. Its product is a precursor protein consisting of pre-, pro-, and mature regions. The mature lunatic Fringe protein is secreted extracellularly, and it induced mesodermal tissue formation in animal cap assays. These results indicate that secreted lunatic Fringe can induce mesoderm and reveal that the Fringe proteins are a family of vertebrate signaling molecules.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2080353/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2080353/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wu, J Y -- Wen, L -- Zhang, W J -- Rao, Y -- R01 CA114197/CA/NCI NIH HHS/ -- R01 CA114197-01A2/CA/NCI NIH HHS/ -- R01 EY014576/EY/NEI NIH HHS/ -- R01 EY014576-03/EY/NEI NIH HHS/ -- R01 GM070967/GM/NIGMS NIH HHS/ -- R01 GM070967-02/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1996 Jul 19;273(5273):355-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatrics, Washington University School of Medicine, St. Louis, MO 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8662522" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Blastocyst/metabolism ; Cell Line ; Culture Media, Conditioned ; Culture Techniques ; Drosophila Proteins ; Embryo, Nonmammalian/metabolism ; Embryonic Development ; *Embryonic Induction ; *Glycosyltransferases ; Mesoderm/*metabolism ; Molecular Sequence Data ; *N-Acetylglucosaminyltransferases ; Polymerase Chain Reaction ; Protein Processing, Post-Translational ; Proteins/chemistry/genetics/*physiology/secretion ; RNA, Messenger/genetics/metabolism ; *Signal Transduction ; Xenopus/*embryology/genetics ; *Xenopus Proteins
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 73
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    HIV-1 Langerhans' cell tropism associated with heterosexual transmission of HIV (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-03-01
    Description: Heterosexual transmission by vaginal intercourse accounts for most transmission of human immunodeficiency virus-type 1 (HIV-1) in Africa and Asia but is less important in the HIV-1 epidemics of the United States and Western Europe. Epithelial Langerhans' cells (LCs) represent a possible source of initial cell contact for vaginal infection. Fifteen primary isolates of HIV-1 from U.S. homosexuals and 18 HIV-1 isolates from Thailand heterosexuals were evaluated for growth in LCs of U.S. origin. All the viruses from the Thai heterosexuals, which were subtype E, grew more efficiently in the LCs than any of the viruses from the U.S. homosexuals, which are subtype B. These results suggest that LC tropism is associated with the efficiency of heterosexual transmission of HIV.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Soto-Ramirez, L E -- Renjifo, B -- McLane, M F -- Marlink, R -- O'Hara, C -- Sutthent, R -- Wasi, C -- Vithayasai, P -- Vithayasai, V -- Apichartpiyakul, C -- Auewarakul, P -- Pena Cruz, V -- Chui, D S -- Osathanondh, R -- Mayer, K -- Lee, T H -- Essex, M -- 5 D43 TW0004/TW/FIC NIH HHS/ -- CA 39805/CA/NCI NIH HHS/ -- HL 33774/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1996 Mar 1;271(5253):1291-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Harvard AIDS Institute, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8638113" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Cells, Cultured ; HIV Core Protein p24/analysis ; HIV Infections/*transmission/virology ; HIV-1/classification/*growth & development/isolation & purification ; Homosexuality, Male ; Humans ; Langerhans Cells/*virology ; Macrophages/virology ; Male ; Monocytes/virology ; *Sexual Behavior ; Sexually Transmitted Diseases, Viral/*transmission/virology ; T-Lymphocytes/virology ; Thailand ; United States ; Virus Replication
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 74
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    RAC regulation of actin polymerization and proliferation by a pathway distinct from Jun kinase (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-11-22
    Description: The RAC guanine nucleotide binding proteins regulate multiple biological activities, including actin polymerization, activation of the Jun kinase (JNK) cascade, and cell proliferation. RAC effector loop mutants were identified that separate the ability of RAC to interact with different downstream effectors. One mutant of activated human RAC protein, RACV12H40 (with valine and histidine substituted at position 12 and 40, respectively), was defective in binding to PAK3, a Ste20-related p21-activated kinase (PAK), but bound to POR1, a RAC-binding protein. This mutant failed to stimulate PAK and JNK activity but still induced membrane ruffling and mediated transformation. A second mutant, RACV12L37 (with leucine substituted at position 37), which bound PAK but not POR1, induced JNK activation but was defective in inducing membrane ruffling and transformation. These results indicate that the effects of RAC on the JNK cascade and on actin polymerization and cell proliferation are mediated by distinct effector pathways that diverge at the level of RAC itself.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Joneson, T -- McDonough, M -- Bar-Sagi, D -- Van Aelst, L -- CA55360/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1996 Nov 22;274(5291):1374-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics and Microbiology, State University of New York, Stony Brook, NY 11794, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8910277" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Actins/*metabolism ; *Adaptor Proteins, Signal Transducing ; Animals ; COS Cells ; Calcium-Calmodulin-Dependent Protein Kinases/*metabolism ; Carrier Proteins/metabolism ; *Cell Division ; Cell Line ; Cell Line, Transformed ; Cell Membrane/ultrastructure ; Enzyme Activation ; GTP-Binding Proteins/genetics/metabolism/*physiology ; Humans ; JNK Mitogen-Activated Protein Kinases ; Mice ; *Mitogen-Activated Protein Kinases ; Mutagenesis ; Protein-Serine-Threonine Kinases/metabolism ; Rats ; Transfection ; p21-Activated Kinases ; rac GTP-Binding Proteins
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  • 75
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    Inhibition of myogenic bHLH and MEF2 transcription factors by the bHLH protein Twist (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-06-07
