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  • 1
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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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  • 2
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    Visualizing antigen-specific and infected cells in situ predicts outcomes in early viral infection (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-03-28
    Description: In the early stages of viral infection, outcomes depend on a race between expansion of infection and the immune response generated to contain it. We combined in situ tetramer staining with in situ hybridization to visualize, map, and quantify relationships between immune effector cells and their targets in tissues. In simian immunodeficiency virus infections in macaques and lymphocytic choriomeningitis virus infections in mice, the magnitude and timing of the establishment of an excess of effector cells versus targets were found to correlate with the extent of control and the infection outcome (i.e., control and clearance versus partial or poor control and persistent infection). This method highlights the importance of the location, timing, and magnitude of the immune response needed for a vaccine to be effective against agents of persistent infection, such as HIV-1.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2753492/" 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/PMC2753492/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Qingsheng -- Skinner, Pamela J -- Ha, Sang-Jun -- Duan, Lijie -- Mattila, Teresa L -- Hage, Aaron -- White, Cara -- Barber, Daniel L -- O'Mara, Leigh -- Southern, Peter J -- Reilly, Cavan S -- Carlis, John V -- Miller, Christopher J -- Ahmed, Rafi -- Haase, Ashley T -- AI066314/AI/NIAID NIH HHS/ -- AI20048/AI/NIAID NIH HHS/ -- AI48484/AI/NIAID NIH HHS/ -- P01 AI066314/AI/NIAID NIH HHS/ -- P01 AI066314-010003/AI/NIAID NIH HHS/ -- P01 AI066314-020003/AI/NIAID NIH HHS/ -- P01 AI066314-030003/AI/NIAID NIH HHS/ -- P01 AI066314-040003/AI/NIAID NIH HHS/ -- P51 RR000169/RR/NCRR NIH HHS/ -- P51 RR000169-430198/RR/NCRR NIH HHS/ -- R01 AI048484/AI/NIAID NIH HHS/ -- R01 AI048484-01/AI/NIAID NIH HHS/ -- R01 AI048484-02/AI/NIAID NIH HHS/ -- R01 AI048484-03/AI/NIAID NIH HHS/ -- R01 AI048484-04/AI/NIAID NIH HHS/ -- RR00169/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2009 Mar 27;323(5922):1726-9. doi: 10.1126/science.1168676.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, Medical School, University of Minnesota, Minneapolis, MN 55455, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19325114" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arenaviridae Infections/*immunology/virology ; Cell Count ; Cervix Uteri/immunology/virology ; Female ; In Situ Hybridization ; Lymph Nodes/immunology/virology ; Lymphocytic choriomeningitis virus/*immunology ; Lymphoid Tissue/immunology/virology ; Macaca mulatta ; Mice ; RNA, Viral/analysis ; Simian Acquired Immunodeficiency Syndrome/*immunology/virology ; Simian Immunodeficiency Virus/*immunology/physiology ; Spleen/immunology/virology ; Staining and Labeling ; T-Lymphocytes, Cytotoxic/*immunology ; Time Factors ; Vagina/immunology/virology ; 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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  • 3
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    A Burkholderia pseudomallei toxin inhibits helicase activity of translation factor eIF4A (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-11-15
    Description: The structure of BPSL1549, a protein of unknown function from Burkholderia pseudomallei, reveals a similarity to Escherichia coli cytotoxic necrotizing factor 1. We found that BPSL1549 acted as a potent cytotoxin against eukaryotic cells and was lethal when administered to mice. Expression levels of bpsl1549 correlate with conditions expected to promote or suppress pathogenicity. BPSL1549 promotes deamidation of glutamine-339 of the translation initiation factor eIF4A, abolishing its helicase activity and inhibiting translation. We propose to name BPSL1549 Burkholderia lethal factor 1.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3364511/" 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/PMC3364511/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cruz-Migoni, Abimael -- Hautbergue, Guillaume M -- Artymiuk, Peter J -- Baker, Patrick J -- Bokori-Brown, Monika -- Chang, Chung-Te -- Dickman, Mark J -- Essex-Lopresti, Angela -- Harding, Sarah V -- Mahadi, Nor Muhammad -- Marshall, Laura E -- Mobbs, George W -- Mohamed, Rahmah -- Nathan, Sheila -- Ngugi, Sarah A -- Ong, Catherine -- Ooi, Wen Fong -- Partridge, Lynda J -- Phillips, Helen L -- Raih, M Firdaus -- Ruzheinikov, Sergei -- Sarkar-Tyson, Mitali -- Sedelnikova, Svetlana E -- Smither, Sophie J -- Tan, Patrick -- Titball, Richard W -- Wilson, Stuart A -- Rice, David W -- 085162/Wellcome Trust/United Kingdom -- BB/D011795/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/D524975/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/E025293/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- WT085162AIA/Wellcome Trust/United Kingdom -- Biotechnology and Biological Sciences Research Council/United Kingdom -- New York, N.Y. -- Science. 