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  • Cell Research
    Guo Key Laboratory of Nutrition and Metabolism Institute for Nutritional Sciences Shanghai Institute for Biological Sciences Chinese Academy of Sciences The Graduate School of the Chinese Academy of Sciences 294 Taiyuan Road Shanghai 200031 China Correspondence Feifan Guo Tel 86 21 54920250 E mail ffguo sibs ac cn Activating transcription factor 4 ATF4 has been shown to play key roles in many physiological processes There are no reports however demonstrating a direct link between ATF4 and lipid metabolism We noticed that Atf4 deficient mice are lean suggesting a possible role for ATF4 in regulating lipid metabolism The goal of our current study is to investigate the involvement of ATF4 in lipid metabolism and elucidate the underlying mechanisms Studies using Atf4 deficient mice revealed increased energy expenditure as measured by oxygen consumption These mice also showed increases in lipolysis expression of uncoupling protein 2 UCP2 and β oxidation genes and decreases in expression of lipogenic genes in white adipose tissue WAT suggesting increased utilization and decreased synthesis of fatty acids respectively Expression of UCP1 2 and 3 was also increased in brown adipose tissue BAT suggesting increased thermogenesis The effect of ATF4 deletion on expression of UCPs in BAT suggests that

    Original URL path: http://www.cell-research.com/arts.asp?id=577 (2016-02-14)
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  • Cell Research
    Hugues de The 2 4 Sai Juan Chen 1 2 Zhu Chen 1 2 Ting Xi Liu 3 and Jun Zhu 2 1 State Key Laboratory of Medical Genomics Institute of Health Science Shanghai Institutes for Biological Sciences and Graduate School Chinese Academy of Sciences and Shanghai Jiao Tong University School of Medicine 225 Chong Qing South Road Shanghai 200025 China 2 CNRS LIA Shanghai Institute of Hematology Rui Jin Hospital 197 Rui Jin Road II Shanghai 200025 China 3 Laboratory of Development and Diseases Institute of Health Science Shanghai Institutes for Biological Sciences and Graduate School Chinese Academy of Sciences and Shanghai Jiao Tong University School of Medicine 225 Chong Qing South Road Shanghai 200025 China 4 CNRS UMR 7151 Hopital Saint Louis 1 Avenue C Vellefaux 75475 Paris Cedex 10 France Correspondence Jun Zhu Ting Xi Liu Zhu Chen E mail jzhu1966 yahoo com cn txliu sibs ac cn zchen stn sh cn The Small ubiquitin related modifier SUMO conjugation to a variety of proteins regulates diverse cellular processes including transcription cell cycle regulation and maintenance of genome integrity To investigate in vivo biological function of SUMO paralogs we inactivated them in the early development of zebrafish While zebrafish embryos deficient for all three SUMO paralogs as Ubc9 deficient ones displayed severe defects loss of individual SUMO paralog was compatible with a normal development SUMO deficient embryos can be rescued by a single human or zebrafish SUMO While key structural basic lysine residues and N terminal unstructured stretch of SUMO are critical for in vivo rescue the consensus K11 sumoylation site of SUMO2 is dispensable implying that chain formation on this potential site is unessential for normal development Inactivation of all three SUMOs triggered p53 dependent apoptosis and further inactivation of p53 restored normal zebrafish development Interestingly we

    Original URL path: http://www.cell-research.com/arts.asp?id=578 (2016-02-14)
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  • Cell Research
    of Biochemistry and Cell Biology Shanghai Institute for Biological Sciences Chinese Academy of Sciences 320 Yue Yang Road Shanghai 200031 China 2 Graduate University of the Chinese Academy of Sciences 320 Yue Yang Road Shanghai 200031 China 3 Department of Medical Microbiology and Parasitology Institutes of Medical Sciences Shanghai Jiao Tong University School of Medicine Shanghai 200025 China 4 State Key Laboratory for Disease and Health Genomics Chinese National Human Genome Center at Shanghai Zhangjiang High Tech Park Shanghai 201203 China Correspondence Rong Zeng Guo Ping Zhao E mail zr sibs ac cn gpzhao sibs ac cn Leptospirosis is a widespread zoonotic disease caused by pathogenic spirochetes of the genus Leptospira that infects humans and a wide range of animals By combining computational prediction and high accuracy tandem mass spectra we revised the genome annotation of Leptospira interrogans serovar Lai a free living pathogenic spirochete responsible for leptospirosis providing substantial peptide evidence for novel genes and new gene boundaries Subsequently we presented a high coverage proteome analysis of protein expression and multiple posttranslational modifications PTMs Approximately 64 3 of the predicted L interrogans proteins were cataloged by detecting 2 540 proteins Meanwhile a profile of multiple PTMs was concurrently established