    Description: The myogenic basic helix-loop-helix (bHLH) and MEF2 transcription factors are expressed in the myotome of developing somites and cooperatively activate skeletal muscle gene expression. The bHLH protein Twist is expressed throughout the epithelial somite and is subsequently excluded from the myotome. Ectopically expressed mouse Twist (Mtwist) was shown to inhibit myogenesis by blocking DNA binding by MyoD, by titrating E proteins, and by inhibiting trans-activation by MEF2. For inhibition of MEF2, Mtwist required heterodimerization with E proteins and an intact basic domain and carboxyl-terminus. Thus, Mtwist inhibits both families of myogenic regulators and may regulate myotome formation temporally or spatially.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Spicer, D B -- Rhee, J -- Cheung, W L -- Lassar, A B -- 5-F32-AR08214-02/AR/NIAMS NIH HHS/ -- New York, N.Y. -- Science. 1996 Jun 7;272(5267):1476-80.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8633239" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Basic Helix-Loop-Helix Transcription Factors ; Cell Differentiation ; Cell Line ; Creatine Kinase/genetics ; DNA/metabolism ; DNA-Binding Proteins/*antagonists & inhibitors/chemistry/genetics/metabolism ; Drosophila ; Drosophila Proteins ; Helix-Loop-Helix Motifs/*physiology ; Inhibitor of Differentiation Protein 1 ; MEF2 Transcription Factors ; Mice ; Muscle, Skeletal/*cytology/metabolism ; MyoD Protein/metabolism/physiology ; Myogenic Regulatory Factors ; Nuclear Proteins/chemistry/metabolism/*physiology ; *Repressor Proteins ; TCF Transcription Factors ; Transcription Factor 7-Like 1 Protein ; Transcription Factors/*antagonists & ; inhibitors/chemistry/genetics/metabolism/physiology ; Transcriptional Activation ; Transfection ; Twist Transcription Factor
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  • 76
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    Stimulation of membrane ruffling and MAP kinase activation by distinct effectors of RAS (1996)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1996-02-09
    Description: The RAS guanine nucleotide binding proteins activate multiple signaling events that regulate cell growth and differentiation. In quiescent fibroblasts, ectopic expression of activated H-RAS (H-RASV12, where V12 indicates valine-12) induces membrane ruffling, mitogen-activated protein (MAP) kinase activation, and stimulation of DNA synthesis. A mutant of activated H-RAS, H-RASV12C40 (where C40 indicates cysteine-40), was identified that was defective for MAP kinase activation and stimulation of DNA synthesis, but retained the ability to induce membrane ruffling. Another mutant of activated H-RAS, H-RASV12S35 (where S35 indicates serine-35), which activates MAP kinase, was defective for stimulation of membrane ruffling and induction of DNA synthesis. Expression of both mutants resulted in a stimulation of DNA synthesis that was comparable to that induced by H-RASV12. These results indicate that membrane ruffling and activation of MAP kinase represent distinct RAS effector pathways and that input from both pathways is required for the mitogenic activity of RAS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Joneson, T -- White, M A -- Wigler, M H -- Bar-Sagi, D -- CA 55360/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1996 Feb 9;271(5250):810-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics and Microbiology, State University of New York at Stony Brook 11794, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8628998" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium-Calmodulin-Dependent Protein Kinases/*metabolism ; Cell Division ; Cell Line ; Cell Membrane/*ultrastructure ; DNA/biosynthesis ; Enzyme Activation ; GTP-Binding Proteins/genetics/metabolism ; Microinjections ; Mutation ; Plasmids ; Protein-Serine-Threonine Kinases/*metabolism ; Proto-Oncogene Proteins/*metabolism ; Proto-Oncogene Proteins c-raf ; Rats ; Signal Transduction ; rac GTP-Binding Proteins ; ras Proteins/genetics/*metabolism
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    An enhanced immune response in mice lacking the transcription factor NFAT1 (1996)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1996-05-10
    Description: Transcription factors of the NFAT family are thought to play a major role in regulating the expression of cytokine genes and other inducible genes during the immune response. The role of NFAT1 was investigated by targeted disruption of the NFAT1 gene. Unexpectedly, cells from NFAT1 -/- mice showed increased primary responses to Leishmania major and mounted increased secondary responses to ovalbumin in vitro. In an in vivo model of allergic inflammation, the accumulation of eosinophils and levels of serum immunoglobulin E were increased in NFAT1 -/- mice. These results suggest that NFAT1 exerts a negative regulatory influence on the immune response.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Xanthoudakis, S -- Viola, J P -- Shaw, K T -- Luo, C -- Wallace, J D -- Bozza, P T -- Luk, D C -- Curran, T -- Rao, A -- CA42471/CA/NCI NIH HHS/ -- GM46227/GM/NIGMS NIH HHS/ -- P30 CA21765/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1996 May 10;272(5263):892-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neurogenetics Program, Department of CNS Research, Hoffmann-LaRoche, Nutley, NJ 07110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8629027" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antigens, Protozoan/immunology ; Cell Line ; Cytokines/biosynthesis ; DNA-Binding Proteins/genetics/*physiology ; Eosinophils/immunology ; Gene Targeting ; Hypersensitivity/*immunology ; *Immunity ; Immunoglobulin E/biosynthesis ; Immunologic Memory ; Leishmania major/immunology ; *Lymphocyte Activation ; Mice ; Molecular Sequence Data ; NFATC Transcription Factors ; *Nuclear Proteins ; Ovalbumin/immunology ; T-Lymphocytes/immunology ; Transcription Factors/genetics/*physiology
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  • 78
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    Coupling of the RAS-MAPK pathway to gene activation by RSK2, a growth factor-regulated CREB kinase (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-08-16
    Description: A signaling pathway has been elucidated whereby growth factors activate the transcription factor cyclic adenosine monophosphate response element-binding protein (CREB), a critical regulator of immediate early gene transcription. Growth factor-stimulated CREB phosphorylation at serine-133 is mediated by the RAS-mitogen-activated protein kinase (MAPK) pathway. MAPK activates CREB kinase, which in turn phosphorylates and activates CREB. Purification, sequencing, and biochemical characterization of CREB kinase revealed that it is identical to a member of the pp90(RSK) family, RSK2. RSK2 was shown to mediate growth factor induction of CREB serine-133 phosphorylation both in vitro and in vivo. These findings identify a cellular function for RSK2 and define a mechanism whereby growth factor signals mediated by RAS and MAPK are transmitted to the nucleus to activate gene expression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Xing, J -- Ginty, D D -- Greenberg, M E -- CA43855/CA/NCI NIH HHS/ -- NS34814-01/NS/NINDS NIH HHS/ -- P30-HD18655/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1996 Aug 16;273(5277):959-63.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program in Biological and Biomedical Sciences, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8688081" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Calcium-Calmodulin-Dependent Protein Kinases/*metabolism ; Cell Line ; Cell Nucleus/metabolism ; Cyclic AMP Response Element-Binding Protein/*metabolism ; Epidermal Growth Factor/pharmacology ; *Gene Expression Regulation ; Growth Substances/*pharmacology ; Humans ; Molecular Sequence Data ; Nerve Growth Factors/pharmacology ; PC12 Cells ; Phosphorylation ; Protein-Serine-Threonine Kinases/*metabolism ; Rats ; Ribosomal Protein S6 Kinases ; *Signal Transduction ; Tetradecanoylphorbol Acetate/pharmacology ; Transcriptional Activation ; Transfection ; Tumor Cells, Cultured ; ras Proteins/metabolism
