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  • 1
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    Bile acids: natural ligands for an orphan nuclear receptor (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-05-21
    Description: Bile acids regulate the transcription of genes that control cholesterol homeostasis through molecular mechanisms that are poorly understood. Physiological concentrations of free and conjugated chenodeoxycholic acid, lithocholic acid, and deoxycholic acid activated the farnesoid X receptor (FXR; NR1H4), an orphan nuclear receptor. As ligands, these bile acids and their conjugates modulated interaction of FXR with a peptide derived from steroid receptor coactivator 1. These results provide evidence for a nuclear bile acid signaling pathway that may regulate cholesterol homeostasis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Parks, D J -- Blanchard, S G -- Bledsoe, R K -- Chandra, G -- Consler, T G -- Kliewer, S A -- Stimmel, J B -- Willson, T M -- Zavacki, A M -- Moore, D D -- Lehmann, J M -- F32 DK09793/DK/NIDDK NIH HHS/ -- R01 DK53366/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1999 May 21;284(5418):1365-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biochemistry, Glaxo Wellcome Research and Development, Research Triangle Park NC, 27709, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10334993" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bile Acids and Salts/chemistry/*metabolism/pharmacology ; Carrier Proteins/metabolism ; Cell Line ; Chenodeoxycholic Acid/*metabolism/pharmacology ; Cholesterol/metabolism ; DNA-Binding Proteins/chemistry/genetics/*metabolism ; Deoxycholic Acid/metabolism/pharmacology ; Histone Acetyltransferases ; Homeostasis ; Humans ; Ligands ; Lithocholic Acid/metabolism/pharmacology ; Mice ; Nuclear Receptor Coactivator 1 ; *Organic Anion Transporters, Sodium-Dependent ; Protein Conformation ; Receptors, Cytoplasmic and Nuclear/chemistry/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Structure-Activity Relationship ; *Symporters ; Transcription Factors/chemistry/genetics/*metabolism ; Transfection
    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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    Signal transduction through prion protein (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-09-16
    Description: The cellular prion protein PrPc is a glycosylphosphatidylinositol-anchored cell-surface protein whose biological function is unclear. We used the murine 1C11 neuronal differentiation model to search for PrPc-dependent signal transduction through antibody-mediated cross-linking. A caveolin-1-dependent coupling of PrPc to the tyrosine kinase Fyn was observed. Clathrin might also contribute to this coupling. The ability of the 1C11 cell line to trigger PrPc-dependent Fyn activation was restricted to its fully differentiated serotonergic or noradrenergic progenies. Moreover, the signaling activity of PrPc occurred mainly at neurites. Thus, PrPc may be a signal transduction protein.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mouillet-Richard, S -- Ermonval, M -- Chebassier, C -- Laplanche, J L -- Lehmann, S -- Launay, J M -- Kellermann, O -- New York, N.Y. -- Science. 2000 Sep 15;289(5486):1925-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Differenciation Cellulaire, CNRS-Institut Pasteur, 75724 Paris Cedex 15, France. srichard@pasteur.fr〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10988071" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caveolin 1 ; *Caveolins ; Cell Compartmentation ; Cell Differentiation ; Enzyme Activation ; Membrane Proteins/metabolism ; Mice ; Neurons/cytology/metabolism ; PrPC Proteins/*metabolism ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins c-fyn ; *Signal Transduction
    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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    Identification of LFA-1 as a candidate autoantigen in treatment-resistant Lyme arthritis (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-07-31
    Description: Treatment-resistant Lyme arthritis is associated with immune reactivity to outer surface protein A (OspA) of Borrelia burgdorferi, the agent of Lyme disease, and the major histocompatibility complex class II allele DRB1*0401. The immunodominant epitope of OspA for T helper cells was identified. A homology search revealed a peptide from human leukocyte function-associated antigen-1 (hLFA-1) as a candidate autoantigen. Individuals with treatment-resistant Lyme arthritis, but not other forms of arthritis, generated responses to OspA, hLFA-1, and their highly related peptide epitopes. Identification of the initiating bacterial antigen and a cross-reactive autoantigen may provide a model for development of autoimmune disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gross, D M -- Forsthuber, T -- Tary-Lehmann, M -- Etling, C -- Ito, K -- Nagy, Z A -- Field, J A -- Steere, A C -- Huber, B T -- R01 AR20358/AR/NIAMS NIH HHS/ -- New York, N.Y. -- Science. 