    Original URL path: http://www.cell-research.com/arts.asp?id=579 (2016-02-14)
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  • Cell Research
    1 3 Zhigang Lu 1 and Zhonghe Zhai 4 1 Laboratory of Chemical Genomics School of Chemical Biology and Biotechnology Shenzhen Graduate School of Peking University Shenzhen 518055 China 2 Institute of Life Sciences YunYang Medical College Tai he Hospital 32 S Renmin Road Shiyan Hubei 442000 China 3 Department of Applied Biology Chemical Technology The Hong Kong Polytechnic University Hung Hom Kowloon Hong Kong 4 College of Life Science Peking University Beijing 100871 China Correspondence Zhigang Lu Tel 86 755 2603 6175 E mail luzg szpku edu cn As a critical apoptosis executioner caspase 3 becomes activated and then enters into the nucleus to exert its function However the molecular mechanism of this nuclear entry of active caspase 3 is still unknown In this study we revealed that caspase 3 harbors a crm 1 independent nuclear export signal NES in its small subunit Using reverse caspase 3 as the study model we found that the function of the NES in caspase 3 was not disturbed by the conformational changes during induced caspase 3 activation Mutations disrupting the cleavage activity or p3 recognition site resulted in a defect in the nuclear entry of active caspase 3 We provide evidence that

    Original URL path: http://www.cell-research.com/arts.asp?id=580 (2016-02-14)
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  • Cell Research
    Chinese Academy of Medical Sciences School of Basic Medicine Peking Union Medical College Beijing 100005 China Correspondence Wei Zhang Tel 86 10 65296417 E mail wzhang pumc edu cn FcαR the Fc receptor for IgA is essential for IgA mediated immune responses Previous studies have shown that IgA and IgA immune complexes can be rapidly endocytosed by FcαR However the underlying mechanism remains unclear Here we investigated the endocytic pathway of FcαR in monocytic cell line U937 that naturally express FcαR and in transfected Chinese hamster ovary CHO COS 7 and Hela cells By using selective chemical inhibitors of different endocytic pathways overexpression of dominant negative mutants of Eps15 and knockdown of clathrin heavy chain CHC via RNA interference we demonstrated that endocytosis of FcαR was through a clathrin mediated pathway The endocytosed FcαR went into Rab5 and Rab11 positive endosomes However endocytosis of FcαR could not be blocked by a dominant negative mutant of Rab5 We also demonstrated that endocytosis of FcαR was dynamin dependent by overexpressing a dominant negative mutant of dynamin The potential endocytic motif for FcαR was also examined Unexpectedly we found that the entire cytoplasmic domain of FcαR was not required for the endocytic process

    Original URL path: http://www.cell-research.com/arts.asp?id=581 (2016-02-14)
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  • Cell Research
    Chen 1 2 3 Qiang Wei 1 2 3 Jing Zhang 1 2 3 Chuangkun Xu 4 Tao Tan 1 2 3 and Weizhi Ji 1 3 1 Kunming Primate Research Center and Laboratory of Reproductive and Developmental Biology Kunming Institute of Zoology Chinese Academy of Sciences Kunming 650223 China 2 Graduate University of the Chinese Academy of Sciences Beijing 100049 China 3 Yunnan Key Laboratory of Animal Reproductive Biology

    Original URL path: http://www.cell-research.com/arts.asp?id=582 (2016-02-14)
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  • Cell Research
    2 2010 242 245 Activation of JNK signaling links lgl mutations to disruption of the cell polarity and epithelial organization in Drosophila imaginal discs Activation of JNK signaling links lgl mutations to disruption of the cell polarity and epithelial organization in Drosophila imaginal discs Activation of JNK signaling links lgl mutations to disruption of the cell polarity and epithelial organization in Drosophila imaginal discs Correspondence Mingfa Li Tel 86 21

    Original URL path: http://www.cell-research.com/arts.asp?id=583 (2016-02-14)
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  • Cell Research

    (No additional info available in detailed archive for this subpage)
    Original URL path: /artsmore1.asp?id=40 (2016-02-14)




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