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  • 79
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    Cooperative DNA binding and sequence-selective recognition conferred by the STAT amino-terminal domain (1996)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1996-08-09
    Description: STAT proteins (signal transducers and activators of transcription) activate distinct target genes despite having similar DNA binding preferences. The transcriptional specificity of STAT proteins was investigated on natural STAT binding sites near the interferon-gamma gene. These sites are arranged in multiple copies and required cooperative interactions for STAT binding. The conserved amino-terminal domain of STAT proteins was required for cooperative DNA binding, although this domain was not essential for dimerization or binding to a single site. Cooperative binding interactions enabled the STAT proteins to recognize variations of the consensus site. These sites can be specific for the different STAT proteins and may function to direct selective transcriptional activation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Xu, X -- Sun, Y L -- Hoey, T -- New York, N.Y. -- Science. 1996 Aug 9;273(5276):794-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Tularik, Two Corporate Drive, South San Francisco, CA 94080, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8670419" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Binding Sites ; Cell Line ; DNA/*metabolism ; DNA-Binding Proteins/chemistry/immunology/*metabolism ; Interferon-gamma/genetics ; Introns ; Molecular Sequence Data ; Mutation ; Oligodeoxyribonucleotides/metabolism ; Promoter Regions, Genetic ; STAT1 Transcription Factor ; STAT4 Transcription Factor ; Sequence Deletion ; Signal Transduction ; Trans-Activators/chemistry/immunology/*metabolism ; *Transcriptional Activation
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  • 80
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    IRAK: a kinase associated with the interleukin-1 receptor (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-02-23
    Description: The pleiotropic biological activities of interleukin-1 (IL-1) are mediated by its type I receptor (IL-1RI). When the ligand binds, IL-1RI initiates a signaling cascade that results in the activation of the transcription regulator nuclear factor kappa B (NF-kappa B). A protein kinase designated IRAK (IL-1 receptor-associated kinase) was purified, and its complementary DNA was molecularly cloned. When human embryonic kidney cells (cell line 293) over-expressing IL-1RI or HeLa cells were exposed to IL-1, IRAK rapidly associated with the IL-1RI complex and was phosphorylated. The primary amino acid sequence of IRAK shares similarity with that of Pelle, a protein kinase that is essential for the activation of a NF-kappa B homolog in Drosophila.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cao, Z -- Henzel, W J -- Gao, X -- New York, N.Y. -- Science. 1996 Feb 23;271(5252):1128-31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Biology Department, Tularik, Incorporated, South San Francisco, CA 94080, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8599092" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cell Line ; Cloning, Molecular ; DNA, Complementary/genetics ; Drosophila ; *Drosophila Proteins ; HeLa Cells ; Humans ; Interleukin-1/*metabolism/pharmacology ; Interleukin-1 Receptor-Associated Kinases ; Molecular Sequence Data ; Phosphorylation ; Protein Kinases/chemistry/genetics/isolation & purification/*metabolism ; Protein-Serine-Threonine Kinases/chemistry ; Receptors, Interleukin-1/*metabolism ; Transfection
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  • 81
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    Binding of zinc finger protein ZPR1 to the epidermal growth factor receptor (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-06-21
    Description: ZPR1 is a zinc finger protein that binds to the cytoplasmic tyrosine kinase domain of the epidermal growth factor receptor (EGFR). Deletion analysis demonstrated that this binding interaction is mediated by the zinc fingers of ZPR1 and subdomains X and XI of the EGFR tyrosine kinase. Treatment of mammalian cells with EGF caused decreased binding of ZPR1 to the EGFR and the accumulation of ZPR1 in the nucleus. The effect of EGF to regulate ZPR1 binding is dependent on tyrosine phosphorylation of the EGFR. ZPR1 therefore represents a prototype for a class of molecule that binds to the EGFR and is released from the receptor after activation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Galcheva-Gargova, Z -- Konstantinov, K N -- Wu, I H -- Klier, F G -- Barrett, T -- Davis, R J -- R01-CA58396/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1996 Jun 21;272(5269):1797-802.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Biology, University of Massachusetts Medical School, Worcester, 01605, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8650580" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Carrier Proteins/chemistry/*metabolism/secretion ; Cell Line ; Cell Nucleus/metabolism ; Cloning, Molecular ; Cytoplasm/metabolism ; Epidermal Growth Factor/pharmacology ; Humans ; Immunoblotting ; Male ; Mice ; Molecular Sequence Data ; Phosphorylation ; Phosphotyrosine/metabolism ; Protein Structure, Secondary ; RNA, Messenger/genetics/metabolism ; Receptor, Epidermal Growth Factor/chemistry/*metabolism ; Testis/metabolism ; Type C Phospholipases/metabolism ; Vanadates/pharmacology ; *Zinc Fingers ; src Homology Domains
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 82
