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  • 1
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    Viral clearance without destruction of infected cells during acute HBV infection (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-30
    Description: Viral clearance during hepatitis B virus (HBV) infection has been thought to reflect the destruction of infected hepatocytes by CD8(+) T lymphocytes. However, in this study, HBV DNA was shown to largely disappear from the liver and the blood of acutely infected chimpanzees long before the peak of T cell infiltration and most of the liver disease. These results demonstrate that noncytopathic antiviral mechanisms contribute to viral clearance during acute viral hepatitis by purging HBV replicative intermediates from the cytoplasm and covalently closed circular viral DNA from the nucleus of infected cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Guidotti, L G -- Rochford, R -- Chung, J -- Shapiro, M -- Purcell, R -- Chisari, F V -- R01 AI20001/AI/NIAID NIH HHS/ -- R01 AI40696/AI/NIAID NIH HHS/ -- R37 CA40489/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1999 Apr 30;284(5415):825-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10221919" target="_blank"〉PubMed〈/a〉
    Keywords: Acute Disease ; Animals ; Cytotoxicity, Immunologic ; DNA, Circular/analysis ; DNA, Viral/analysis/blood ; Hepatitis B/*immunology/pathology/virology ; Hepatitis B Antibodies/blood ; Hepatitis B Core Antigens/analysis ; Hepatitis B virus/genetics/*immunology/isolation & purification/physiology ; Killer Cells, Natural/immunology ; Liver/immunology/pathology/*virology ; Mice ; Mice, Transgenic ; Pan troglodytes ; T-Lymphocytes/immunology ; Time Factors ; Virus Replication
    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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    The chromatin remodeller ACF acts as a dimeric motor to space nucleosomes (2009)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2009-12-25
    Description: Evenly spaced nucleosomes directly correlate with condensed chromatin and gene silencing. The ATP-dependent chromatin assembly factor (ACF) forms such structures in vitro and is required for silencing in vivo. ACF generates and maintains nucleosome spacing by constantly moving a nucleosome towards the longer flanking DNA faster than the shorter flanking DNA. How the enzyme rapidly moves back and forth between both sides of a nucleosome to accomplish bidirectional movement is unknown. Here we show that nucleosome movement depends cooperatively on two ACF molecules, indicating that ACF functions as a dimer of ATPases. Further, the nucleotide state determines whether the dimer closely engages one or both sides of the nucleosome. Three-dimensional reconstruction by single-particle electron microscopy of the ATPase-nucleosome complex in an activated ATP state reveals a dimer architecture in which the two ATPases face each other. Our results indicate a model in which the two ATPases work in a coordinated manner, taking turns to engage either side of a nucleosome, thereby allowing processive bidirectional movement. This novel dimeric motor mechanism differs from that of dimeric motors such as kinesin and dimeric helicases that processively translocate unidirectionally and reflects the unique challenges faced by motors that move nucleosomes.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2869534/" 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/PMC2869534/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Racki, Lisa R -- Yang, Janet G -- Naber, Nariman -- Partensky, Peretz D -- Acevedo, Ashley -- Purcell, Thomas J -- Cooke, Roger -- Cheng, Yifan -- Narlikar, Geeta J -- R01 GM073767/GM/NIGMS NIH HHS/ -- R01 GM073767-01/GM/NIGMS NIH HHS/ -- R01 GM073767-02/GM/NIGMS NIH HHS/ -- R01 GM073767-03/GM/NIGMS NIH HHS/ -- R01 GM073767-03S1/GM/NIGMS NIH HHS/ -- R01 GM073767-04/GM/NIGMS NIH HHS/ -- R01 GM073767-05/GM/NIGMS NIH HHS/ -- England -- Nature. 2009 Dec 24;462(7276):1016-21. doi: 10.1038/nature08621.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Biophysics, University of California, San Francisco, California 94158, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20033039" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphatases/metabolism ; Adenosine Triphosphate/metabolism ; Animals ; Cell Line ; Chromatin Assembly and Disassembly/*physiology ; Dimerization ; Gene Silencing/physiology ; Histones/metabolism ; Humans ; Microscopy, Electron, Transmission ; *Models, Molecular ; Multiprotein Complexes/*metabolism ; Nucleosomes/chemistry/*metabolism ; Protein Binding ; Protein Structure, Tertiary ; Transcription Factors/chemistry/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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  • 3
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    APJ acts as a dual receptor in cardiac hypertrophy (2012)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2012-07-20