1998 Jul 31;281(5377):703-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Tufts University, Boston, MA 02111 USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9685265" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Algorithms ; Amino Acid Sequence ; Animals ; Antigen Presentation ; Antigens, Surface/immunology/metabolism ; Arthritis, Reactive/drug therapy/*immunology ; Autoantigens/*immunology ; Autoimmune Diseases/*immunology ; Bacterial Outer Membrane Proteins/immunology/metabolism ; Bacterial Vaccines ; Borrelia burgdorferi Group/immunology ; Child ; Cross Reactions ; Female ; HLA-DR Antigens/genetics/immunology/metabolism ; HLA-DRB1 Chains ; Humans ; Immunodominant Epitopes ; *Lipoproteins ; Lyme Disease/drug therapy/*immunology ; Lymphocyte Function-Associated Antigen-1/chemistry/*immunology/metabolism ; Male ; Mice ; Mice, Transgenic ; Molecular Sequence Data ; Synovial Fluid/immunology ; T-Lymphocytes, Helper-Inducer/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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  • 4
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    Modulation of gene expression via disruption of NF-kappaB signaling by a bacterial small molecule (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-06-21
    Description: The control of innate immune responses through activation of the nuclear transcription factor NF-kappaB is essential for the elimination of invading microbial pathogens. We showed that the bacterial N-(3-oxo-dodecanoyl) homoserine lactone (C12) selectively impairs the regulation of NF-kappaB functions in activated mammalian cells. The consequence is specific repression of stimulus-mediated induction of NF-kappaB-responsive genes encoding inflammatory cytokines and other immune regulators. These findings uncover a strategy by which C12-producing opportunistic pathogens, such as Pseudomonas aeruginosa, attenuate the innate immune system to establish and maintain local persistent infection in humans, for example, in cystic fibrosis patients.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kravchenko, Vladimir V -- Kaufmann, Gunnar F -- Mathison, John C -- Scott, David A -- Katz, Alexander Z -- Grauer, David C -- Lehmann, Mandy -- Meijler, Michael M -- Janda, Kim D -- Ulevitch, Richard J -- New York, N.Y. -- Science. 2008 Jul 11;321(5886):259-63. doi: 10.1126/science.1156499. Epub 2008 Jun 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology and Microbial Sciences, 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/18566250" target="_blank"〉PubMed〈/a〉
    Keywords: 4-Butyrolactone/*analogs & derivatives/physiology ; Adult ; Animals ; Cyclic AMP Response Element-Binding Protein/metabolism ; Cystic Fibrosis/microbiology ; Female ; *Gene Expression Regulation ; Homoserine/*analogs & derivatives/physiology ; Humans ; I-kappa B Kinase/metabolism ; I-kappa B Proteins/metabolism ; Immunity, Innate ; Interferon-gamma/immunology ; Lipopolysaccharides/immunology ; Macrophage Activation ; Macrophages/*immunology/*metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Middle Aged ; NF-kappa B/*metabolism ; Phosphorylation ; Pseudomonas Infections/immunology/microbiology ; Pseudomonas aeruginosa/immunology/*pathogenicity/physiology ; *Signal Transduction ; Toll-Like Receptors/metabolism ; Transcription Factor RelA/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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  • 5
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    An endogenous tumour-promoting ligand of the human aryl hydrocarbon receptor (2011)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2011-10-07
    Description: Activation of the aryl hydrocarbon receptor (AHR) by environmental xenobiotic toxic chemicals, for instance 2,3,7,8-tetrachlorodibenzo-p-dioxin (dioxin), has been implicated in a variety of cellular processes such as embryogenesis, transformation, tumorigenesis and inflammation. But the identity of an endogenous ligand activating the AHR under physiological conditions in the absence of environmental toxic chemicals is still unknown. Here we identify the tryptophan (Trp) catabolite kynurenine (Kyn) as an endogenous ligand of the human AHR that is constitutively generated by human tumour cells via tryptophan-2,3-dioxygenase (TDO), a liver- and neuron-derived Trp-degrading enzyme not yet implicated in cancer biology. TDO-derived Kyn suppresses antitumour immune responses and promotes tumour-cell survival and motility through the AHR in an autocrine/paracrine fashion. The TDO-AHR pathway is active in human brain tumours and is associated with malignant progression and poor survival. Because Kyn is produced during cancer progression and inflammation in the local microenvironment in amounts sufficient for activating the human AHR, these results provide evidence for a previously unidentified pathophysiological function of the AHR with profound implications for cancer and immune biology.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Opitz, Christiane A -- Litzenburger, Ulrike M -- Sahm, Felix -- Ott, Martina -- Tritschler, Isabel -- Trump, Saskia -- Schumacher, Theresa -- Jestaedt, Leonie -- Schrenk, Dieter -- Weller, Michael -- Jugold, Manfred -- Guillemin, Gilles J -- Miller, Christine L -- Lutz, Christian -- Radlwimmer, Bernhard -- Lehmann, Irina -- von Deimling, Andreas -- Wick, Wolfgang -- Platten, Michael -- England -- Nature. 2011 Oct 5;478(7368):197-203. doi: 10.1038/nature10491.