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    Enter Listeria, unruffled (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-03-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gallagher, R B -- New York, N.Y. -- Science. 1996 Mar 29;271(5257):1825.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8596949" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/metabolism ; Bacterial Proteins/*metabolism ; Cadherins/*metabolism ; Cell Line ; Fibroblasts/microbiology ; Listeria monocytogenes/*metabolism/ultrastructure ; *Phagocytosis
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  • 83
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    Identification of a putative target for Rho as the serine-threonine kinase protein kinase N (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-02-02
    Description: Rho, a Ras-like small guanosine triphosphatase, has been implicated in cytoskeletal responses to extracellular signals such as lysophosphatidic acid (LPA) to form stress fibers and focal contacts. The form of RhoA bound to guanosine triphosphate directly bound to and activated a serine-threonine kinase, protein kinase N (PKN). Activated RhoA formed a complex with PKN and activated it in COS-7 cells. PKN was phosphorylated in Swiss 3T3 cells stimulated with LPA, and this phosphorylation was blocked by treatment of cells with botulinum C3 exoenzyme. Activation of Rho may be linked directly to a serine-threonine kinase pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Amano, M -- Mukai, H -- Ono, Y -- Chihara, K -- Matsui, T -- Hamajima, Y -- Okawa, K -- Iwamatsu, A -- Kaibuchi, K -- New York, N.Y. -- Science. 1996 Feb 2;271(5249):648-50.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Signal Transduction, Nara Institute of Science and Technology, Ikoma, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8571127" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; ADP Ribose Transferases/pharmacology ; Amino Acid Sequence ; Animals ; *Botulinum Toxins ; Cell Line ; Chromatography, Affinity ; Enzyme Activation ; GTP Phosphohydrolases/*metabolism ; GTP-Binding Proteins/*metabolism ; Guanosine Triphosphate/metabolism ; Lysophospholipids/pharmacology ; Mice ; Molecular Sequence Data ; Phosphorylation ; Protein Kinase C/*metabolism ; Recombinant Fusion Proteins/metabolism ; rhoA GTP-Binding Protein
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  • 84
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    Requirement for the adapter protein GRB2 in EGF receptor endocytosis (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-06-28
    Description: Activated epidermal growth factor (EGF) receptors induce the formation of various complexes of intracellular signaling proteins that are mediated by SRC homology 2 (SH2) and SH3 domains. The activated receptors are also rapidly internalized into the endocytotic compartment and degraded in lysosomes. EGF stimulation of canine epithelial cells induced a rapid and transient association of the SH3-SH2-SH3 protein GRB2 with dynamin, a guanosine triphosphatase that regulates endocytosis. Disruption of GRB2 interactions by microinjection of a peptide corresponding to the GRB2 SH2 domain or its phosphopeptide ligand blocked EGF receptor endocytosis; other SH2 domains that bind EGF receptors or antibodies that neutralize RAS did not. Both activation and termination of EGF signaling appear to be regulated by the diverse interactions of GRB2.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Z -- Moran, M F -- New York, N.Y. -- Science. 1996 Jun 28;272(5270):1935-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Banting and Best Department of Medical Research, University of Toronto, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8658166" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptor Proteins, Signal Transducing ; Animals ; Antibodies, Monoclonal ; Cell Line ; Dogs ; Dynamins ; *Endocytosis/drug effects ; Epidermal Growth Factor/pharmacology ; GRB2 Adaptor Protein ; GTP Phosphohydrolases/metabolism ; Microinjections ; Peptide Fragments/pharmacology ; Proteins/*metabolism ; Receptor, Epidermal Growth Factor/*metabolism ; Receptors, Transferrin/metabolism ; Recombinant Fusion Proteins/pharmacology ; Signal Transduction ; ras Proteins/immunology/physiology ; src Homology Domains/physiology
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  • 85
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    Gene perplexes epilepsy researchers (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-03-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉O'Brien, C -- New York, N.Y. -- Science. 1996 Mar 22;271(5256):1672.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8596927" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Chromosome Mapping ; Chromosomes, Human, Pair 21/*genetics ; Cystatin B ; Cystatins/*genetics ; Cysteine Proteinase Inhibitors/*genetics ; Epilepsies, Myoclonic/*genetics ; Female ; Humans ; Male ; Mutation ; Pedigree ; RNA, Messenger/genetics/metabolism
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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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    Protein kinase N (PKN) and PKN-related protein rhophilin as targets of small GTPase Rho (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-02-02
    Description: The Rho guanosine 5'-triphosphatase (GTPase) cycles between the active guanosine triphosphate (GTP)-bound form and the inactive guanosine diphosphate-bound form and regulates cell adhesion and cytokinesis, but how it exerts these actions is unknown. The yeast two-hybrid system was used to clone a complementary DNA for a protein (designated Rhophilin) that specifically bound to GTP-Rho. The Rho-binding domain of this protein has 40 percent identity with a putative regulatory domain of a protein kinase, PKN. PKN itself bound to GTP-Rho and was activated by this binding both in vitro and in vivo. This study indicates that a serine-threonine protein kinase is a Rho effector and presents an amino acid sequence motif for binding to GTP-Rho that may be shared by a family of Rho target proteins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Watanabe, G -- Saito, Y -- Madaule, P -- Ishizaki, T -- Fujisawa, K -- Morii, N -- Mukai, H -- Ono, Y -- Kakizuka, A -- Narumiya, S -- New York, N.Y. -- Science. 1996 Feb 2;271(5249):645-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, Kyoto University Faculty of Medicine, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8571126" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; Amino Acid Sequence ; Animals ; Cell Line ; Cloning, Molecular ; Enzyme Activation ; GTP Phosphohydrolases/*metabolism ; GTP-Binding Proteins/chemistry/*metabolism ; Guanosine Triphosphate/metabolism ; Humans ; Membrane Proteins/*metabolism ; Mice ; Molecular Sequence Data ; Phosphorylation ; Protein Kinase C/chemistry/*metabolism ; *Protein-Serine-Threonine Kinases ; Recombinant Fusion Proteins/metabolism ; Saccharomyces cerevisiae/genetics ; Signal Transduction ; ras Proteins ; *rho GTP-Binding Proteins ; rhoA GTP-Binding Protein ; rhoB GTP-Binding Protein
