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  • 1
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    Methylation of histone H4 at arginine 3 facilitating transcriptional activation by nuclear hormone receptor (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-06-02
    Description: Acetylation of core histone tails plays a fundamental role in transcription regulation. In addition to acetylation, other posttranslational modifications, such as phosphorylation and methylation, occur in core histone tails. Here, we report the purification, molecular identification, and functional characterization of a histone H4-specific methyltransferase PRMT1, a protein arginine methyltransferase. PRMT1 specifically methylates arginine 3 (Arg 3) of H4 in vitro and in vivo. Methylation of Arg 3 by PRMT1 facilitates subsequent acetylation of H4 tails by p300. However, acetylation of H4 inhibits its methylation by PRMT1. Most important, a mutation in the S-adenosyl-l-methionine-binding site of PRMT1 substantially crippled its nuclear receptor coactivator activity. Our finding reveals Arg 3 of H4 as a novel methylation site by PRMT1 and indicates that Arg 3 methylation plays an important role in transcriptional regulation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, H -- Huang, Z Q -- Xia, L -- Feng, Q -- Erdjument-Bromage, H -- Strahl, B D -- Briggs, S D -- Allis, C D -- Wong, J -- Tempst, P -- Zhang, Y -- GM63067-01/GM/NIGMS NIH HHS/ -- P30 CA08748/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2001 Aug 3;293(5531):853-7. Epub 2001 May 31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Biophysics, Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599-7295, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11387442" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Amino Acid Sequence ; Animals ; Arginine/*metabolism ; Binding Sites ; Cell Nucleus/metabolism ; HeLa Cells ; Histones/chemistry/*metabolism ; Humans ; Hydroxamic Acids/pharmacology ; Intracellular Signaling Peptides and Proteins ; Lysine/metabolism ; Methylation ; Methyltransferases/chemistry/genetics/isolation & purification/*metabolism ; Molecular Sequence Data ; Mutation ; Oocytes ; Protein-Arginine N-Methyltransferases ; Receptors, Androgen/*metabolism ; Recombinant Proteins/metabolism ; S-Adenosylmethionine/metabolism ; *Transcriptional Activation ; 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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  • 2
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    The growth factor progranulin binds to TNF receptors and is therapeutic against inflammatory arthritis in mice (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-03-12
    Description: The growth factor progranulin (PGRN) has been implicated in embryonic development, tissue repair, tumorigenesis, and inflammation, but its receptors remain unidentified. We report that PGRN bound directly to tumor necrosis factor receptors (TNFRs) and disturbed the TNFalpha-TNFR interaction. PGRN-deficient mice were susceptible to collagen-induced arthritis, and administration of PGRN reversed inflammatory arthritis. Atsttrin, an engineered protein composed of three PGRN fragments, exhibited selective TNFR binding. PGRN and Atsttrin prevented inflammation in multiple arthritis mouse models and inhibited TNFalpha-activated intracellular signaling. Collectively, these findings demonstrate that PGRN is a ligand of TNFR, an antagonist of TNFalpha signaling, and plays a critical role in the pathogenesis of inflammatory arthritis in mice. They also suggest new potential therapeutic interventions for various TNFalpha-mediated pathologies and conditions, including rheumatoid arthritis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3104397/" 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/PMC3104397/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tang, Wei -- Lu, Yi -- Tian, Qing-Yun -- Zhang, Yan -- Guo, Feng-Jin -- Liu, Guang-Yi -- Syed, Nabeel Muzaffar -- Lai, Yongjie -- Lin, Edward Alan -- Kong, Li -- Su, Jeffrey -- Yin, Fangfang -- Ding, Ai-Hao -- Zanin-Zhorov, Alexandra -- Dustin, Michael L -- Tao, Jian -- Craft, Joseph -- Yin, Zhinan -- Feng, Jian Q -- Abramson, Steven B -- Yu, Xiu-Ping -- Liu, Chuan-ju -- AI43542/AI/NIAID NIH HHS/ -- AR040072/AR/NIAMS NIH HHS/ -- AR050620/AR/NIAMS NIH HHS/ -- AR053210/AR/NIAMS NIH HHS/ -- GM061710/GM/NIGMS NIH HHS/ -- R01 AI030165/AI/NIAID NIH HHS/ -- R01 AI030165-20/AI/NIAID NIH HHS/ -- R01 GM061710/GM/NIGMS NIH HHS/ -- R01 GM061710-08/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2011 Apr 22;332(6028):478-84. doi: 10.1126/science.1199214. Epub 2011 Mar 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Orthopaedic Surgery, New York University School of Medicine and NYU Hospital for Joint Diseases, New York, NY 10003, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21393509" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Aged ; Animals ; Anti-Inflammatory Agents, Non-Steroidal/metabolism/pharmacology/therapeutic use ; Arthritis, Experimental/*drug therapy/*immunology/pathology/physiopathology ; Cartilage, Articular/metabolism/pathology ; Female ; Humans ; Intercellular Signaling Peptides and ; Proteins/chemistry/genetics/*metabolism/therapeutic use ; Ligands ; Male ; Mice ; Mice, Inbred Strains ; Mice, Knockout ; Mice, Transgenic ; Middle Aged ; Protein Interaction Domains and Motifs ; Receptors, Tumor Necrosis Factor, Type I/genetics/*metabolism ; Receptors, Tumor Necrosis Factor, Type II/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism/pharmacology/therapeutic use ; Recombinant Proteins/therapeutic use ; Signal Transduction ; T-Lymphocytes, Regulatory/immunology/physiology ; Tumor Necrosis Factor-alpha/*metabolism ; Young Adult
