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  • Cell Research
    Education and Institutes of Biomedical Sciences Shanghai Medical College College of Life Science Fudan University Shanghai 200032 China 2 China Novartis Institutes for BioMedical Research Shanghai China 3 Department of Chemistry Institute of Stem Cell Research and Regenerative Medicine Fudan University Shanghai 200032 China 4 Department of Biochemistry and Molecular Biology Institute of Stem Cell Research and Regenerative Medicine Fudan University Shanghai 200032 China 5 Department of Pharmacology and Moores Cancer Center University of California San Diego La Jolla California 92093 USA 6 Lineberger Comprehensive Cancer Center Department of Biochemistry and Biophysics University of North Carolina at Chapel Hill North Carolina 27599 USA Correspondence Dan Ye E mail yedan fudan edu cn DNA methylation suppresses gene expression and plays a broad and important role in diverse biological processes such as development and tumor suppression1 2 DNA methylation is generally thought to be relatively stable and heritable This view is recently changed by the discovery of TET ten eleven translocation family of dioxygenases which catalyze three sequential oxidation reactions converting 5mC first to 5hmC and then 5 formylcytosine 5fC and finally 5 carboxylcytosine 5caC 3 4 5 6 7 A subsequent decarboxylation of 5caC could then lead to DNA demethylation3 While the biological function and catalytic mechanism of TET enzymes are being extensively investigated much less is currently known about their regulation TET proteins are the members of Fe II α ketoglutarate α KG dependent dioxygenases which require Fe II as a metal cofactor and α KG as a co substrate8 9 In various types of tumors pathological accumulation of three metabolites 2 HG succinate and fumurate that share structural similarity with α KG results in a competitive inhibition of α KG dependent TET activity leading to a hypermethylation phenotype10 11 α KG is produced and consumed mainly by four different

    Original URL path: http://www.cell-research.com/arts.asp?id=1976 (2016-02-14)
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  • Cell Research

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    Original URL path: /artsmore1.asp?id=174 (2016-02-14)


  • Cell Research
    Neuhuber 3 and Alexander Flügel 1 2 1 Institute for Multiple Sclerosis Research Department of Neuroimmunology Gemeinnützige Hertie Stiftung and University Medical Centre Göttingen Göttingen Germany 2 Max Planck Institute for Experimental Medicine Göttingen Germany 3 Institute for Anatomy I Friedrich Alexander University Erlangen Germany Correspondence Alexander Flügel E mail fluegel med uni goettingen de A recent paper published in Nature reports sensory nerve fibers in the skin that give

    Original URL path: http://www.cell-research.com/arts.asp?id=1977 (2016-02-14)
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  • Cell Research
    1025 1026 Phosphorylated ubiquitin a new shade of PINK1 in Parkin activation FREE Véronique Sauvé 1 and Kalle Gehring 1 1 Department of Biochemistry and GRASP McGill University Montréal QC H3G 0B1 Canada Correspondence Kalle Gehring E mail kalle gehring mcgill ca The Parkinson s disease PD associated proteins Parkin and PINK1 together comprise a mitochondrial quality control pathway that promotes neuronal survival through autophagy of damaged mitochondria Three recent

    Original URL path: http://www.cell-research.com/arts.asp?id=1979 (2016-02-14)
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  • Cell Research
    of Cellular Biology La Jolla Institute for Allergy and Immunology La Jolla CA 92037 USA Correspondence Nunzio Bottini Tel 1 858 752 6815 E mail nunzio lji org The emerging concept of molecular barcodes refers to the dynamic combination of post translational modifications often of different nature e g phosphorylation and ubiquitination that gives rise to multiple forms of a protein which can relay distinct signals throughout a cell In