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  • 87
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    PIN: an associated protein inhibitor of neuronal nitric oxide synthase (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-11-01
    Description: The neurotransmitter functions of nitric oxide are dependent on dynamic regulation of its biosynthetic enzyme, neuronal nitric oxide synthase (nNOS). By means of a yeast two-hybrid screen, a 10-kilodalton protein was identified that physically interacts with and inhibits the activity of nNOS. This inhibitor, designated PIN, appears to be one of the most conserved proteins in nature, showing 92 percent amino acid identity with the nematode and rat homologs. Binding of PIN destabilizes the nNOS dimer, a conformation necessary for activity. These results suggest that PIN may regulate numerous biological processes through its effects on nitric oxide synthase activity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jaffrey, S R -- Snyder, S H -- DA00074/DA/NIDA NIH HHS/ -- GM-07309/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1996 Nov 1;274(5288):774-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, Johns Hopkins University School of Medicine, 725 North Wolfe Street, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8864115" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Carrier Proteins/chemistry/genetics/*metabolism/pharmacology ; Cell Line ; Cyclic GMP/metabolism ; Dimerization ; *Drosophila Proteins ; Dyneins ; Enzyme Inhibitors/chemistry/*metabolism/pharmacology ; Humans ; Molecular Sequence Data ; Molecular Weight ; Neurons/enzymology ; Nitric Oxide Synthase/*antagonists & inhibitors/metabolism ; Rats ; Recombinant Fusion Proteins/metabolism/pharmacology ; Saccharomyces cerevisiae ; Transfection
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 88
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    Identification of MAP kinase domains by redirecting stress signals into growth factor responses (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-06-14
    Description: Mitogen-activated protein kinase (MAPK) cascades, termed MAPK modules, channel extracellular signals into specific cellular responses. Chimeric molecules were constructed between p38 and p44 MAPKs, which transduce stress and growth factor signals, respectively. A discrete region of 40 residues located in the amono-terminal p38MAPK lobe directed the specificity of response to extracellular signals, whereas the p44MAPK chimera, expressed in vivo, redirected stress signals into early mitogenic responses, demonstrating the functional independence of these domains.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brunet, A -- Pouyssegur, J -- New York, N.Y. -- Science. 1996 Jun 14;272(5268):1652-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre de Biochemie-CNRS, UMR134, Parc Valrose, Faculte des Sciences, Nice, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8658140" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Anisomycin/pharmacology ; Binding Sites ; Calcium-Calmodulin-Dependent Protein Kinases/genetics/*metabolism ; Cell Division ; Cell Line ; Cricetinae ; Cricetulus ; Enzyme Activation ; Gene Expression Regulation ; Genes, fos ; Growth Substances/metabolism ; Mice ; Mitogen-Activated Protein Kinase 3 ; *Mitogen-Activated Protein Kinases ; Molecular Sequence Data ; Phosphorylation/drug effects ; Protein Kinases/metabolism ; Protein-Serine-Threonine Kinases/metabolism ; Recombinant Fusion Proteins/genetics/metabolism ; Ribosomal Protein S6 Kinases ; Signal Transduction ; Sorbitol/pharmacology ; Substrate Specificity ; p38 Mitogen-Activated Protein Kinases
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  • 89
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    Association of Src tyrosine kinase with a human potassium channel mediated by SH3 domain (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-12-20
    Description: The human Kv1.5 potassium channel (hKv1.5) contains proline-rich sequences identical to those that bind to Src homology 3 (SH3) domains. Direct association of the Src tyrosine kinase with cloned hKv1.5 and native hKv1.5 in human myocardium was observed. This interaction was mediated by the proline-rich motif of hKv1.5 and the SH3 domain of Src. Furthermore, hKv1.5 was tyrosine phosphorylated, and the channel current was suppressed, in cells coexpressing v-Src. These results provide direct biochemical evidence for a signaling complex composed of a potassium channel and a protein tyrosine kinase.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Holmes, T C -- Fadool, D A -- Ren, R -- Levitan, I B -- F32 NS009952/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1996 Dec 20;274(5295):2089-91.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Volen Center for Complex Systems, Brandeis University, Waltham, MA 02254, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8953041" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Cell Line ; Cloning, Molecular ; Humans ; Kv1.5 Potassium Channel ; Molecular Sequence Data ; Myocardium/chemistry ; Oncogene Protein pp60(v-src)/metabolism ; Patch-Clamp Techniques ; Phosphorylation ; Phosphotyrosine/metabolism ; Potassium Channels/chemistry/*metabolism ; *Potassium Channels, Voltage-Gated ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Transfection ; src Homology Domains/*physiology ; src-Family Kinases/chemistry/*metabolism
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  • 90
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    Failure of the cystic fibrosis transmembrane conductance regulator to conduct ATP (1996)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1996-03-29
