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  • 1
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    Ecology: The Convention on Biological Diversity's 2010 target (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-01-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Balmford, Andrew -- Bennun, Leon -- Brink, Ben Ten -- Cooper, David -- Cote, Isabelle M -- Crane, Peter -- Dobson, Andrew -- Dudley, Nigel -- Dutton, Ian -- Green, Rhys E -- Gregory, Richard D -- Harrison, Jeremy -- Kennedy, Elizabeth T -- Kremen, Claire -- Leader-Williams, Nigel -- Lovejoy, Thomas E -- Mace, Georgina -- May, Robert -- Mayaux, Phillipe -- Morling, Paul -- Phillips, Joanna -- Redford, Kent -- Ricketts, Taylor H -- Rodriguez, Jon Paul -- Sanjayan, M -- Schei, Peter J -- van Jaarsveld, Albert S -- Walther, Bruno A -- New York, N.Y. -- Science. 2005 Jan 14;307(5707):212-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cambridge University and University of Cape Town.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15653489" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biodiversity ; *Conservation of Natural Resources ; *Ecology ; Ecosystem ; Humans ; Interdisciplinary Communication ; International Cooperation ; Models, Biological ; Models, Theoretical ; Public Policy
    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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    In vivo imaging of Treg cells providing immune privilege to the haematopoietic stem-cell niche (2011)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2011-06-10
    Description: Stem cells reside in a specialized regulatory microenvironment or niche, where they receive appropriate support for maintaining self-renewal and multi-lineage differentiation capacity. The niche may also protect stem cells from environmental insults including cytotoxic chemotherapy and perhaps pathogenic immunity. The testis, hair follicle and placenta are all sites of residence for stem cells and are immune-suppressive environments, called immune-privileged sites, where multiple mechanisms cooperate to prevent immune attack, even enabling prolonged survival of foreign allografts without immunosuppression. We sought to determine if somatic stem-cell niches more broadly are immune-privileged sites by examining the haematopoietic stem/progenitor cell (HSPC) niche in the bone marrow, a site where immune reactivity exists. We observed persistence of HSPCs from allogeneic donor mice (allo-HSPCs) in non-irradiated recipient mice for 30 days without immunosuppression with the same survival frequency compared to syngeneic HSPCs. These HSPCs were lost after the depletion of FoxP3 regulatory T (T(reg)) cells. High-resolution in vivo imaging over time demonstrated marked co-localization of HSPCs with T(reg) cells that accumulated on the endosteal surface in the calvarial and trabecular bone marrow. T(reg) cells seem to participate in creating a localized zone where HSPCs reside and where T(reg) cells are necessary for allo-HSPC persistence. In addition to processes supporting stem-cell function, the niche will provide a relative sanctuary from immune attack.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3725645/" 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/PMC3725645/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fujisaki, Joji -- Wu, Juwell -- Carlson, Alicia L -- Silberstein, Lev -- Putheti, Prabhakar -- Larocca, Rafael -- Gao, Wenda -- Saito, Toshiki I -- Lo Celso, Cristina -- Tsuyuzaki, Hitoshi -- Sato, Tatsuyuki -- Cote, Daniel -- Sykes, Megan -- Strom, Terry B -- Scadden, David T -- Lin, Charles P -- AI041521/AI/NIAID NIH HHS/ -- CA111519/CA/NCI NIH HHS/ -- HL097748/HL/NHLBI NIH HHS/ -- HL97794/HL/NHLBI NIH HHS/ -- P01 AI041521/AI/NIAID NIH HHS/ -- P01 AI073748/AI/NIAID NIH HHS/ -- P01 CA111519/CA/NCI NIH HHS/ -- P01 CA111519-05/CA/NCI NIH HHS/ -- R01 HL097748/HL/NHLBI NIH HHS/ -- R01 HL097748-02/HL/NHLBI NIH HHS/ -- R01 HL097794/HL/NHLBI NIH HHS/ -- R01 HL097794-02/HL/NHLBI NIH HHS/ -- England -- Nature. 2011 Jun 8;474(7350):216-9. doi: 10.1038/nature10160.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Advanced Microscopy Program, Center for Systems Biology and Wellman Center for Photomedicine, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts 02114, USA. jfujisaki@partners.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21654805" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Survival/immunology ; Cells, Cultured ; Forkhead Transcription Factors/metabolism ; Graft Survival/*immunology ; Hematopoietic Stem Cells/cytology/*immunology ; Humans ; *Imaging, Three-Dimensional ; Interleukin-10/deficiency/genetics/immunology/metabolism ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Stem Cell Niche/cytology/*immunology ; T-Lymphocytes, Regulatory/*immunology/metabolism ; Time Factors ; Transplantation, Homologous/immunology