2011 Nov 11;334(6057):821-4. doi: 10.1126/science.1211915.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology and Biotechnology, Krebs Institute, University of Sheffield, Sheffield S10 2TN, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22076380" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Animals ; Bacterial Proteins/*chemistry/genetics/metabolism/*toxicity ; Bacterial Toxins/*chemistry/genetics/metabolism/*toxicity ; Burkholderia pseudomallei/*chemistry/*pathogenicity ; Catalytic Domain ; Cell Line ; Crystallography, X-Ray ; Cytotoxins/chemistry/genetics/metabolism/toxicity ; Escherichia coli Proteins/chemistry ; Eukaryotic Initiation Factor-4A/*antagonists & inhibitors/metabolism ; Glutamine/metabolism ; Humans ; Mice ; Mice, Inbred BALB C ; Models, Molecular ; Mutant Proteins/toxicity ; Peptide Chain Initiation, Translational/drug effects ; Protein Binding ; Protein Conformation ; Protein Structure, Secondary ; Protein Structure, Tertiary
    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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    Genomic instability in mice lacking histone H2AX (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-04-06
    Description: Higher order chromatin structure presents a barrier to the recognition and repair of DNA damage. Double-strand breaks (DSBs) induce histone H2AX phosphorylation, which is associated with the recruitment of repair factors to damaged DNA. To help clarify the physiological role of H2AX, we targeted H2AX in mice. Although H2AX is not essential for irradiation-induced cell-cycle checkpoints, H2AX-/- mice were radiation sensitive, growth retarded, and immune deficient, and mutant males were infertile. These pleiotropic phenotypes were associated with chromosomal instability, repair defects, and impaired recruitment of Nbs1, 53bp1, and Brca1, but not Rad51, to irradiation-induced foci. Thus, H2AX is critical for facilitating the assembly of specific DNA-repair complexes on damaged DNA.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4721576/" 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/PMC4721576/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Celeste, Arkady -- Petersen, Simone -- Romanienko, Peter J -- Fernandez-Capetillo, Oscar -- Chen, Hua Tang -- Sedelnikova, Olga A -- Reina-San-Martin, Bernardo -- Coppola, Vincenzo -- Meffre, Eric -- Difilippantonio, Michael J -- Redon, Christophe -- Pilch, Duane R -- Olaru, Alexandru -- Eckhaus, Michael -- Camerini-Otero, R Daniel -- Tessarollo, Lino -- Livak, Ferenc -- Manova, Katia -- Bonner, William M -- Nussenzweig, Michel C -- Nussenzweig, Andre -- Z99 CA999999/Intramural NIH HHS/ -- New York, N.Y. -- Science. 2002 May 3;296(5569):922-7. Epub 2002 Apr 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Experimental Immunology Branch, National Cancer Institute, NIH, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11934988" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; B-Lymphocytes/immunology/physiology ; Base Sequence ; Cell Aging ; Cell Cycle ; Cells, Cultured ; *Chromosome Aberrations ; DNA Damage ; *DNA Repair ; Female ; Gene Targeting ; Histones/chemistry/*genetics/*physiology ; Immunoglobulin Class Switching ; Infertility, Male/genetics/physiopathology ; Lymphocyte Count ; Male ; Meiosis ; Mice ; Mice, Knockout ; Molecular Sequence Data ; Mutation ; Phosphorylation ; *Recombination, Genetic ; Spermatocytes/physiology ; T-Lymphocytes/immunology/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
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  • 5
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    Mutations in dynein link motor neuron degeneration to defects in retrograde transport (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-05-06
    Description: Degenerative disorders of motor neurons include a range of progressive fatal diseases such as amyotrophic lateral sclerosis (ALS), spinal-bulbar muscular atrophy (SBMA), and spinal muscular atrophy (SMA). Although the causative genetic alterations are known for some cases, the molecular basis of many SMA and SBMA-like syndromes and most ALS cases is unknown. Here we show that missense point mutations in the cytoplasmic dynein heavy chain result in progressive motor neuron degeneration in heterozygous mice, and in homozygotes this is accompanied by the formation of Lewy-like inclusion bodies, thus resembling key features of human pathology. These mutations exclusively perturb neuron-specific functions of dynein.