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  • Artikel  (2)
  • Animals  (1)
  • Cell Cycle Proteins/genetics/*metabolism  (1)
  • 2-phenylethanol
  • Applications
  • EAG
  • Food Science, Agricultural, Medicinal and Pharmaceutical Chemistry
  • 2015-2019  (2)
  • 1995-1999
  • 2015  (2)
  • 1
    Publikationsdatum: 2015-09-12
    Beschreibung: Chromosomal instability (CIN) is a major trait of cancer cells and a potent driver of tumor progression. However, the molecular mechanisms underlying CIN still remain elusive. We found that a number of CIN(+) cell lines have impairments in the integrity of the conserved inner centromere-shugoshin (ICS) network, which coordinates sister chromatid cohesion and kinetochore-microtubule attachment. These defects are caused mostly by the loss of histone H3 lysine 9 trimethylation at centromeres and sometimes by a reduction in chromatin-associated cohesin; both pathways separately sustain centromeric shugoshin stability. Artificial restoration of the ICS network suppresses chromosome segregation errors in a wide range of CIN(+) cells, including RB- and BRCA1-deficient cells. Thus, dysfunction of the ICS network might be a key mechanism underlying CIN in human tumorigenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tanno, Yuji -- Susumu, Hiroaki -- Kawamura, Miyuki -- Sugimura, Haruhiko -- Honda, Takashi -- Watanabe, Yoshinori -- New York, N.Y. -- Science. 2015 Sep 11;349(6253):1237-40. doi: 10.1126/science.aaa2655.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Chromosome Dynamics, Institute of Molecular and Cellular Biosciences, University of Tokyo, Yayoi, Tokyo 113-0032, Japan. ; Laboratory of Chromosome Dynamics, Institute of Molecular and Cellular Biosciences, University of Tokyo, Yayoi, Tokyo 113-0032, Japan. Department of Biological Sciences, Graduate School of Science, University of Tokyo, Yayoi, Tokyo 113-0032, Japan. ; First Department of Pathology, Hamamatsu University School of Medicine, Hamamatsu, Shizuoka 431-3192, Japan. ; Laboratory of Chromosome Dynamics, Institute of Molecular and Cellular Biosciences, University of Tokyo, Yayoi, Tokyo 113-0032, Japan. Department of Biological Sciences, Graduate School of Science, University of Tokyo, Yayoi, Tokyo 113-0032, Japan. ywatanab@iam.u-tokyo.ac.jp.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26359403" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): BRCA1 Protein/genetics ; Carcinogenesis/genetics/*metabolism ; Cell Cycle Proteins/genetics/*metabolism ; Centromere/genetics/*metabolism ; Chromatids/metabolism ; Chromatin/metabolism ; *Chromosomal Instability ; Chromosomal Proteins, Non-Histone/metabolism ; *Chromosome Segregation ; HeLa Cells ; Histones/metabolism ; Humans ; Kinetochores/metabolism ; Lysine/metabolism ; Methylation ; Microtubules/metabolism ; Retinoblastoma Protein/genetics
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
    BibTip Andere fanden auch interessant ...
  • 2
    Publikationsdatum: 2015-07-15
    Beschreibung: Changes to the symbiotic microbiota early in life, or the absence of it, can lead to exacerbated type 2 immunity and allergic inflammations. Although it is unclear how the microbiota regulates type 2 immunity, it is a strong inducer of proinflammatory T helper 17 (T(H)17) cells and regulatory T cells (T(regs)) in the intestine. Here, we report that microbiota-induced T(regs) express the nuclear hormone receptor RORgammat and differentiate along a pathway that also leads to T(H)17 cells. In the absence of RORgammat(+) T(regs), T(H)2-driven defense against helminths is more efficient, whereas T(H)2-associated pathology is exacerbated. Thus, the microbiota regulates type 2 responses through the induction of type 3 RORgammat(+) T(regs) and T(H)17 cells and acts as a key factor in balancing immune responses at mucosal surfaces.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ohnmacht, Caspar -- Park, Joo-Hong -- Cording, Sascha -- Wing, James B -- Atarashi, Koji -- Obata, Yuuki -- Gaboriau-Routhiau, Valerie -- Marques, Rute -- Dulauroy, Sophie -- Fedoseeva, Maria -- Busslinger, Meinrad -- Cerf-Bensussan, Nadine -- Boneca, Ivo G -- Voehringer, David -- Hase, Koji -- Honda, Kenya -- Sakaguchi, Shimon -- Eberl, Gerard -- New York, N.Y. -- Science. 2015 Aug 28;349(6251):989-93. doi: 10.1126/science.aac4263. Epub 2015 Jul 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut Pasteur, Microenvironment and Immunity Unit, 75724 Paris, France. ; Laboratory of Experimental Immunology, Immunology Frontier Research Center, Osaka University, Suita 565-0871, Japan. ; RIKEN Center for Integrative Medical Sciences (IMS-RCAI), Yokohama, Kanagawa 230-0045, Japan. PRESTO, Japan Science and Technology Agency, Saitama 332-0012, Japan. ; The Institute of Medical Science, The University of Tokyo, Tokyo 108-8639, Japan. ; INSERM, U1163, Laboratory of Intestinal Immunity, Paris, France. Universite Paris Descartes-Sorbonne Paris Cite and Institut Imagine, Paris, France. INRA Micalis UMR1319, Jouy-en-Josas, France. ; Center of Allergy and Environment (ZAUM), Technische Universitat and Helmholtz Zentrum Munchen, Munich, Germany. ; Research Institute of Molecular Pathology, Vienna Biocenter, 1030 Vienna, Austria. ; INSERM, U1163, Laboratory of Intestinal Immunity, Paris, France. Universite Paris Descartes-Sorbonne Paris Cite and Institut Imagine, Paris, France. ; Institut Pasteur, Biology and Genetics of Bacterial Cell Wall, 75724 Paris, France. INSERM, Groupe Avenir, 75015 Paris, France. ; Department of Infection Biology at the Institute of Clinical Microbiology, Immunology and Hygiene, University Clinic Erlangen and Friedrich-Alexander University Erlangen-Nuremberg, 91054 Erlangen, Germany. ; RIKEN Center for Integrative Medical Sciences (IMS-RCAI), Yokohama, Kanagawa 230-0045, Japan. CREST, Japan Science and Technology Agency, 4-1-8 Honcho Kawaguchi, Saitama 332-0012, Japan. ; Laboratory of Experimental Immunology, Immunology Frontier Research Center, Osaka University, Suita 565-0871, Japan. Department of Experimental Pathology, Institute for Frontier Medical Sciences, Kyoto University, Kyoto 606-8507, Japan. ; Institut Pasteur, Microenvironment and Immunity Unit, 75724 Paris, France. gerard.eberl@pasteur.fr.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26160380" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Colitis, Ulcerative/immunology ; Colon/immunology/microbiology ; Germ-Free Life ; Homeostasis ; *Immunity, Mucosal ; Intestinal Mucosa/*immunology/*microbiology ; Intestine, Small/immunology/microbiology ; Intestines/immunology/*microbiology ; Mice ; Microbiota/*immunology ; Models, Immunological ; Nematospiroides dubius ; Nuclear Receptor Subfamily 1, Group F, Member 3/*metabolism ; Specific Pathogen-Free Organisms ; Strongylida Infections/immunology ; T-Lymphocyte Subsets/immunology ; T-Lymphocytes, Regulatory/*immunology/metabolism ; Th17 Cells/immunology ; Th2 Cells/immunology ; Vitamin A/metabolism
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
    BibTip Andere fanden auch interessant ...
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