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  • 1
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    Cell activation and apoptosis by bacterial lipoproteins through toll-like receptor-2 (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-31
    Description: Apoptosis is implicated in the generation and resolution of inflammation in response to bacterial pathogens. All bacterial pathogens produce lipoproteins (BLPs), which trigger the innate immune response. BLPs were found to induce apoptosis in THP-1 monocytic cells through human Toll-like receptor-2 (hTLR2). BLPs also initiated apoptosis in an epithelial cell line transfected with hTLR2. In addition, BLPs stimulated nuclear factor-kappaB, a transcriptional activator of multiple host defense genes, and activated the respiratory burst through hTLR2. Thus, hTLR2 is a molecular link between microbial products, apoptosis, and host defense mechanisms.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Aliprantis, A O -- Yang, R B -- Mark, M R -- Suggett, S -- Devaux, B -- Radolf, J D -- Klimpel, G R -- Godowski, P -- Zychlinsky, A -- AI 37720-04/AI/NIAID NIH HHS/ -- AI-38894/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1999 Jul 30;285(5428):736-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Skirball Institute and Department of Microbiology, New York University School of Medicine, 540 First Avenue, New York, NY 10016, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10426996" target="_blank"〉PubMed〈/a〉
    Keywords: Antibodies, Monoclonal ; Antigens, CD14/analysis ; *Apoptosis ; Bacterial Proteins/metabolism/*pharmacology ; Cell Line/metabolism ; Cycloheximide/pharmacology ; Cytotoxicity, Immunologic ; *Drosophila Proteins ; Genes, Reporter ; Humans ; Lipopolysaccharides/immunology ; Lipoproteins/metabolism/*pharmacology ; Membrane Glycoproteins/immunology/*metabolism ; Monocytes/*cytology/immunology/metabolism ; NF-kappa B/metabolism ; Protein Synthesis Inhibitors/pharmacology ; Reactive Oxygen Species/metabolism ; Receptors, Cell Surface/immunology/*metabolism ; Signal Transduction ; Tetradecanoylphorbol Acetate/pharmacology ; Toll-Like Receptor 2 ; Toll-Like Receptors ; Transfection ; Tumor Cells, Cultured
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Anti-inflammatory properties of cytochrome P450 epoxygenase-derived eicosanoids (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-08-24
    Description: The epoxyeicosatrienoic acids (EETs) are products of cytochrome P450 epoxygenases that have vasodilatory properties similar to that of endothelium-derived hyperpolarizing factor. The cytochrome P450 isoform CYP2J2 was cloned and identified as a potential source of EETs in human endothelial cells. Physiological concentrations of EETs or overexpression of CYP2J2 decreased cytokine-induced endothelial cell adhesion molecule expression, and EETs prevented leukocyte adhesion to the vascular wall by a mechanism involving inhibition of transcription factor NF-kappaB and IkappaB kinase. The inhibitory effects of EETs were independent of their membrane-hyperpolarizing effects, suggesting that these molecules play an important nonvasodilatory role in vascular inflammation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2720027/" 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/PMC2720027/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Node, K -- Huo, Y -- Ruan, X -- Yang, B -- Spiecker, M -- Ley, K -- Zeldin, D C -- Liao, J K -- HL-52233/HL/NHLBI NIH HHS/ -- HL-58108/HL/NHLBI NIH HHS/ -- P01 HL048743/HL/NHLBI NIH HHS/ -- P01 HL048743-080008/HL/NHLBI NIH HHS/ -- P01 HL048743-090008/HL/NHLBI NIH HHS/ -- R01 HL052233/HL/NHLBI NIH HHS/ -- R01 HL052233-05/HL/NHLBI NIH HHS/ -- R01 HL052233-06/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1999 Aug 20;285(5431):1276-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Vascular Medicine and Atherosclerosis Unit, Cardiovascular Division, Brigham and Women's Hospital and Harvard Medical School, 221 Longwood Avenue, LMRC-322, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10455056" target="_blank"〉PubMed〈/a〉
    Keywords: 8,11,14-Eicosatrienoic Acid/analogs & derivatives/*metabolism/*pharmacology ; Animals ; *Anti-Inflammatory Agents, Non-Steroidal/metabolism/pharmacology ; Carotid Arteries/cytology ; Cattle ; Cell Adhesion/drug effects ; Cell Adhesion Molecules/biosynthesis ; Cells, Cultured ; Coronary Vessels/enzymology ; Cytochrome P-450 Enzyme System/genetics/*metabolism ; DNA-Binding Proteins/metabolism ; Endothelium, Vascular/enzymology/*metabolism ; Humans ; Hydroxyeicosatetraenoic Acids/pharmacology ; I-kappa B Kinase ; *I-kappa B Proteins ; Mice ; Mice, Inbred C57BL ; NF-kappa B/antagonists & inhibitors/metabolism ; Oxygenases/genetics/*metabolism ; Protein-Serine-Threonine Kinases/antagonists & inhibitors/metabolism ; Tumor Necrosis Factor-alpha/antagonists & inhibitors/pharmacology ; Vascular Cell Adhesion Molecule-1/biosynthesis/genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    Host defense mechanisms triggered by microbial lipoproteins through toll-like receptors (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-31
