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  • 1
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-11-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ganz, T -- New York, N.Y. -- Science. 1999 Oct 15;286(5439):420-1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, UCLA School of Medicine, Los Angeles, CA 90095, USA. tganz@mednet.ucla.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10577203" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anti-Infective Agents/*chemistry/pharmacology ; Cell Membrane/metabolism ; Chemotaxis ; Defensins ; Dendritic Cells/immunology ; Epithelial Cells/metabolism ; Evolution, Molecular ; Humans ; *Immunity, Innate ; Immunologic Memory ; Matrix Metalloproteinase 7/deficiency/genetics ; Paneth Cells/metabolism ; Proteins/*chemistry/genetics/pharmacology/*physiology ; 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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  • 2
    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
    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
    Publication Date: 2004-10-30
    Description: Hepcidin is a peptide hormone secreted by the liver in response to iron loading and inflammation. Decreased hepcidin leads to tissue iron overload, whereas hepcidin overproduction leads to hypoferremia and the anemia of inflammation. Ferroportin is an iron exporter present on the surface of absorptive enterocytes, macrophages, hepatocytes, and placental cells. Here we report that hepcidin bound to ferroportin in tissue culture cells. After binding, ferroportin was internalized and degraded, leading to decreased export of cellular iron. The posttranslational regulation of ferroportin by hepcidin may thus complete a homeostatic loop: Iron regulates the secretion of hepcidin, which in turn controls the concentration of ferroportin on the cell surface.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nemeth, Elizabeta -- Tuttle, Marie S -- Powelson, Julie -- Vaughn, Michael B -- Donovan, Adriana -- Ward, Diane McVey -- Ganz, Tomas -- Kaplan, Jerry -- DK065029/DK/NIDDK NIH HHS/ -- DK30534/DK/NIDDK NIH HHS/ -- HL26922/HL/NHLBI NIH HHS/ -- T35HL007744/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2004 Dec 17;306(5704):2090-3. Epub 2004 Oct 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15514116" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antimicrobial Cationic Peptides/chemical ; synthesis/genetics/*metabolism/pharmacology ; Biological Transport ; Cation Transport Proteins/*metabolism ; Cell Line ; Cell Membrane/metabolism ; Cytosol/metabolism ; Ferritins/metabolism ; HeLa Cells ; Hepcidins ; Homeostasis ; Humans ; Iron/*metabolism ; Iron Regulatory Protein 2/metabolism ; Lysosomes/metabolism ; Mice ; Protein Binding ; RNA, Messenger/genetics/metabolism ; Receptor, Epidermal Growth Factor/metabolism ; Recombinant Fusion Proteins/metabolism ; Transfection ; Transferrin/metabolism
    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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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 2002-11-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ganz, Tomas -- New York, N.Y. -- Science. 2002 Nov 1;298(5595):977-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of California, Los Angeles, CA 90095, USA. tganz@mednet.ucla.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12411693" target="_blank"〉PubMed〈/a〉
    Keywords: Adjuvants, Immunologic ; Animals ; Antigens, Neoplasm/immunology ; Antiviral Agents/physiology ; CD8-Positive T-Lymphocytes/*immunology ; Dendritic Cells/immunology/metabolism ; *Drosophila Proteins ; HIV/*physiology ; HIV Infections/*immunology/virology ; HIV Long-Term Survivors ; Humans ; Immunity, Cellular ; Ligands ; Lymphocyte Activation ; Membrane Glycoproteins/metabolism ; Membrane Microdomains/metabolism ; Mice ; Neoplasms/*immunology ; Receptors, CCR6 ; Receptors, Cell Surface/metabolism ; Receptors, Chemokine/metabolism ; Toll-Like Receptors ; Virus Replication ; alpha-Defensins/*physiology ; beta-Defensins/*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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  • 5
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Genomics 5 (1989), S. 240-244 
    ISSN: 0888-7543
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Medicine
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Palo Alto, Calif. : Annual Reviews
    Annual Review of Physiology 54 (1992), S. 331-350 
    ISSN: 0066-4278
    Source: Annual Reviews Electronic Back Volume Collection 1932-2001ff
    Topics: Medicine , Biology
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Palo Alto, Calif. : Annual Reviews
    Annual Review of Immunology 11 (1993), S. 105-128 
    ISSN: 0732-0582
    Source: Annual Reviews Electronic Back Volume Collection 1932-2001ff
    Topics: Biology , Medicine
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    FEBS Letters 356 (1994), S. 169-173 
    ISSN: 0014-5793
    Keywords: C1 complement ; C1 inhibitor ; Defensin ; Inflammation
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
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  • 9
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    FEBS Letters 326 (1993), S. 299 
    ISSN: 0014-5793
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    FEBS Letters 321 (1993), S. 267-273 
    ISSN: 0014-5793
    Keywords: Defensin ; Gene structure ; Neutrophil
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
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