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurooncology, Neurology Clinic and National Center for Tumor Diseases, University Hospital of Heidelberg, 69120 Heidelberg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21976023" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autocrine Communication ; Brain Neoplasms/genetics/immunology/*metabolism/*pathology ; Cell Line, Tumor ; Cell Survival ; Disease Progression ; Gene Expression Regulation, Neoplastic ; Glioma/genetics/immunology/*metabolism/*pathology ; Humans ; Kynurenine/immunology/*metabolism/pharmacology/secretion ; Ligands ; Mice ; Mice, Inbred C57BL ; Mice, Nude ; Neoplasm Transplantation ; Paracrine Communication ; Receptors, Aryl Hydrocarbon/immunology/*metabolism ; Tryptophan/metabolism ; Tryptophan Oxygenase/deficiency/genetics/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 6
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    Differential targeting of Gbetagamma-subunit signaling with small molecules (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-04-22
    Description: G protein betagamma subunits have potential as a target for therapeutic treatment of a number of diseases. We performed virtual docking of a small-molecule library to a site on Gbetagamma subunits that mediates protein interactions. We hypothesized that differential targeting of this surface could allow for selective modulation of Gbetagamma subunit functions. Several compounds bound to Gbetagamma subunits with affinities from 0.1 to 60 muM and selectively modulated functional Gbetagamma-protein-protein interactions in vitro, chemotactic peptide signaling pathways in HL-60 leukocytes, and opioid receptor-dependent analgesia in vivo. These data demonstrate an approach for modulation of G protein-coupled receptor signaling that may represent an important therapeutic strategy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bonacci, Tabetha M -- Mathews, Jennifer L -- Yuan, Chujun -- Lehmann, David M -- Malik, Sundeep -- Wu, Dianqing -- Font, Jose L -- Bidlack, Jean M -- Smrcka, Alan V -- GM60286/GM/NIGMS NIH HHS/ -- HL-T3207949/HL/NHLBI NIH HHS/ -- HL080706/HL/NHLBI NIH HHS/ -- K05-DA00360/DA/NIDA NIH HHS/ -- R01 CA132317/CA/NCI NIH HHS/ -- R01 GM054597/GM/NIGMS NIH HHS/ -- R01 GM054597-09/GM/NIGMS NIH HHS/ -- R01 HL080706/HL/NHLBI NIH HHS/ -- R01 HL080706-10/HL/NHLBI NIH HHS/ -- R01 HL080706-11/HL/NHLBI NIH HHS/ -- T32DA07232/DA/NIDA NIH HHS/ -- New York, N.Y. -- Science. 2006 Apr 21;312(5772):443-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology and Physiology, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16627746" target="_blank"〉PubMed〈/a〉
    Keywords: Analgesics/pharmacology ; Animals ; Binding Sites ; Binding, Competitive ; Cell Line ; Computer Simulation ; Cyclohexanes/chemistry/*metabolism/*pharmacology ; Drug Evaluation, Preclinical/*methods ; Enzyme-Linked Immunosorbent Assay ; G-Protein-Coupled Receptor Kinase 2 ; GTP-Binding Protein alpha Subunits/metabolism ; GTP-Binding Protein beta Subunits/chemistry/*metabolism ; GTP-Binding Protein gamma Subunits/chemistry/*metabolism ; HL-60 Cells ; Humans ; Isoenzymes/metabolism ; Mice ; Mice, Inbred ICR ; Mitogen-Activated Protein Kinases/metabolism ; Molecular Structure ; Morphine/pharmacology ; N-Formylmethionine Leucyl-Phenylalanine/metabolism ; Peptide Library ; Peptides/*metabolism ; Phosphatidylinositol 3-Kinases/metabolism ; Phospholipase C beta ; Protein Binding ; Protein Interaction Mapping ; *Signal Transduction ; Software ; Structure-Activity Relationship ; Type C Phospholipases/metabolism ; Xanthenes/chemistry/*metabolism/*pharmacology ; beta-Adrenergic Receptor Kinases/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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  • 7
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    Induction of TH1 and TH2 immunity in neonatal mice (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-03-22
    Description: The neonatal period has been thought of as a window in ontogeny, during which the developing immune system is particularly susceptible to tolerization. In the present study, the classic system for induction of neonatal tolerance to protein antigens was reexamined in mice. The presumably tolerogenic protocol was found to trigger a vigorous T helper cell type 2 (TH2) immune response. Thus, neonatal "tolerization" induces immune deviation, not tolerance in the immunological sense. Neonates are not immune privileged but generate TH2 or TH1 responses, depending on the mode of immunization.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Forsthuber, T -- Yip, H C -- Lehmann, P V -- AI36219-02/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1996 Mar 22;271(5256):1728-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Case Western Reserve University, Cleveland, OH 44106-4943, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8596934" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn/*immunology ; Antibody Formation ; Freund's Adjuvant ; *Immune Tolerance ; Immunization ; Immunoglobulin G/biosynthesis ; Immunologic Memory ; Lymph Nodes/immunology ; Mice ; Mice, Inbred BALB C ; Muramidase/immunology ; Spleen/immunology ; Th1 Cells/*immunology ; Th2 Cells/*immunology
    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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