    Description: The generation of cell-mediated immunity against many infectious pathogens involves the production of interleukin-12 (IL-12), a key signal of the innate immune system. Yet, for many pathogens, the molecules that induce IL-12 production by macrophages and the mechanisms by which they do so remain undefined. Here it is shown that microbial lipoproteins are potent stimulators of IL-12 production by human macrophages, and that induction is mediated by Toll-like receptors (TLRs). Several lipoproteins stimulated TLR-dependent transcription of inducible nitric oxide synthase and the production of nitric oxide, a powerful microbicidal pathway. Activation of TLRs by microbial lipoproteins may initiate innate defense mechanisms against infectious pathogens.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brightbill, H D -- Libraty, D H -- Krutzik, S R -- Yang, R B -- Belisle, J T -- Bleharski, J R -- Maitland, M -- Norgard, M V -- Plevy, S E -- Smale, S T -- Brennan, P J -- Bloom, B R -- Godowski, P J -- Modlin, R L -- New York, N.Y. -- Science. 1999 Jul 30;285(5428):732-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, Howard Hughes Medical Institute, University of California Los Angeles School of Medicine, Los Anges, CA 90095, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10426995" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Bacterial/chemistry/*immunology/metabolism ; Cell Line ; *Drosophila Proteins ; Gene Expression Regulation ; Humans ; Interleukin-12/*biosynthesis/genetics ; Lipopolysaccharides/immunology ; Lipoproteins/chemistry/*immunology/metabolism ; Macrophages/*immunology/metabolism ; Membrane Glycoproteins/*metabolism ; Mice ; Monocytes/*immunology/metabolism ; Mycobacterium tuberculosis/*immunology ; NF-kappa B/biosynthesis ; Nitric Oxide Synthase/genetics ; Nitric Oxide Synthase Type II ; Promoter Regions, Genetic ; Receptors, Cell Surface/*metabolism ; Signal Transduction ; Toll-Like Receptors ; Transcription, Genetic ; Transfection ; Tumor Cells, Cultured
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    Requirement for the leukocyte-specific adapter protein SLP-76 for normal T cell development (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-07-17
    Description: The leukocyte-specific adapter molecule SLP-76 (Src homology 2 domain-containing leukocyte protein of 76 kilodaltons) is rapidly phosphorylated on tyrosine residues after receptor ligation in several hematopoietically derived cell types. Mice made deficient for SLP-76 expression contained no peripheral T cells as a result of an early block in thymopoiesis. Macrophage and natural killer cell compartments were intact in SLP-76-deficient mice, despite SLP-76 expression in these lineages in wild-type mice. Thus, the SLP-76 adapter protein is required for normal thymocyte development and plays a crucial role in translating signals mediated by pre-T cell receptors into distal biochemical events.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Clements, J L -- Yang, B -- Ross-Barta, S E -- Eliason, S L -- Hrstka, R F -- Williamson, R A -- Koretzky, G A -- GM53256/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1998 Jul 17;281(5375):416-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Internal Medicine, University of Iowa College of Medicine, Iowa City, IA 52242, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9665885" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; Animals ; B-Lymphocytes/cytology/immunology ; Gene Targeting ; Immunoglobulin M/blood ; Killer Cells, Natural/cytology ; *Leukopoiesis ; Lymph Nodes/cytology ; Lymphocyte Activation ; Lymphocyte Count ; Macrophages/cytology ; Mice ; Mice, Inbred C57BL ; Phosphoproteins/genetics/*physiology ; Protein-Tyrosine Kinases/metabolism ; Receptors, Antigen, T-Cell/metabolism ; Signal Transduction ; Spleen/cytology ; T-Lymphocytes/*cytology ; Thymus Gland/cytology ; ZAP-70 Protein-Tyrosine Kinase
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 5
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    El Nino and infectious disease (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-02-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yang, X B -- Scherm, H -- New York, N.Y. -- Science. 1997 Feb 7;275(5301):739.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9036530" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cholera/*epidemiology ; *Climate ; *Disease Outbreaks ; Humans ; *Plant Diseases
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 6
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    Aquaporins and ion conductance (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-03-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Verkman, A S -- Yang, B -- New York, N.Y. -- Science. 1997 Mar 7;275(5305):1491; author reply 1492.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9072811" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aquaporin 1 ; *Aquaporins ; Blood Group Antigens ; *Cell Membrane Permeability/drug effects ; Colforsin/pharmacology ; Cyclic AMP/agonists/metabolism ; Cyclic AMP-Dependent Protein Kinases/metabolism ; Erythrocyte Membrane/metabolism ; Humans ; Ion Channels/genetics/*physiology ; Oocytes ; Patch-Clamp Techniques ; RNA, Complementary ; Water/*metabolism ; Xenopus
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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