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  • Cell Research

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    Original URL path: /artsmore1.asp?id=190 (2016-02-14)



  • Cell Research
    China Correspondence dsli sibs ac cn In this issue of Cell Research we are proud to announce the winners of the 6th Sanofi Cell Research Outstanding Paper Award which were selected from papers published in the 2014 print issues of Cell Research The 2014 Sanofi Cell Research Outstanding Review Article Award goes to Dr Kun Liang Guan for his review paper entitled Autophagy regulation by nutrient signaling The winners of

    Original URL path: http://www.cell-research.com/arts.asp?id=2170 (2016-02-14)
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  • Cell Research
    FREE Ben Z Stanger 1 1 Departments of Medicine and Cell and Developmental Biology BRB II III Rm 512 421 Curie Boulevard Perelman School of Medicine at the University of Pennsylvania Philadelphia PA 19104 To maintain homeostasis organs replace cells lost through normal cellular turnover often through the straightforward replication of existing cells A recent paper in Nature shows that cells in the liver are not equivalent when it comes

    Original URL path: http://www.cell-research.com/arts.asp?id=2171 (2016-02-14)
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  • Cell Research
    awaited executioner of pyroptosis FREE Si Ming Man 1 and Thirumala Devi Kanneganti 1 1 Department of Immunology St Jude Children s Research Hospital MS 351 262 Danny Thomas Place Memphis TN 38105 USA Correspondence Thirumala Devi Kanneganti Tel 1 901 595 3634 Fax 1 901 595 5766 E mail Thirumala Devi Kanneganti stjude org Inflammatory caspases drive a lytic form of cell death called pyroptosis in response to microbial

    Original URL path: http://www.cell-research.com/arts.asp?id=2172 (2016-02-14)
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  • Cell Research
    from an old dog Another synaptotoxic fragment from APP FREE Sheue Houy Tyan 1 and Edward H Koo 1 2 1 Department of Medicine National University of Singapore Singapore 2 Department of Neurosciences University of California San Diego La Jolla USA Correspondence Edward H Koo Tel 1 858 822 1024 Fax 1 858 822 1021 E mail edkoo ucsd edu In a surprising twist a hitherto unrecognized cleavage of the

    Original URL path: http://www.cell-research.com/arts.asp?id=2173 (2016-02-14)
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  • Cell Research
    Engelke 1 2 and Arul M Chinnaiyan 1 2 3 4 5 1 Michigan Center for Translational Pathology Ann Arbor MI 48109 USA 2 Department of Pathology Ann Arbor MI 48109 USA 3 Department of Urology University of Michigan Ann Arbor MI 48109 USA 4 Howard Hughes Medical Institute University of Michigan Medical School Ann Arbor MI 48109 USA 5 Comprehensive Cancer Center University of Michigan Medical School Ann Arbor MI 48109 USA Correspondence Arul M Chinnaiyan E mail arul umich edu In a recent issue of Nature two reports investigate the mechanisms by which acute myeloid leukemia AML develops resistance to therapeutic inhibition of bromodomain and extra terminal BET proteins Small molecules in this class such as JQ1 and I BET bind and inhibit the bromodomain modules deep hydrophobic pockets that recognize acetylated lysine residues on histones and transcription factors to disrupt the productive transcription of key proliferative genes1 In particular BET inhibition has emerged as one of the most promising strategies to target the potent oncogene MYC at the transcriptional level2 although other action models have emerged including disruption of the binding of BRD4 to super enhancers3 or to transcription factors4 Now two groups working from different angles

    Original URL path: http://www.cell-research.com/arts.asp?id=2174 (2016-02-14)
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  • Cell Research
    Limei Guo 1 Qian Su 2 Yujie Sun 2 Michael A McNutt 1 and Yuxin Yin 1 1 Institute of Systems Biomedicine Department of Pathology School of Basic Medical Sciences Peking Tsinghua Center for Life Sciences Peking University Health Science Center Beijing 100191 China 2 Biodynamic Optical Imaging Center Peking University Beijing 100871 China Correspondence Yuxin Yin Tel 86 10 8280 1237 Fax 86 10 8280 1380 E mail yinyuxin hsc pku edu cn Tumor suppressor PTEN regulates cellular activities and controls genome stability through multiple mechanisms In this study we report that PTEN is necessary for the protection of DNA replication forks against replication stress We show that deletion of PTEN leads to replication fork collapse and chromosomal instability upon fork stalling following nucleotide depletion induced by hydroxyurea PTEN is physically associated with replication protein A 1 RPA1 via the RPA1 C terminal domain STORM and iPOND reveal that PTEN is localized at replication sites and promotes RPA1 accumulation on replication forks PTEN recruits the deubiquitinase OTUB1 to mediate RPA1 deubiquitination RPA1 deletion confers a phenotype like that observed in PTEN knockout cells with stalling of replication forks Expression of PTEN and RPA1 shows strong correlation in colorectal cancer

    Original URL path: http://www.cell-research.com/arts.asp?id=2175 (2016-02-14)
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  • Cell Research
    2200 Copenhagen Denmark 3 Centre for Epigenetics University of Copenhagen Ole Maaløes Vej 5 2200 Copenhagen Denmark 4 The Danish Stem Cell Center Danstem University of Copenhagen Blegdamsvej 3 2200 Copenhagen Denmark 5 Centre for Epigenetics Department of Biochemistry and Molecular Biology University of Southern Denmark Campusvej 55 5230 Odense M Denmark 6 MDS and MPN Centre Institute of Hematology and Blood Diseases Hospital Chinese Academy of Medical Sciences Peking Union Medical College Tianjin 300020 China 7 The Second Affiliated Hospital to Nanchang University 1 Minde Road Nanchang Jiangxi 330006 China 8 Wellcome Trust Centre for Cell Biology University of Edinburgh Edinburgh EH9 3BF UK 9 Department of Bioanalytics Institute of Biotechnology Technische Universität Berlin 13355 Berlin Germany 10 Cognitive Systems DTU Compute Technical University of Denmark 2800 Lyngby Denmark 11 Bioinformatics Centre University of Copenhagen Ole Maaløes Vej 5 2200 Copenhagen Denmark 12 Present address Epigenetics Program Department of Biochemistry and Biophysics Perelman School of Medicine University of Pennsylvania 3400 Civic Center Blvd Philadelphia PA USA 13 Present address The Novo Nordisk Foundation Center for Basic Metabolic Research University of Copenhagen Blegdamsvej 3 2200 Copenhagen Denmark Correspondence Kristian Helin E mail kristian helin bric ku dk Tel 45 3532 5666 Fax 45 3532 5669 Xudong Wu E mail wuxudong tijmu edu cn E mail 86 8333 6825 ASXL1 mutations are frequently found in hematological tumors and loss of Asxl1 promotes myeloid transformation in mice Here we present data supporting a role for an ASXL1 BAP1 complex in the deubiqutinylation of mono ubiquitinylated lysine 119 on Histone H2A H2AK119ub1 in vivo The Polycomb group proteins control the expression of the INK4B ARF INK4A locus during normal development in part through catalyzing mono ubiquitinylation of H2AK119 Since the activation of the locus INK4B ARF INK4A plays a fail safe mechanism protecting

    Original URL path: http://www.cell-research.com/arts.asp?id=2176 (2016-02-14)
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