    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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    Small molecule inhibitors reveal Niemann-Pick C1 is essential for Ebola virus infection (2011)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2011-08-26
    Description: Ebola virus (EboV) is a highly pathogenic enveloped virus that causes outbreaks of zoonotic infection in Africa. The clinical symptoms are manifestations of the massive production of pro-inflammatory cytokines in response to infection and in many outbreaks, mortality exceeds 75%. The unpredictable onset, ease of transmission, rapid progression of disease, high mortality and lack of effective vaccine or therapy have created a high level of public concern about EboV. Here we report the identification of a novel benzylpiperazine adamantane diamide-derived compound that inhibits EboV infection. Using mutant cell lines and informative derivatives of the lead compound, we show that the target of the inhibitor is the endosomal membrane protein Niemann-Pick C1 (NPC1). We find that NPC1 is essential for infection, that it binds to the virus glycoprotein (GP), and that antiviral compounds interfere with GP binding to NPC1. Combined with the results of previous studies of GP structure and function, our findings support a model of EboV infection in which cleavage of the GP1 subunit by endosomal cathepsin proteases removes heavily glycosylated domains to expose the amino-terminal domain, which is a ligand for NPC1 and regulates membrane fusion by the GP2 subunit. Thus, NPC1 is essential for EboV entry and a target for antiviral therapy.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3230319/" 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/PMC3230319/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cote, Marceline -- Misasi, John -- Ren, Tao -- Bruchez, Anna -- Lee, Kyungae -- Filone, Claire Marie -- Hensley, Lisa -- Li, Qi -- Ory, Daniel -- Chandran, Kartik -- Cunningham, James -- 5-T32-HL007623/HL/NHLBI NIH HHS/ -- 5K08AI079381/AI/NIAID NIH HHS/ -- K08 AI079381/AI/NIAID NIH HHS/ -- K12-HD052896/HD/NICHD NIH HHS/ -- R01 AI088027/AI/NIAID NIH HHS/ -- R01 CA104266/CA/NCI NIH HHS/ -- U54 AI057159/AI/NIAID NIH HHS/ -- U54 AI057159-09/AI/NIAID NIH HHS/ -- England -- Nature. 2011 Aug 24;477(7364):344-8. doi: 10.1038/nature10380.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Hematology, Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21866101" target="_blank"〉PubMed〈/a〉
    Keywords: Adamantane/analogs & derivatives/chemistry ; Animals ; Antiviral Agents/*chemistry/*pharmacology ; Carrier Proteins/*metabolism ; Cathepsins/metabolism ; Cell Line ; Cercopithecus aethiops ; Ebolavirus/*drug effects/*physiology ; Endosomes/enzymology ; Glycoproteins/metabolism ; Hemorrhagic Fever, Ebola/drug therapy/metabolism ; Humans ; Membrane Fusion/drug effects ; Membrane Glycoproteins/*metabolism ; Molecular Weight ; Piperazines/chemistry ; Vero Cells ; Viral Fusion Proteins/metabolism ; Virus Internalization/*drug effects
    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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    Large-scale prediction and testing of drug activity on side-effect targets (2012)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2012-06-23