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hafezparast, Majid -- Klocke, Rainer -- Ruhrberg, Christiana -- Marquardt, Andreas -- Ahmad-Annuar, Azlina -- Bowen, Samantha -- Lalli, Giovanna -- Witherden, Abi S -- Hummerich, Holger -- Nicholson, Sharon -- Morgan, P Jeffrey -- Oozageer, Ravi -- Priestley, John V -- Averill, Sharon -- King, Von R -- Ball, Simon -- Peters, Jo -- Toda, Takashi -- Yamamoto, Ayumu -- Hiraoka, Yasushi -- Augustin, Martin -- Korthaus, Dirk -- Wattler, Sigrid -- Wabnitz, Philipp -- Dickneite, Carmen -- Lampel, Stefan -- Boehme, Florian -- Peraus, Gisela -- Popp, Andreas -- Rudelius, Martina -- Schlegel, Juergen -- Fuchs, Helmut -- Hrabe de Angelis, Martin -- Schiavo, Giampietro -- Shima, David T -- Russ, Andreas P -- Stumm, Gabriele -- Martin, Joanne E -- Fisher, Elizabeth M C -- New York, N.Y. -- Science. 2003 May 2;300(5620):808-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurodegenerative Disease, Institute of Neurology, National Hospital for Neurology and Neurosurgery, Queen Square, London WC1N 3BG, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12730604" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anterior Horn Cells/pathology ; Apoptosis ; *Axonal Transport ; Cell Differentiation ; Cell Movement ; Central Nervous System/embryology ; Chromosome Mapping ; Dimerization ; Dyneins/chemistry/*genetics/*physiology ; Female ; Ganglia, Spinal/pathology ; Golgi Apparatus/metabolism/ultrastructure ; Heterozygote ; Homozygote ; Lewy Bodies/pathology ; Male ; Mice ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Motor Neuron Disease/*genetics/pathology/physiopathology ; Motor Neurons/*physiology/ultrastructure ; Mutation ; Mutation, Missense ; *Nerve Degeneration ; Peptide Fragments/metabolism ; Phenotype ; Point Mutation ; Spinal Nerves/growth & development ; Tetanus Toxin/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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  • 6
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    Imaging sites of receptor dephosphorylation by PTP1B on the surface of the endoplasmic reticulum (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-03-02
    Description: When bound by extracellular ligands, receptor tyrosine kinases (RTKs) on the cell surface transmit critical signals to the cell interior. Although signal termination is less well understood, protein tyrosine phosphatase-1B (PTP1B) is implicated in the dephosphorylation and inactivation of several RTKs. However, PTP1B resides on the cytoplasmic surface of the endoplasmic reticulum (ER), so how and when it accesses RTKs has been unclear. Using fluorescence resonance energy transfer (FRET) methods, we monitored interactions between the epidermal- and platelet-derived growth factor receptors and PTP1B. PTP1B-catalyzed dephosphorylation required endocytosis of the receptors and occurred at specific sites on the surface of the ER. Most of the RTKs activated at the cell surface showed interaction with PTP1B after internalization, establishing that RTK activation and inactivation are spatially and temporally partitioned within cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Haj, Fawaz G -- Verveer, Peter J -- Squire, Anthony -- Neel, Benjamin G -- Bastiaens, Philippe I H -- R01 CA49152/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2002 Mar 1;295(5560):1708-11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Biology Program, Division of Hematology-Oncology, Department of Medicine, Beth Israel-Deaconess Medical Center, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11872838" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Substitution ; Animals ; Catalytic Domain ; Cell Membrane/enzymology ; Cells, Cultured ; *Endocytosis ; Endoplasmic Reticulum/*enzymology ; Energy Transfer ; Epidermal Growth Factor/metabolism/pharmacology ; Fluorescence ; Mice ; Microscopy, Confocal ; Microscopy, Fluorescence ; Phosphorylation ; Platelet-Derived Growth Factor/metabolism/pharmacology ; Protein Transport ; Protein Tyrosine Phosphatase, Non-Receptor Type 1 ; Protein Tyrosine Phosphatases/chemistry/genetics/*metabolism ; Receptor, Epidermal Growth Factor/*metabolism ; Receptors, Platelet-Derived Growth Factor/*metabolism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction
    Print ISSN: 0036-8075
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  • 7
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    Induction of direct antimicrobial activity through mammalian toll-like receptors (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-02-27
    Description: The mammalian innate immune system retains from Drosophila a family of homologous Toll-like receptors (TLRs) that mediate responses to microbial ligands. Here, we show that TLR2 activation leads to killing of intracellular Mycobacterium tuberculosis in both mouse and human macrophages, through distinct mechanisms. In mouse macrophages, bacterial lipoprotein activation of TLR2 leads to a nitric oxide-dependent killing of intracellular tubercle bacilli, but in human monocytes and alveolar macrophages, this pathway was nitric oxide-independent. Thus, mammalian TLRs respond (as Drosophila Toll receptors do) to microbial ligands and also have the ability to activate antimicrobial effector pathways at the site of infection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thoma-Uszynski, S -- Stenger, S -- Takeuchi, O -- Ochoa, M T -- Engele, M -- Sieling, P A -- Barnes, P F -- Rollinghoff, M -- Bolcskei, P L -- Wagner, M -- Akira, S -- Norgard, M V -- Belisle, J T -- Godowski, P J -- Bloom, B R -- Modlin, R L -- AI 07118/AI/NIAID NIH HHS/ -- AI 22553/AI/NIAID NIH HHS/ -- AI 47868/AI/NIAID NIH HHS/ -- AR 40312/AR/NIAMS NIH HHS/ -- New York, N.Y. -- Science. 