    Original URL path: http://www.cell-research.com/arts.asp?id=1980 (2016-02-14)
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  • Cell Research
    UMR 8253 Institut Necker Enfants Malades INEM Université Paris Descartes Sorbonne Paris Cité Paris 75993 Paris cedex 14 France Correspondence Etienne Morel E mail etienne morel inserm fr Patrice Codogno E mail patrice codogno inserm fr The phosphatidylinositol 3 kinase complex I PI3K complex I is a crucial regulator of autophagy which contains Beclin 1 or ATG6 ATG14L VPS34 or the class III phosphatidylinositol 3 kinase and its adaptor VPS15

    Original URL path: http://www.cell-research.com/arts.asp?id=1981 (2016-02-14)
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  • Cell Research
    Zhimin Lu 1 2 3 and Tony Hunter 4 1 Brain Tumor Center and Department of Neuro Oncology The University of Texas Graduate School of Biomedical Sciences at Houston Houston TX 77030 USA 2 Department of Molecular and Cellular Oncology The University of Texas Graduate School of Biomedical Sciences at Houston Houston TX 77030 USA 3 Cancer Biology Program The University of Texas Graduate School of Biomedical Sciences at Houston Houston TX 77030 USA 4 Molecular and Cell Biology Laboratory Salk Institute for Biological Studies La Jolla CA 92037 USA Correspondence Zhimin Lu Tel 713 834 6231 Fax 713 834 6230 E mail zhiminlu mdanderson org Tony Hunter Tel 858 453 4100 Fax 713 834 6230 E mail hunter salk edu Proline directed phosphorylation is a posttranslational modification that is instrumental in regulating signaling from the plasma membrane to the nucleus and its dysregulation contributes to cancer development Protein interacting with never in mitosis A1 Pin1 which is overexpressed in many types of cancer isomerizes specific phosphorylated Ser Thr Pro bonds in many substrate proteins including glycolytic enzyme protein kinases protein phosphatases methyltransferase lipid kinase ubiquitin E3 ligase DNA endonuclease RNA polymerase and transcription activators and regulators This Pin1 mediated

    Original URL path: http://www.cell-research.com/arts.asp?id=1983 (2016-02-14)
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  • Cell Research
    Honghe Chen 1 Zilong Wang 1 Rongjuan Pei 1 Qian Wang 5 Lei Pan 2 Junqi Niu 3 Xinwen Chen 1 and Hong Tang 1 2 1 State Key Laboratory of Virology and the Center for Viral Pathology Wuhan Institute of Virology Chinese Academy of Sciences Wuhan Hubei 430071 China 2 Key Laboratory of Infection and Immunity Institute of Biophysics Chinese Academy of Sciences Beijing 100101 China 3 Department of Hepatology The First Hospital of Jilin University Changchun Jilin 130021 China 4 The Institute of Biotechnology Shanxi University Taiyuan Shanxi 030006 China 5 Key Laboratory of Human Functional Genomics of Jiangsu Province School of Basic Medical Science Nanjing Medical University Nanjing Jiangsu 210093 China Correspondence Hong Tang Tel 86 10 64888438 Fax 86 10 64848357 E mail tanghong moon ibp ac cn Xinwen Chen Tel 86 10 64888438 Fax 86 10 64848357 E mail chenxw wh iov cn The majority of hepatitis C virus HCV infection develops chronic infection which causes steatosis cirrhosis and hepatocellular carcinoma However understanding HCV chronicity and pathogenesis is hampered by its narrow host range mostly restricted to human and chimpanzee Recent endeavour to infect a variety of humanized mice has not been able to achieve persistent HCV infection unless the essential innate immune responsive genes are knocked out Nevertheless such immune compromised humanized mice still lacked HCV infection induced hepatopathogenesis Here we report that transgenic mice in ICR background harboring both human CD81 and occludin genes C OTg are permissive to HCV infection at a chronicity rate comparable to humans In this mouse model HCV accomplishes its replication cycle leading to sustained viremia and infectivity for more than 12 months post infection with expected fibrotic and cirrhotic progression Host factors favorable for HCV replication and inadequate innate immune response may contribute to the persistence Lastly

    Original URL path: http://www.cell-research.com/arts.asp?id=1984 (2016-02-14)
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