    Description: The cystic fibrosis transmembrane conductance regulator (CFTR) is a chloride ion channel regulated by protein kinase A and adenosine triphosphate (ATP). Loss of CFTR-mediated chloride ion conductance from the apical plasma membrane of epithelial cells is a primary physiological lesion in cystic fibrosis. CFTR has also been suggested to function an an ATP channel, although the size of the ATP anion is much larger than the estimated size of the CFTR pore. ATP was not conducted through CFTR in intact organs, polarized human lung cell lines, stably transfected mammalian cell lines, or planar lipid bilayers reconstituted with CFTR protein. These findings suggest that ATP permeation through the CFTR is unlikely to contribute to the normal function of CFTR or to the pathogenesis of cystic fibrosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Reddy, M M -- Quinton, P M -- Haws, C -- Wine, J J -- Grygorczyk, R -- Tabcharani, J A -- Hanrahan, J W -- Gunderson, K L -- Kopito, R R -- DK43994/DK/NIDDK NIH HHS/ -- DK45913/DK/NIDDK NIH HHS/ -- HL42368/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1996 Mar 29;271(5257):1876-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biomedical Sciences, University of California, Riverside, 92521, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8596959" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/*metabolism ; Animals ; CHO Cells ; Cell Line ; Cell Membrane/metabolism ; Cell Polarity ; Chlorides/metabolism ; Cricetinae ; Cystic Fibrosis Transmembrane Conductance Regulator/*metabolism ; Humans ; Lipid Bilayers/metabolism ; Lung/cytology/metabolism ; Patch-Clamp Techniques ; Recombinant Proteins/metabolism
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  • 91
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    A quasi-monoclonal mouse (1996)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1996-06-14
    Description: As a model for studying the generation of antibody diversity, a gene-targeted mouse was produced that is hemizygous for a rearranged V(D)J segment at the immunoglobulin (Ig) heavy chain locus, the other allele being nonfunctional. The mouse also has no functional kappa light chain allele. The heavy chain, when paired with any lambda light chain, is specific for the hapten (4-hydroxy-3-nitrophenyl) acetyl (NP). The primary repertoire of this quasi-monoclonal mouse is monospecific, but somatic hypermutation and secondary rearrangements change the specificity of 20 percent of the antigen receptors on B cells. The serum concentrations of the Ig isotypes are similar to those in nontransgenic littermates, but less than half of the serum IgM binds to NP, and none of the other isotypes do. Thus, neither network interactions nor random activation of a small fraction of the B cell population can account for serum Ig concentrations.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cascalho, M -- Ma, A -- Lee, S -- Masat, L -- Wabl, M -- 1R01 GM37699/GM/NIGMS NIH HHS/ -- P60 AR20684/AR/NIAMS NIH HHS/ -- New York, N.Y. -- Science. 1996 Jun 14;272(5268):1649-52.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, University of California, San Francisco 94143-0670, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8658139" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/*genetics/immunology ; *Antigens, CD ; Antigens, CD43 ; Antigens, CD45/immunology ; B-Lymphocytes/cytology/immunology ; Base Sequence ; Cell Line ; Cloning, Molecular ; Dna ; Flow Cytometry ; Gene Rearrangement, B-Lymphocyte, Heavy Chain ; Haptens/immunology ; Immunoglobulin Heavy Chains/*genetics/immunology ; Immunoglobulin Isotypes/genetics ; Immunoglobulin J-Chains/genetics ; Immunoglobulin Light Chains/genetics/immunology ; Immunoglobulin Variable Region/genetics ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Knockout/genetics/*immunology ; Molecular Sequence Data ; Nitrophenols/immunology ; Phenylacetates ; Recombinant Proteins/genetics/immunology ; Sialoglycoproteins/immunology
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  • 92
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    Cholesterol modification of hedgehog signaling proteins in animal development (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-10-11
    Description: Hedgehog (Hh) proteins comprise a family of secreted signaling molecules essential for patterning a variety of structures in animal embryogenesis. During biosynthesis, Hh undergoes an autocleavage reaction, mediated by its carboxyl-terminal domain, that produces a lipid-modified amino-terminal fragment responsible for all known Hh signaling activity. Here it is reported that cholesterol is the lipophilic moiety covalently attached to the amino-terminal signaling domain during autoprocessing and that the carboxyl-terminal domain acts as an intramolecular cholesterol transferase. This use of cholesterol to modify embryonic signaling proteins may account for some of the effects of perturbed cholesterol biosynthesis on animal development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Porter, J A -- Young, K E -- Beachy, P A -- New York, N.Y. -- Science. 1996 Oct 11;274(5285):255-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Molecular Biology and Genetics, Johns Hopkins School of Medicine, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8824192" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cells, Cultured ; Cholesterol/*metabolism ; Dithiothreitol/pharmacology ; Drosophila ; *Drosophila Proteins ; *Embryonic Induction ; Embryonic and Fetal Development ; Hedgehog Proteins ; Humans ; Protein Processing, Post-Translational ; Proteins/genetics/*metabolism ; Signal Transduction ; *Trans-Activators
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  • 93
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    Lymphocyte apoptosis: mediation by increased type 3 inositol 1,4,5-trisphosphate receptor (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-07-26
    Description: B and T lymphocytes undergoing apoptosis in response to anti-immunoglobulin M antibodies and dexamethasone, respectively, were found to have increased amounts of messenger RNA for the inositol 1,4,5-trisphosphate receptor (IP3R) and increased amounts of IP3R protein. Immunohistochemical analysis revealed that the augmented receptor population was localized to the plasma membrane. Type 3 IP3R (IP3R3) was selectively increased during apoptosis, with no enhancement of type 1 IP3R (IP3R1). Expression of IP3R3 antisense constructs in S49 T cells blocked dexamethasone-induced apoptosis, whereas IP3R3 sense, IP3R1 sense, or IP3R1 antisense control constructs did not block cell death. Thus, the increases in IP3R3 may be causally related to apoptosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Khan, A A -- Soloski, M J -- Sharp, A H -- Schilling, G -- Sabatini, D M -- Li, S H -- Ross, C A -- Snyder, S H -- AI-20922/AI/NIAID NIH HHS/ -- AI-37934/AI/NIAID NIH HHS/ -- MH43040/MH/NIMH NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1996 Jul 26;273(5274):503-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8662540" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; *Apoptosis ; B-Lymphocytes/*cytology/metabolism ; Base Sequence ; Calcium/metabolism ; Calcium Channels/genetics/immunology/*metabolism ; Cell Line ; Cell Membrane/metabolism ; Cells, Cultured ; DNA, Antisense ; Dexamethasone/pharmacology ; Immunoblotting ; Inositol 1,4,5-Trisphosphate/*metabolism ; Inositol 1,4,5-Trisphosphate Receptors ; Mice ; Molecular Sequence Data ; Receptors, Cytoplasmic and Nuclear/genetics/immunology/*metabolism ; T-Lymphocytes/*cytology/metabolism ; Transfection ; Tumor Cells, Cultured