    Description: Cardiac hypertrophy is initiated as an adaptive response to sustained overload but progresses pathologically as heart failure ensues. Here we report that genetic loss of APJ, a G-protein-coupled receptor, confers resistance to chronic pressure overload by markedly reducing myocardial hypertrophy and heart failure. In contrast, mice lacking apelin (the endogenous APJ ligand) remain sensitive, suggesting an apelin-independent function of APJ. Freshly isolated APJ-null cardiomyocytes exhibit an attenuated response to stretch, indicating that APJ is a mechanosensor. Activation of APJ by stretch increases cardiomyocyte cell size and induces molecular markers of hypertrophy. Whereas apelin stimulates APJ to activate Galphai and elicits a protective response, stretch signals in an APJ-dependent, G-protein-independent fashion to induce hypertrophy. Stretch-mediated hypertrophy is prevented by knockdown of beta-arrestins or by pharmacological doses of apelin acting through Galphai. Taken together, our data indicate that APJ is a bifunctional receptor for both mechanical stretch and the endogenous peptide apelin. By sensing the balance between these stimuli, APJ occupies a pivotal point linking sustained overload to cardiomyocyte hypertrophy.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3422434/" 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/PMC3422434/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Scimia, Maria Cecilia -- Hurtado, Cecilia -- Ray, Saugata -- Metzler, Scott -- Wei, Ke -- Wang, Jianming -- Woods, Chris E -- Purcell, Nicole H -- Catalucci, Daniele -- Akasaka, Takeshi -- Bueno, Orlando F -- Vlasuk, George P -- Kaliman, Perla -- Bodmer, Rolf -- Smith, Layton H -- Ashley, Euan -- Mercola, Mark -- Brown, Joan Heller -- Ruiz-Lozano, Pilar -- NS05422/NS/NINDS NIH HHS/ -- P01 HL085577/HL/NHLBI NIH HHS/ -- R01 HL054732/HL/NHLBI NIH HHS/ -- R01 HL086879/HL/NHLBI NIH HHS/ -- R01HL054732/HL/NHLBI NIH HHS/ -- R01HL083463/HL/NHLBI NIH HHS/ -- R01HL086879/HL/NHLBI NIH HHS/ -- R01HL28143/HL/NHLBI NIH HHS/ -- R37 HL028143/HL/NHLBI NIH HHS/ -- R37HL059502/HL/NHLBI NIH HHS/ -- England -- Nature. 2012 Aug 16;488(7411):394-8. doi: 10.1038/nature11263.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Sanford-Burnham Medical Research Institute, La Jolla, California 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22810587" target="_blank"〉PubMed〈/a〉
    Keywords: Adipokines ; Animals ; Aorta/pathology ; Arrestins/deficiency/genetics/metabolism ; Blood Pressure ; Cardiomegaly/*metabolism/pathology/physiopathology/prevention & control ; Female ; GTP-Binding Protein alpha Subunits, Gi-Go/metabolism ; Intercellular Signaling Peptides and ; Proteins/deficiency/genetics/metabolism/pharmacology ; Male ; Mechanoreceptors/metabolism ; Mechanotransduction, Cellular/drug effects/physiology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Myocytes, Cardiac/drug effects/pathology ; Receptors, G-Protein-Coupled/agonists/deficiency/genetics/*metabolism ; Signal Transduction/drug effects
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 4
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    Linear ubiquitination prevents inflammation and regulates immune signalling (2011)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2011-04-02
    Description: Members of the tumour necrosis factor (TNF) receptor superfamily have important functions in immunity and inflammation. Recently linear ubiquitin chains assembled by a complex containing HOIL-1 and HOIP (also known as RBCK1 and RNF31, respectively) were implicated in TNF signalling, yet their relevance in vivo remained uncertain. Here we identify SHARPIN as a third component of the linear ubiquitin chain assembly complex, recruited to the CD40 and TNF receptor signalling complexes together with its other constituents, HOIL-1 and HOIP. Mass spectrometry of TNF signalling complexes revealed RIP1 (also known as RIPK1) and NEMO (also known as IKKgamma or IKBKG) to be linearly ubiquitinated. Mutation of the Sharpin gene (Sharpin(cpdm/cpdm)) causes chronic proliferative dermatitis (cpdm) characterized by inflammatory skin lesions and defective lymphoid organogenesis. Gene induction by TNF, CD40 ligand and interleukin-1beta was attenuated in cpdm-derived cells which were rendered sensitive to TNF-induced death. Importantly, Tnf gene deficiency prevented skin lesions in cpdm mice. We conclude that by enabling linear ubiquitination in the TNF receptor signalling complex, SHARPIN interferes with TNF-induced cell death and, thereby, prevents inflammation. Our results provide evidence for the relevance of linear ubiquitination in vivo in preventing inflammation and regulating immune signalling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gerlach, Bjorn -- Cordier, Stefanie M -- Schmukle, Anna C -- Emmerich, Christoph H -- Rieser, Eva -- Haas, Tobias L -- Webb, Andrew I -- Rickard, James A -- Anderton, Holly -- Wong, Wendy W-L -- Nachbur, Ueli -- Gangoda, Lahiru -- Warnken, Uwe -- Purcell, Anthony W -- Silke, John -- Walczak, Henning -- 10950/Cancer Research UK/United Kingdom -- England -- Nature. 2011 Mar 31;471(7340):591-6. doi: 10.1038/nature09816.