2001 Feb 23;291(5508):1544-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Dermatology, Department of Microbiology and Immunology and Molecular Biology Institute, 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/11222859" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacterial Proteins/immunology ; Cell Line ; Cells, Cultured ; *Drosophila Proteins ; Humans ; Interferon-gamma/immunology/pharmacology ; Ligands ; Lipoproteins/*immunology ; Macrophage Activation ; Macrophages/immunology/metabolism/*microbiology ; Macrophages, Alveolar/immunology/metabolism/microbiology ; Macrophages, Peritoneal/immunology/metabolism/microbiology ; Membrane Glycoproteins/*metabolism ; Mice ; Monocytes/immunology/metabolism/*microbiology ; Mycobacterium tuberculosis/growth & development/*immunology ; Nitric Oxide/*metabolism ; Nitric Oxide Synthase/antagonists & inhibitors/metabolism ; Nitric Oxide Synthase Type II ; Receptors, Cell Surface/*metabolism ; Signal Transduction ; Toll-Like Receptor 2 ; Toll-Like Receptors ; Tumor Necrosis Factor-alpha/immunology/pharmacology
    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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  • 8
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    Microbiology. Subversion of Schwann cells and the leper's bell (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-05-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brophy, Peter J -- New York, N.Y. -- Science. 2002 May 3;296(5569):862-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Preclinical Veterinary Sciences, University of Edinburgh, Summerhall, Edinburgh EH9 1QH, UK. peter.brophy@ed.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11988561" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antigens, Bacterial ; Axons/physiology ; Cell Death ; Cell Differentiation ; Cell Membrane/metabolism ; Coculture Techniques ; Cytoskeletal Proteins/metabolism ; Demyelinating Diseases/*microbiology ; Dystroglycans ; Dystrophin/metabolism ; Glycolipids/metabolism ; Humans ; Laminin/metabolism ; Leprosy/*microbiology/pathology/*physiopathology ; Membrane Glycoproteins/metabolism ; Membrane Proteins/metabolism ; Mice ; *Muscle Proteins ; Mycobacterium leprae/growth & development/metabolism/*pathogenicity ; Myelin Sheath/*physiology ; Schwann Cells/cytology/*microbiology/*physiology ; Utrophin
    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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  • 9
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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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  • 10
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    Imaging protein kinase Calpha activation in cells (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-03-26
    Description: Spatially resolved fluorescence resonance energy transfer (FRET) measured by fluorescence lifetime imaging microscopy (FLIM), provides a method for tracing the catalytic activity of fluorescently tagged proteins inside live cell cultures and enables determination of the functional state of proteins in fixed cells and tissues. Here, a dynamic marker of protein kinase Calpha (PKCalpha) activation is identified and exploited. Activation of PKCalpha is detected through the binding of fluorescently tagged phosphorylation site-specific antibodies; the consequent FRET is measured through the donor fluorophore on PKCalpha by FLIM. This approach enabled the imaging of PKCalpha activation in live and fixed cultured cells and was also applied to pathological samples.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ng, T -- Squire, A -- Hansra, G -- Bornancin, F -- Prevostel, C -- Hanby, A -- Harris, W -- Barnes, D -- Schmidt, S -- Mellor, H -- Bastiaens, P I -- Parker, P J -- New York, N.Y. -- Science. 1999 Mar 26;283(5410):2085-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Protein Phosphorylation Laboratory and Cell Biophysics Laboratory, Imperial Cancer Research Fund (ICRF), 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/10092232" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Animals ; Breast Neoplasms/enzymology ; COS Cells ; Catalysis ; Cytoplasm/enzymology ; Endoplasmic Reticulum/enzymology ; Energy Transfer ; Enzyme Activation ; Fluorescence ; Fluorescent Dyes ; Golgi Apparatus/enzymology ; Green Fluorescent Proteins ; Humans ; Immune Sera ; Isoenzymes/immunology/*metabolism ; Luminescent Proteins ; Mice ; *Microscopy, Fluorescence ; Phosphorylation ; Phosphothreonine/immunology/metabolism ; Protein Kinase C/immunology/*metabolism ; Protein Kinase C-alpha ; Tetradecanoylphorbol Acetate/pharmacology ; 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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