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  • 94
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    Requirement of an ICE-like protease for induction of apoptosis and ceramide generation by REAPER (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-02-09
    Description: Genetic studies indicated that the Drosophila melanogaster protein REAPER (RPR) controls apoptosis during embryo development. Induction of RPR expression in Drosophila Schneider cells rapidly stimulated apoptosis. RPR-mediated apoptosis was blocked by N-benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone (Z-VAD-fmk), which suggests that an interleukin-1 beta converting enzyme (ICE)-like protease is required for RPR function. RPR-induced apoptosis was associated with increased ceramide production that was also blocked by Z-VAD-fmk, which suggests that ceramide generation requires an ICE-like protease as well. Thus, the intracellular RPR protein uses cell death signaling pathways similar to those used by the vertebrate transmembrane receptors Fas (CD95) and tumor necrosis factor receptor type 1.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pronk, G J -- Ramer, K -- Amiri, P -- Williams, L T -- New York, N.Y. -- Science. 1996 Feb 9;271(5250):808-10.〈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/8628997" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Chloromethyl Ketones/pharmacology ; Amino Acid Sequence ; Animals ; *Apoptosis/drug effects ; Caspase 1 ; Cell Line ; Ceramides/*metabolism/pharmacology ; Copper/pharmacology ; Copper Sulfate ; Cysteine Endopeptidases/*metabolism ; *Drosophila Proteins ; Drosophila melanogaster/*cytology/embryology/genetics/metabolism ; Enzyme Activation ; Gene Expression ; Molecular Sequence Data ; Peptides/genetics/*physiology ; Protease Inhibitors/pharmacology ; Signal Transduction ; 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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  • 95
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    Nonselective and G betagamma-insensitive weaver K+ channels (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-06-28
    Description: Homozygous weaver mice are profoundly ataxic because of the loss of granule cell neurons during cerebellar development. This granule cell loss appears to be caused by a genetic defect in the pore region (Gly156--〉Ser) of the heterotrimeric guanine nucleotide-binding protein (G protein)-gated inwardly rectifying potassium (K+) channel subunit (GIRK2). A related subunit, GIRK1, associates with GIRK2 to constitute a neuronal G protein-gated inward rectifier K+ channel. The weaver allele of the GIRK2 subunit (wvGIRK2) caused loss of K+ selectivity when expressed either as wvGIRK2 homomultimers or as GIRK1-wvGIRK2 heteromultimers. The mutation also let to loss of sensitivity to G protein betagamma dimers. Expression of wvGIRK2 subunits let to increased cell death, presumably as a result of basal nonselective channel opening.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Navarro, B -- Kennedy, M E -- Velimirovic, B -- Bhat, D -- Peterson, A S -- Clapham, D E -- New York, N.Y. -- Science. 1996 Jun 28;272(5270):1950-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, Mayo Foundation, Rochester, Minnesota 55905, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8658170" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antisense Elements (Genetics) ; CHO Cells ; Cell Death ; Cell Line ; Cerebellum/cytology/*metabolism ; Cricetinae ; G Protein-Coupled Inwardly-Rectifying Potassium Channels ; GTP-Binding Proteins/*physiology ; Membrane Potentials ; Mice ; Mice, Neurologic Mutants ; Molecular Sequence Data ; Neurons/cytology/metabolism ; Oocytes/cytology ; Patch-Clamp Techniques ; Point Mutation ; Potassium Channels/genetics/*metabolism ; *Potassium Channels, Inwardly Rectifying ; 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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  • 96
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    In vitro development of primitive and definitive erythrocytes from different precursors (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-05-03
    Description: During mouse embryogenesis the production of "primitive" erythrocytes (EryP) precedes the production of "definitive" erythrocytes (EryD) in parallel with the transition of the hematopoietic site from the yolk sac to the fetal liver. On a macrophage colony-stimulating factor-deficient stromal cell line OP9, mouse embryonic stem cells were shown to give rise to EryP and EryD sequentially with a time course similar to that seen in murine ontogeny. Studies of the different growth factor requirements and limiting dilution analysis of precursor frequencies indicate that most EryP and EryD probably developed from different precursors by way of distinct differentiation pathways.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nakano, T -- Kodama, H -- Honjo, T -- New York, N.Y. -- Science. 1996 May 3;272(5262):722-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Chemistry, Faculty of Medicine, Kyoto University, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8614833" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cell Division ; Cell Line ; Cell Lineage ; Cell Separation ; Cells, Cultured ; Coculture Techniques ; Erythroid Precursor Cells/*cytology ; *Erythropoiesis ; Erythropoietin/pharmacology ; Kinetics ; Mice ; Signal Transduction ; Stem Cell Factor/physiology
    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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  • 97
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    T cell activation determined by T cell receptor number and tunable thresholds (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-07-05
    Description: The requirements for T cell activation have been reported to vary widely depending on the state of the T cell, the type of antigen-presenting cell, and the nature of the T cell receptor (TCR) ligand. A unitary requirement for T cell responses was revealed by measurement of the number of triggered TCRs. Irrespective of the nature of the triggering ligand, T cells "counted" the number of triggered TCRs and responded when a threshold of approximately 8000 TCRs was reached. The capacity to reach the activation threshold was severely compromised by a reduction in the number of TCRs. Costimulatory signals lowered the activation threshold to approximately 1500 TCRs, thus making T cells more sensitive to antigenic stimulation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Viola, A -- Lanzavecchia, A -- New York, N.Y. -- Science. 1996 Jul 5;273(5271):104-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Basel Institute for Immunology, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8658175" target="_blank"〉PubMed〈/a〉