    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 genetically humanized mouse model for hepatitis C virus infection (2011)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2011-06-10
    Description: Hepatitis C virus (HCV) remains a major medical problem. Antiviral treatment is only partially effective and a vaccine does not exist. Development of more effective therapies has been hampered by the lack of a suitable small animal model. Although xenotransplantation of immunodeficient mice with human hepatocytes has shown promise, these models are subject to important challenges. Building on the previous observation that CD81 and occludin comprise the minimal human factors required to render mouse cells permissive to HCV entry in vitro, we attempted murine humanization via a genetic approach. Here we show that expression of two human genes is sufficient to allow HCV infection of fully immunocompetent inbred mice. We establish a precedent for applying mouse genetics to dissect viral entry and validate the role of scavenger receptor type B class I for HCV uptake. We demonstrate that HCV can be blocked by passive immunization, as well as showing that a recombinant vaccinia virus vector induces humoral immunity and confers partial protection against heterologous challenge. This system recapitulates a portion of the HCV life cycle in an immunocompetent rodent for the first time, opening opportunities for studying viral pathogenesis and immunity and comprising an effective platform for testing HCV entry inhibitors in vivo.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3159410/" 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/PMC3159410/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dorner, Marcus -- Horwitz, Joshua A -- Robbins, Justin B -- Barry, Walter T -- Feng, Qian -- Mu, Kathy -- Jones, Christopher T -- Schoggins, John W -- Catanese, Maria Teresa -- Burton, Dennis R -- Law, Mansun -- Rice, Charles M -- Ploss, Alexander -- F32DK081193/DK/NIDDK NIH HHS/ -- F32DK082155/DK/NIDDK NIH HHS/ -- R01 AI071084/AI/NIAID NIH HHS/ -- R01 AI071084-04/AI/NIAID NIH HHS/ -- R01 AI072613/AI/NIAID NIH HHS/ -- R01 AI072613-05/AI/NIAID NIH HHS/ -- R01 AI079031/AI/NIAID NIH HHS/ -- R01 AI079031-04/AI/NIAID NIH HHS/ -- R01 DK085713/DK/NIDDK NIH HHS/ -- R01 DK085713-03/DK/NIDDK NIH HHS/ -- R01AI071084/AI/NIAID NIH HHS/ -- R01AI072613/AI/NIAID NIH HHS/ -- R01AI079031/AI/NIAID NIH HHS/ -- RC1 DK087193/DK/NIDDK NIH HHS/ -- RC1 DK087193-02/DK/NIDDK NIH HHS/ -- RC1DK087193/DK/NIDDK NIH HHS/ -- England -- Nature. 2011 Jun 8;474(7350):208-11. doi: 10.1038/nature10168.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for the Study of Hepatitis C, The Rockefeller University, New York, New York 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21654804" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoviridae/genetics/physiology ; Animals ; Antibodies, Blocking/immunology ; Antigens, CD/genetics/metabolism ; Antigens, CD81 ; Cells, Cultured ; Claudin-1 ; *Disease Models, Animal ; Genotype ; Hepacivirus/genetics/metabolism/*physiology ; Hepatitis C/*genetics/*virology ; Hepatocytes/cytology/*metabolism/*virology ; Humans ; Immunization, Passive ; Membrane Proteins/genetics/metabolism ; Mice ; Receptors, Virus/genetics/metabolism ; Scavenger Receptors, Class B/genetics/metabolism ; Transfection ; Viral Tropism
    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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  • 4
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    Suppression of cotton bollworm in multiple crops in China in areas with Bt toxin-containing cotton (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-09-20
    Description: Transgenic cotton that has been engineered to produce insecticidal toxins from Bacillus thuringiensis (Bt) and so to resist the pest cotton bollworm (Helicoverpa armigera) has been widely planted in Asia. Analysis of the population dynamics of H. armigera from 1992 to 2007 in China indicated that a marked decrease in regional outbreaks of this pest in multiple crops was associated with the planting of Bt cotton. The study area included six provinces in northern China with an annual total of 3 million hectares of cotton and 22 million hectares of other crops (corn, peanuts, soybeans, and vegetables) grown by more than 10 million resource-poor farmers. Our data suggest that Bt cotton not only controls H. armigera on transgenic cotton designed to resist this pest but also may reduce its presence on other host crops and may decrease the need for insecticide sprays in general.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wu, Kong-Ming -- Lu, Yan-Hui -- Feng, Hong-Qiang -- Jiang, Yu-Ying -- Zhao, Jian-Zhou -- New York, N.Y. -- Science. 2008 Sep 19;321(5896):1676-8. doi: 10.1126/science.1160550.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉State Key Laboratory for Biology of Plant Diseases and Insect Pests, Institute of Plant Protection, Chinese Academy of Agricultural Sciences, Beijing, 100193, People's Republic of China. kmwu@ippcaas.cn〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18801998" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Bacterial Proteins/genetics ; China ; Crops, Agricultural/*genetics ; *Endotoxins/genetics ; Gossypium/*genetics ; *Hemolysin Proteins/genetics ; Insecticides ; *Moths ; *Pest Control, Biological ; Plant Diseases/*statistics & numerical data ; *Plants, Genetically Modified ; Population Density ; Population Dynamics ; Rain ; Temperature
    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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