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  • Cell Research
    2012 impact factor 10 526 Thomson Reuters 2013 Free Sample Issue Submission Advanced Online Publication Current Issue Top 10 VOLUME 25 ISSUE 3 3 2015 398 398 Structural basis of AMPK regulation by adenine nucleotides and glycogen FREE Xiaodan Li Lili Wang X Edward Zhou Jiyuan Ke Parker W de Waal Xin Gu M H Eileen Tan Dongye Wang Donghai Wu H Eric Xu and Karsten Melcher 10 1038 cr

    Original URL path: http://www.cell-research.com/arts.asp?id=2081 (2016-02-14)
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  • Cell Research
    2015 399 400 Anticancer immunotherapy by CTLA 4 blockade obligatory contribution of IL 2 receptors and negative prognostic impact of soluble CD25 FREE Dalil Hannani Marie Vétizou David Enot Sylvie Rusakiewicz Nathalie Chaput David Klatzmann Melanie Desbois Nicolas Jacquelot Nadège Vimond Salem Chouaib Christine Mateus James P Allison Antoni Ribas Jedd D Wolchok Jianda Yuan Philip Wong Michael Postow Andrzej Mackiewicz Jacek Mackiewicz Dirk Schadendorff Dirk Jaeger Alan J Korman

    Original URL path: http://www.cell-research.com/arts.asp?id=2082 (2016-02-14)
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  • Cell Research

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    Original URL path: /artsmore1.asp?id=181 (2016-02-14)


  • Cell Research
    of Bio membrane and Membrane Biotechnology Beijing 100084 China 2 Center for Structural Biology Tsinghua Peking Joint Center for Life Sciences School of Life Sciences and School of Medicine Tsinghua University Beijing 100084 China 3 Department of Cell Biology Johns Hopkins University School of Medicine Baltimore MD 21205 USA Correspondence Nieng Yan Peter Espenshade E mail nyan tsinghua edu cn peter espenshade jhmi edu The sterol regulatory element binding protein SREBP and SREBP cleavage activating protein SCAP are central players in the SREBP pathway which control the cellular lipid homeostasis SCAP binds to SREBP through their carboxyl C domains and escorts SREBP from the endoplasmic reticulum to the Golgi upon sterol depletion A conserved pathway with the homologues of SREBP and SCAP being Sre1 and Scp1 was identified in fission yeast Schizosaccharomyces pombe Here we report the in vitro reconstitution of the complex between the C domains of Sre1 and Scp1 as well as the crystal structure of the WD40 domain of Scp1 at 2 1 Å resolution The structure reveals an eight bladed β propeller that exhibits several distinctive features from a canonical WD40 repeat domain Structural and biochemical characterization led to the identification of two Scp1 elements that

    Original URL path: http://www.cell-research.com/arts.asp?id=2083 (2016-02-14)
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  • Cell Research
    Genetics KU Leuven Leuven B 3000 Belgium 3 Centre de Recherche en Cancérologie de Marseille CRCM Aix Marseille Université Marseille F 13284 France Inserm U1068 Institut Paoli Calmettes CNRS UMR7258 Marseille F 13009 France Correspondence Guido David Tel 32 472 636349 E mail guido david med kuleuven be Pascale Zimmermann E mail pascale zimmermann med kuleuven be Exosomes are secreted vesicles of endosomal origin involved in signaling processes We recently showed that the syndecan heparan sulfate proteoglycans control the biogenesis of exosomes through their interaction with syntenin 1 and the endosomal sorting complex required for transport accessory component ALIX Here we investigated the role of heparanase the only mammalian enzyme able to cleave heparan sulfate internally in the syndecan syntenin ALIX exosome biogenesis pathway We show that heparanase stimulates the exosomal secretion of syntenin 1 syndecan and certain other exosomal cargo such as CD63 in a concentration dependent manner In contrast exosomal CD9 CD81 and flotillin 1 are not affected Conversely reduction of endogenous heparanase reduces the secretion of syntenin 1 containing exosomes The ability of heparanase to stimulate exosome production depends on syntenin 1 and ALIX Syndecans but not glypicans support exosome biogenesis in heparanase exposed cells Finally heparanase