    Keywords: Antibodies/immunology ; Antigen-Presenting Cells/immunology ; Antigens, CD3/immunology ; Antigens, CD80/immunology ; *Bacterial Toxins ; Cell Line ; Clone Cells ; Down-Regulation ; Enterotoxins/immunology ; Histocompatibility Antigens Class II/immunology ; Humans ; Interferon-gamma/biosynthesis ; *Lymphocyte Activation ; Peptides/immunology ; Receptors, Antigen, T-Cell/*immunology ; Receptors, Antigen, T-Cell, alpha-beta/immunology ; Superantigens/immunology ; T-Lymphocytes/*immunology
    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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  • 98
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    Interfering with apoptosis: Ca(2+)-binding protein ALG-2 and Alzheimer's disease gene ALG-3 (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-01-26
    Description: Two apoptosis-linked genes, named ALG-2 and ALG-3, were identified by means of a functional selection strategy. ALG-2 codes for a Ca(2+)-binding protein required for T cell receptor-, Fas-, and glucocorticoid-induced cell death. ALG-3, a partial complementary DNA that is homologous to the familial Alzheimer's disease gene STM2, rescues a T cell hybridoma from T cell receptor- and Fas-induced apoptosis. These findings suggest that ALG-2 may mediate Ca(2+)-regulated signals along the death pathway and that cell death may play a role in Alzheimer's disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vito, P -- Lacana, E -- D'Adamio, L -- New York, N.Y. -- Science. 1996 Jan 26;271(5248):521-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉T Cell Molecular Biology Unit, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8560270" target="_blank"〉PubMed〈/a〉
    Keywords: Alkaloids/pharmacology ; Alzheimer Disease/*genetics ; Amino Acid Sequence ; Animals ; Antigens, CD95/metabolism ; *Apoptosis/drug effects ; Apoptosis Regulatory Proteins ; Calcium/metabolism ; Calcium-Binding Proteins/chemistry/genetics/*physiology ; Cell Line ; Cloning, Molecular ; DNA, Complementary ; Dactinomycin/pharmacology ; Dexamethasone/pharmacology ; Fas Ligand Protein ; Hybridomas ; Interleukin-2/metabolism ; Membrane Glycoproteins/metabolism ; Membrane Proteins/chemistry/genetics/*physiology ; Mice ; Molecular Sequence Data ; Presenilin-2 ; Receptors, Antigen, T-Cell/physiology ; Signal Transduction ; Staurosporine ; T-Lymphocytes ; Transfection ; Up-Regulation
    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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  • 99
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    Blockage by adenovirus E4orf6 of transcriptional activation by the p53 tumor suppressor (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-06-07
    Description: The adenovirus E4orf6 protein is shown here to interact with the cellular tumor suppressor protein p53 and to block p53-mediated transcriptional activation. The adenovirus protein inhibited the ability of p53 to bind to human TAFII31, a component of transcription factor IID (TFIID). Earlier work demonstrated that the interaction of p53 with TAFII31 involves a sequence near the NH2-terminus of p53, whereas the E4orf6-p53 interaction occurs within amino acids 318 to 360 of p53. Thus, the E4orf6 protein interacts at a site on p53 distinct from the domain that binds to TAFII31 but nevertheless inhibits the p53-TAFII31 interaction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dobner, T -- Horikoshi, N -- Rubenwolf, S -- Shenk, T -- New York, N.Y. -- Science. 1996 Jun 7;272(5267):1470-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut fur Medizinische Mikrobiologie und Hygiene, Universitat Regensburg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8633237" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoviridae/physiology ; Adenovirus E4 Proteins/immunology/*metabolism ; Cell Line ; DNA/metabolism ; Genes, p53 ; HeLa Cells ; Humans ; Immunoblotting ; Recombinant Fusion Proteins/metabolism ; *TATA-Binding Protein Associated Factors ; Trans-Activators/*metabolism ; *Transcription Factor TFIID ; *Transcriptional Activation ; Transfection ; Tumor Suppressor Protein p53/chemistry/*metabolism
    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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  • 100
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    Luteinizing hormone deficiency and female infertility in mice lacking the transcription factor NGFI-A (Egr-1) (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-08-30
    Description: The immediate-early transcription factor NGFI-A (also called Egr-1, zif/268, or Krox-24) is thought to couple extracellular signals to changes in gene expression. Although activins and inhibins regulate follicle-stimulating hormone (FSH) synthesis, no factor has been identified that exclusively regulates luteinizing hormone (LH) synthesis. An analysis of NGFI-A-deficient mice derived from embryonic stem cells demonstrated female infertility that was secondary to LH-beta deficiency. Ovariectomy led to increased amounts of FSH-beta but not LH-beta messenger RNA, which suggested a pituitary defect. A conserved, canonical NGFI-A site in the LH-beta promoter was required for synergistic activation by NGFI-A and steroidogenic factor-1 (SF-1). NGFI-A apparently influences female reproductive capacity through its regulation of LH-beta transcription.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, S L -- Sadovsky, Y -- Swirnoff, A H -- Polish, J A -- Goda, P -- Gavrilina, G -- Milbrandt, J -- CA53524/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1996 Aug 30;273(5279):1219-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Washington University School of Medicine, St. Louis, MO 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8703054" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cell Line ; DNA-Binding Proteins/*genetics ; Early Growth Response Protein 1 ; Female ; Follicle Stimulating Hormone/genetics ; Follicle Stimulating Hormone, beta Subunit ; Fushi Tarazu Transcription Factors ; *Gene Expression Regulation ; Gene Targeting ; Gonadotropins/pharmacology ; Homeodomain Proteins ; *Immediate-Early Proteins ; Infertility, Female/*genetics ; Luteinizing Hormone/analysis/*deficiency/*genetics ; Male ; Mice ; Molecular Sequence Data ; Ovary/drug effects/physiology ; Pituitary Gland/metabolism ; Promoter Regions, Genetic ; Receptors, Cytoplasmic and Nuclear ; Steroidogenic Factor 1 ; Transcription Factors/*genetics ; Transfection ; Uterus/drug effects ; Zinc Fingers
    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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