    Description: Discovering the unintended 'off-targets' that predict adverse drug reactions is daunting by empirical methods alone. Drugs can act on several protein targets, some of which can be unrelated by conventional molecular metrics, and hundreds of proteins have been implicated in side effects. Here we use a computational strategy to predict the activity of 656 marketed drugs on 73 unintended 'side-effect' targets. Approximately half of the predictions were confirmed, either from proprietary databases unknown to the method or by new experimental assays. Affinities for these new off-targets ranged from 1 nM to 30 muM. To explore relevance, we developed an association metric to prioritize those new off-targets that explained side effects better than any known target of a given drug, creating a drug-target-adverse drug reaction network. Among these new associations was the prediction that the abdominal pain side effect of the synthetic oestrogen chlorotrianisene was mediated through its newly discovered inhibition of the enzyme cyclooxygenase-1. The clinical relevance of this inhibition was borne out in whole human blood platelet aggregation assays. This approach may have wide application to de-risking toxicological liabilities in drug discovery.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3383642/" 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/PMC3383642/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lounkine, Eugen -- Keiser, Michael J -- Whitebread, Steven -- Mikhailov, Dmitri -- Hamon, Jacques -- Jenkins, Jeremy L -- Lavan, Paul -- Weber, Eckhard -- Doak, Allison K -- Cote, Serge -- Shoichet, Brian K -- Urban, Laszlo -- AG002132/AG/NIA NIH HHS/ -- GM71896/GM/NIGMS NIH HHS/ -- GM93456/GM/NIGMS NIH HHS/ -- P01 AG002132/AG/NIA NIH HHS/ -- R01 GM071896/GM/NIGMS NIH HHS/ -- England -- Nature. 2012 Jun 10;486(7403):361-7. doi: 10.1038/nature11159.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Novartis Institutes for Biomedical Research, Cambridge, Massachusetts 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22722194" target="_blank"〉PubMed〈/a〉
    Keywords: Blood Platelets/drug effects ; Chlorotrianisene/adverse effects/chemistry/pharmacology ; Cyclooxygenase 1/metabolism ; Cyclooxygenase Inhibitors/adverse effects/pharmacology ; Databases, Factual ; Drug Evaluation, Preclinical/*methods ; *Drug-Related Side Effects and Adverse Reactions ; Estrogens, Non-Steroidal/adverse effects/pharmacology ; Forecasting ; Humans ; Models, Biological ; Molecular Targeted Therapy/adverse effects ; Platelet Aggregation/drug effects ; Reproducibility of Results ; Substrate Specificity ; Toxicity Tests/*methods
    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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  • 5
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    Mutations in the sulfonylurea receptor gene in familial persistent hyperinsulinemic hypoglycemia of infancy (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-04-21
    Description: Familial persistent hyperinsulinemic hypoglycemia of infancy (PHHI), an autosomal recessive disorder characterized by unregulated insulin secretion, is linked to chromosome 11p14-15.1. The newly cloned high-affinity sulfonylurea receptor (SUR) gene, a regulator of insulin secretion, was mapped to 11p15.1 by means of fluorescence in situ hybridization. Two separate SUR gene splice site mutations, which segregated with disease phenotype, were identified in affected individuals from nine different families. Both mutations resulted in aberrant processing of the RNA sequence and disruption of the putative second nucleotide binding domain of the SUR protein. Abnormal insulin secretion in PHHI appears to be caused by mutations in the SUR gene.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thomas, P M -- Cote, G J -- Wohllk, N -- Haddad, B -- Mathew, P M -- Rabl, W -- Aguilar-Bryan, L -- Gagel, R F -- Bryan, J -- DK38146/DK/NIDDK NIH HHS/ -- DK44311/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1995 Apr 21;268(5209):426-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Specialties, University of Texas M.D. Anderson Cancer Center, Houston 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7716548" target="_blank"〉PubMed〈/a〉
    Keywords: *ATP-Binding Cassette Transporters ; Amino Acid Sequence ; Base Sequence ; Chromosome Mapping ; Chromosomes, Human, Pair 11 ; DNA Mutational Analysis ; DNA, Complementary/genetics ; Genotype ; Humans ; Hyperinsulinism/*genetics ; Hypoglycemia/*genetics ; Infant ; Insulin/secretion ; Molecular Sequence Data ; Mutation ; Pancreatic Diseases/*genetics ; Phenotype ; Point Mutation ; Potassium Channels/chemistry/*genetics ; *Potassium Channels, Inwardly Rectifying ; RNA Splicing ; Receptors, Drug/chemistry/*genetics ; Sulfonylurea Compounds/metabolism ; Sulfonylurea Receptors
    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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