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Tumour Immunology Unit, Department of Medicine, Imperial College London, W12 0NN London, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21455173" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CD40 Ligand/metabolism ; Carrier Proteins/chemistry/metabolism ; Cell Line ; Humans ; I-kappa B Kinase/metabolism ; Immunity/*immunology ; Inflammation/*metabolism/pathology/prevention & control ; Interleukin-1beta/metabolism ; Mice ; Multiprotein Complexes/chemistry/metabolism ; NF-kappa B/metabolism ; Nerve Tissue Proteins/chemistry/genetics/metabolism ; Phenotype ; Receptor-Interacting Protein Serine-Threonine Kinases/metabolism ; Receptors, Tumor Necrosis Factor/deficiency/genetics/metabolism ; *Signal Transduction ; Skin/cytology/immunology/metabolism/pathology ; Tumor Necrosis Factor-alpha/deficiency/genetics ; Ubiquitin/chemistry/metabolism ; Ubiquitin-Protein Ligase Complexes/chemistry/metabolism ; Ubiquitin-Protein Ligases/chemistry/metabolism ; *Ubiquitination
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
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    Creating a buzz about insect genomes (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-03-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Robinson, Gene E -- Hackett, Kevin J -- Purcell-Miramontes, Mary -- Brown, Susan J -- Evans, Jay D -- Goldsmith, Marian R -- Lawson, Daniel -- Okamuro, Jack -- Robertson, Hugh M -- Schneider, David J -- R01 HD029594/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 2011 Mar 18;331(6023):1386. doi: 10.1126/science.331.6023.1386.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21415334" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arthropods/genetics ; Genome ; *Genome, Insect ; Insects/*genetics ; *Sequence Analysis, DNA
    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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    Non-A, non-B hepatitis: ultrastructural evidence for two agents in experimentally infected chimpanzees (1979)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1979-07-13
    Description: Two different ultrastructural alterations were observed in liver cells of chimpanzees inoculated with plasma derived from two different patients with non-A, non-B hepatitis. During the acute phase of illness in one group of four chimpanzees, peculiar tubular structures, composed of two unit membranes with electron-opaque material in between, were observed in the cytoplasm of hepatocytes. In contrast, these structures were never detected in the liver cells of the second group of five chimpanzees that received the second inoculum, However, nuclear changes, usually associated with aggregates of 20- to 27-nanometer particles, were found in hepatocytes of the latter animals. Although these particles resembled viruses, they were not as uniform as small virus particles often appear. In five other chimpanzees inoculated with non-A, non-B hepatitis material not known to be related to the first two inocula, cytoplasmic structures were found in four, and nuclear structures were found in the remaining one. Thus, all 14 chimpanzees inoculated with transmissible non-A, non-B hepatitis agents could be classified as having either nuclear or cytoplasmic changes. These observations add support to epidemiologic data suggesting that there may be more than one agent of non-A, non-B hepatitis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shimizu, Y K -- Feinstone, S M -- Purcell, R H -- Alter, H J -- London, W T -- New York, N.Y. -- Science. 1979 Jul 13;205(4402):197-200.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/451589" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Nucleus/ultrastructure ; Cytoplasm/ultrastructure ; Hepatitis, Viral, Animal/*microbiology ; Hepatitis, Viral, Human/*microbiology ; Inclusion Bodies, Viral/ultrastructure ; Liver/microbiology/ultrastructure ; Microscopy, Electron ; Pan troglodytes
    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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    Pierce's disease of grapevines: isolation of the causal bacterium (1978)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1978-01-06
    Description: A Gram-negative, rod-shaped bacterium has been consistently isolated from grapevines with Pierce's disease. Grapevines inoculated with the bacterium developed Pierce's disease, and the bacterium was reisolated from the plants. The bacterium was serologically and ultrastructurallv indistinguishable from the one in naturally infected plants, and also indistinguishable from a bacterium isolated from almonds with almond leaf scorch disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Davis, M J -- Purcell, A H -- Thomson, S V -- New York, N.Y. -- Science. 1978 Jan 6;199(4324):75-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Plant Pathology, University of California, Berkeley, CA 94720, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17569487" target="_blank"〉PubMed〈/a〉
    Keywords: Agglutination Tests ; Animals ; Cell Wall/ultrastructure ; Gram-Negative Bacteria/cytology/immunology/*isolation & ; purification/pathogenicity ; Hemiptera/microbiology ; Insect Vectors/microbiology ; Male ; Mice ; Plant Diseases/*microbiology ; Prunus/microbiology ; Rabbits ; Vitis/*microbiology
    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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