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  • *Gene Silencing  (1)
  • *Insecticides/pharmacology  (1)
  • Models, Biological
  • American Association for the Advancement of Science (AAAS)  (3)
  • American Chemical Society
  • Cell Press
  • National Academy of Sciences
  • 2010-2014  (3)
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Verlag/Herausgeber
  • American Association for the Advancement of Science (AAAS)  (3)
  • American Chemical Society
  • Cell Press
  • National Academy of Sciences
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Jahr
  • 1
    Publikationsdatum: 2011-10-15
    Beschreibung: Persistence of human fetal hemoglobin (HbF, alpha(2)gamma(2)) in adults lessens the severity of sickle cell disease (SCD) and the beta-thalassemias. Here, we show that the repressor BCL11A is required in vivo for silencing of gamma-globin expression in adult animals, yet dispensable for red cell production. BCL11A serves as a barrier to HbF reactivation by known HbF inducing agents. In a proof-of-principle test of BCL11A as a potential therapeutic target, we demonstrate that inactivation of BCL11A in SCD transgenic mice corrects the hematologic and pathologic defects associated with SCD through high-level pancellular HbF induction. Thus, interference with HbF silencing by manipulation of a single target protein is sufficient to reverse SCD.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3746545/" 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/PMC3746545/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Xu, Jian -- Peng, Cong -- Sankaran, Vijay G -- Shao, Zhen -- Esrick, Erica B -- Chong, Bryan G -- Ippolito, Gregory C -- Fujiwara, Yuko -- Ebert, Benjamin L -- Tucker, Philip W -- Orkin, Stuart H -- K01 DK093543/DK/NIDDK NIH HHS/ -- T32 CA009172/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2011 Nov 18;334(6058):993-6. doi: 10.1126/science.1211053. Epub 2011 Oct 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Hematology/Oncology, Children's Hospital Boston and Department of Pediatric Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21998251" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Anemia, Sickle Cell/blood/*genetics/pathology/*therapy ; Animals ; Carrier Proteins/genetics/*physiology ; DNA Methylation ; Embryo, Mammalian ; Epigenesis, Genetic ; Erythroid Cells/metabolism ; Fetal Hemoglobin/*genetics/metabolism ; *Gene Expression Regulation ; *Gene Silencing ; Histones/metabolism ; Humans ; Mice ; Mice, Knockout ; Mice, Transgenic ; Molecular Targeted Therapy ; Nuclear Proteins/genetics/*physiology ; gamma-Globins/*genetics
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 2
    Publikationsdatum: 2012-11-10
    Beschreibung: Phosphine is a small redox-active gas that is used to protect global grain reserves, which are threatened by the emergence of phosphine resistance in pest insects. We find that polymorphisms responsible for genetic resistance cluster around the redox-active catalytic disulfide or the dimerization interface of dihydrolipoamide dehydrogenase (DLD) in insects (Rhyzopertha dominica and Tribolium castaneum) and nematodes (Caenorhabditis elegans). DLD is a core metabolic enzyme representing a new class of resistance factor for a redox-active metabolic toxin. It participates in four key steps of core metabolism, and metabolite profiles indicate that phosphine exposure in mutant and wild-type animals affects these steps differently. Mutation of DLD in C. elegans increases arsenite sensitivity. This specific vulnerability may be exploited to control phosphine-resistant insects and safeguard food security.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schlipalius, David I -- Valmas, Nicholas -- Tuck, Andrew G -- Jagadeesan, Rajeswaran -- Ma, Li -- Kaur, Ramandeep -- Goldinger, Anita -- Anderson, Cameron -- Kuang, Jujiao -- Zuryn, Steven -- Mau, Yosep S -- Cheng, Qiang -- Collins, Patrick J -- Nayak, Manoj K -- Schirra, Horst Joachim -- Hilliard, Massimo A -- Ebert, Paul R -- R01NS060129/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2012 Nov 9;338(6108):807-10. doi: 10.1126/science.1224951.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Agri-Science Queensland, Department of Agriculture, Fisheries and Forestry, Ecosciences Precinct, Brisbane, QLD 4001, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23139334" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Arsenicals/pharmacology ; Arsenites/pharmacology ; Beetles/drug effects/*enzymology/genetics/metabolism ; Caenorhabditis elegans/drug effects/*enzymology/genetics/metabolism ; Caenorhabditis elegans Proteins/chemistry/genetics/metabolism ; Catalytic Domain ; Dihydrolipoamide Dehydrogenase/chemistry/*genetics/metabolism ; Insect Proteins/chemistry/genetics/metabolism ; Insecticide Resistance/*genetics ; *Insecticides/pharmacology ; Metabolic Networks and Pathways ; Molecular Sequence Data ; Mutation ; Oxidation-Reduction ; Pesticides ; *Phosphines/pharmacology ; Polymorphism, Genetic ; Protein Multimerization ; Tribolium/drug effects/*enzymology/genetics/metabolism
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 3
    Publikationsdatum: 2013-02-09
    Beschreibung: Mutations in IDH1 and IDH2, the genes coding for isocitrate dehydrogenases 1 and 2, are common in several human cancers, including leukemias, and result in overproduction of the (R)-enantiomer of 2-hydroxyglutarate [(R)-2HG]. Elucidation of the role of IDH mutations and (R)-2HG in leukemogenesis has been hampered by a lack of appropriate cell-based models. Here, we show that a canonical IDH1 mutant, IDH1 R132H, promotes cytokine independence and blocks differentiation in hematopoietic cells. These effects can be recapitulated by (R)-2HG, but not (S)-2HG, despite the fact that (S)-2HG more potently inhibits enzymes, such as the 5'-methylcytosine hydroxylase TET2, that have previously been linked to the pathogenesis of IDH mutant tumors. We provide evidence that this paradox relates to the ability of (S)-2HG, but not (R)-2HG, to inhibit the EglN prolyl hydroxylases. Additionally, we show that transformation by (R)-2HG is reversible.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3836459/" 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/PMC3836459/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Losman, Julie-Aurore -- Looper, Ryan E -- Koivunen, Peppi -- Lee, Sungwoo -- Schneider, Rebekka K -- McMahon, Christine -- Cowley, Glenn S -- Root, David E -- Ebert, Benjamin L -- Kaelin, William G Jr -- P30 DK049216/DK/NIDDK NIH HHS/ -- R01 CA068490/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2013 Mar 29;339(6127):1621-5. doi: 10.1126/science.1231677. Epub 2013 Feb 7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA 02215, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23393090" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Cell Line, Tumor ; Cell Transformation, Neoplastic/genetics/*metabolism ; Glutarates/*metabolism ; *Hematopoiesis ; Humans ; Isocitrate Dehydrogenase/genetics/*metabolism ; Leukemia/*enzymology/genetics ; Models, Biological ; Procollagen-Proline Dioxygenase/*antagonists & inhibitors
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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