    Original URL path: http://www.cell-research.com/arts.asp?id=2084 (2016-02-14)
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  • Cell Research
    Michael Hölzel 2 4 Wouter Nijkamp 2 Lodewyk FA Wessels 2 Roderick L Beijersbergen 2 Rene Bernards 2 and Sidong Huang 1 1 Department of Biochemistry The Rosalind and Morris Goodman Cancer Centre McGill University Montreal QC H3G 1Y6 Canada 2 Division of Molecular Carcinogenesis Cancer Systems Biology Centre and Cancer Genomics Centre The Netherlands Cancer Institute Plesmanlaan 121 1066 CX Amsterdam The Netherlands 3 Institute for Systems Biology 401 Terry Avenue North Seattle WA 98109 5234 USA 4 Current address Unit for RNA Biology Department of Clinical Chemistry and Clinical Pharmacology University of Bonn 53105 Bonn Germany Correspondence Sidong Huang Tel 1 514 398 4447 Rene Bernards Tel 31 20 512 1952 E mail sidong huang mcgill ca r bernards nki nl Recurrent inactivating mutations in components of SWI SNF chromatin remodeling complexes have been identified across cancer types supporting their roles as tumor suppressors in modulating oncogenic signaling pathways We report here that SMARCE1 loss induces EGFR expression and confers resistance to MET and ALK inhibitors in non small cell lung cancers NSCLCs We found that SMARCE1 binds to regulatory regions of the EGFR locus and suppresses EGFR transcription in part through regulating expression of Polycomb Repressive Complex

    Original URL path: http://www.cell-research.com/arts.asp?id=2086 (2016-02-14)
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  • Cell Research
    of Molecular Biology Shanghai Key Laboratory of Molecular Andrology Institute of Biochemistry and Cell Biology Shanghai Institutes for Biological Sciences Chinese Academy of Sciences Shanghai 200031 China 2 CAS Key Laboratory of Computational Biology CAS Center for Excellence in Brain Science CAS MPG Partner Institute for Computational Biology Shanghai Institutes for Biological Sciences Chinese Academy of Sciences Shanghai 200031 China 3 Department of Neuroscience University of Connecticut Stem Cell Institute University of Connecticut Health Center Farmington CT 06030 USA 4 School of Life Science and Technology ShanghaiTech University Shanghai 200031 China Correspondence Li Yang Ling Ling Chen E mail liyang picb ac cn linglingchen sibcb ac cn Adenosine deaminases acting on RNA ADARs are involved in adenosine to inosine RNA editing and are implicated in development and diseases Here we observed that ADAR1 deficiency in human embryonic stem cells hESCs significantly affected hESC differentiation and neural induction with widespread changes in mRNA and miRNA expression including upregulation of self renewal related miRNAs such as miR302s Global editing analyses revealed that ADAR1 editing activity contributes little to the altered miRNA mRNA expression in ADAR1 deficient hESCs upon neural induction Genome wide iCLIP studies identified that ADAR1 binds directly to pri miRNAs

    Original URL path: http://www.cell-research.com/arts.asp?id=2087 (2016-02-14)
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  • Cell Research
    Biology Shanghai Institute of Biochemistry and Cell Biology Shanghai Institutes for Biological Sciences Chinese Academic of Sciences Shanghai 200031 China 2 Eastern Hepatobilliary Surgery Hospital Second Military Medical University Shanghai 200438 China 3 Key Laboratory of Systems Biology Shanghai Institutes for Biological Sciences Chinese Academy of Sciences Shanghai 200031 China 4 Department of Hepatobiliary Surgery the Affiliated Drum Tower Hospital of Nanjing University Medical School Nanjing 210000 China 5 Fudan University Shanghai Cancer Center and Institutes of Biomedical Sciences Shanghai Medical College Fudan University Shanghai 200032 China Correspondence Lijian Hui Xiaolei Shi E mail ljhui sibcb ac cn njsxl2000 163 com Liver and kidney cancers are notorious for drug resistance Due to the complexity redundancy and interpatient heterogeneity of resistance mechanisms most efforts targeting a single pathway were unsuccessful Novel personalized therapies targeting multiple essential drug resistance pathways in parallel hold a promise for future cancer treatment Exploiting the multitarget characteristic of microRNAs miRNAs we developed a new therapeutic strategy by the combinational use of miRNA and anticancer drugs to increase drug response By a systems approach we identified that miR 27b a miRNA deleted in liver and kidney cancers sensitizes cancer cells to a broad spectrum of anticancer drugs

    Original URL path: http://www.cell-research.com/arts.asp?id=2088 (2016-02-14)
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