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  • Cell Research
    2013 597 598 Proteasome independent p53 degradation Mais M Nuaaman 1 and Samuel Benchimol 1 1 Department of Biology York University Toronto ON M3J 1P3 Canada Correspondence Samuel Benchimol E mail benchimo yorku ca The intracellular levels of the p53 tumor suppressor protein are regulated through various pathways and involve numerous regulatory components A recent study published in Cell Research identifies a proteasome independent pathway of p53 protein degradation in

    Original URL path: http://www.cell-research.com/arts.asp?id=1658 (2016-02-14)
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  • Cell Research
    of Radiation Oncology University of Michigan 4424B Medical Science I 1301 Catherine Street Ann Arbor MI 48109 USA 2 Department of Oncology the Second Affiliated Hospital of Nanchang University 1 Minde Road Nanchang Jiangxi 330006 China 3 Department of Pathology Beth Israel Deaconess Medical Center Harvard Medical School Boston MA 02215 USA Correspondence Yi Sun E mail sunyi umich edu The SCF SKP1 S phase kinase associated protein 1 Cullin 1 F box protein E3 ubiquitin ligases the founding member of Cullin RING ligases CRLs are the largest family of E3 ubiquitin ligases in mammals Each individual SCF E3 ligase consists of one adaptor protein SKP1 one scaffold protein cullin 1 the first family member of the eight cullins one F box protein out of 69 family members and one out of two RING Really Interesting New Gene family proteins RBX1 ROC1 or RBX2 ROC2 SAG RNF7 Various combinations of these four components construct a large number of SCF E3s that promote the degradation of many key regulatory proteins in cell context temporally and spatially dependent manners thus controlling precisely numerous important cellular processes including cell cycle progression apoptosis gene transcription signal transduction DNA replication maintenance of genome integrity and tumorigenesis To understand how the SCF E3 ligases regulate these cellular processes and embryonic development under in vivo physiological conditions a number of mouse models with transgenic Tg expression or targeted deletion of components of SCF have been established and characterized In this review we will provide a brief introduction to the ubiquitin proteasome system UPS and the SCF E3 ubiquitin ligases followed by a comprehensive overview on the existing Tg and knockout KO mouse models of the SCF E3s and discuss the role of each component in mouse embryogenesis cell proliferation apoptosis carcinogenesis as well as other pathogenic processes

    Original URL path: http://www.cell-research.com/arts.asp?id=1659 (2016-02-14)
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  • Cell Research
    College of Animal Sciences Ministry of Education Zhejiang University 866 Yu Hang Tang Road Hangzhou Zhejiang 310058 China 2 College of Life Sciences Zhejiang University 866 Yu Hang Tang Road Hangzhou Zhejiang 310058 China 3 p53 Laboratory Agency for Science and Technology Research 8A Biomedical Grove 6 06 Immunos Singapore 138648 Correspondence Jinrong Peng Jun Chen David P Lane E mail pengjr zju edu cn chenjun2009 zju edu cn dplane p53Lab a star edu sg p53 protein turnover through the ubiquitination pathway is a vital mechanism in the regulation of its transcriptional activity however little is known about p53 turnover through proteasome independent pathway s The digestive organ expansion factor Def protein is essential for the development of digestive organs In zebrafish loss of function of def selectively upregulates the expression of p53 response genes which raises a question as to what is the relationship between Def and p53 We report here that Def is a nucleolar protein and that loss of function of def leads to the upregulation of p53 protein which surprisingly accumulates in the nucleoli Our extensive studies have demonstrated that Def can mediate the degradation of p53 protein and that this process is independent of the

    Original URL path: http://www.cell-research.com/arts.asp?id=1660 (2016-02-14)
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  • Cell Research
    Shi 1 2 3 1 Ministry of Education Key Laboratory of Protein Science School of Life Sciences and School of Medicine Tsinghua University Beijing 100084 China 2 Tsinghua Peking Joint Center for Life Sciences School of Life Sciences and School of Medicine Tsinghua University Beijing 100084 China 3 Center for Structural Biology School of Life Sciences and School of Medicine Tsinghua University Beijing 100084 China 4 Ministry of Education Key Laboratory of Bioinformatics School of Life Sciences and School of Medicine Tsinghua University Beijing 100084 China Correspondence Yigong Shi E mail shi lab tsinghua edu cn Bacteria exemplified by enteropathogenic Escherichia coli E coli rely on elaborate acid resistance systems to survive acidic environment such as the stomach Comprehensive understanding of bacterial acid resistance is important for prevention and clinical treatment In this study we report a previously uncharacterized type of acid resistance system in E coli that relies on L glutamine Gln one of the most abundant food borne free amino acids Upon uptake into E coli Gln is converted to L glutamate Glu by the acid activated glutaminase YbaS with concomitant release of gaseous ammonia The free ammonia neutralizes proton resulting in elevated intracellular pH under acidic environment

    Original URL path: http://www.cell-research.com/arts.asp?id=1661 (2016-02-14)
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  • Cell Research
    3 4 1 College of Life Sciences Beijing Normal University Beijing 100875 China 2 National Institute of Biological Sciences Zhongguancun Life Science Park Beijing 102206 China 3 Tsinghua Peking Center for Life Sciences Beijing 100084 China 4 School of Life Sciences Tsinghua University Beijing 100084 China 5 Graduate Program Chinese Academy of Medical Sciences and Peking Union Medical College Beijing 100730 China 6 College of Biological Sciences China Agricultural University Beijing 100193 China 7 Shanghai Institute of Plant Physiology and Ecology Chinese Academy of Sciences Shanghai 200032 China 8 Michael Smith Laboratories University of British Columbia Vancouver BC Canada V6T 1Z4 Correspondence Yijun Qi Tel 86 10 62793132 E mail qiyijun biomed tsinghua edu cn microRNAs miRNAs play important roles in the regulation of gene expression In Arabidopsis mature miRNAs are processed from primary miRNA transcripts pri miRNAs by nuclear HYL1 SE DCL1 complexes that form Dicing bodies D bodies Here we report that an RNA binding protein MOS2 binds to pri miRNAs and is involved in efficient processing of pri miRNAs MOS2 does not interact with HYL1 SE and DCL1 and is not localized in D bodies Interestingly in the absence of MOS2 the recruitment of pri miRNAs by

    Original URL path: http://www.cell-research.com/arts.asp?id=1662 (2016-02-14)
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  • Cell Research
    Regenerative Medicine MC1528B Department of Medicine Loma Linda University Loma Linda CA 92354 USA 2 Division of Anatomy Loma Linda University Loma Linda CA 92354 USA 3 Center for Health Disparities and Molecular Medicine Loma Linda University Loma Linda CA 92354 USA 4 Stem Cells and Regeneration Program School of Biomedical Sciences Department of Orthopaedics and Traumatology Li Ka Shing Institute of Health Sciences The Chinese University of Hong Kong Prince of Wales Hospital Shatin Hong Kong SAR China 5 Department of Radiation Medicine Loma Linda University Loma Linda CA 92354 USA 6 Department of Pathology Loma Linda University Loma Linda CA 92354 USA 7 Musculoskeletal Disease Center Jerry L Pettis Memorial VA Medical Center Loma Linda CA 92354 USA Correspondence Xiao Bing Zhang Tel 1 909 651 5886 E mail xzhang llu edu The direct conversion of skin cells into somatic stem cells has opened new therapeutic possibilities in regenerative medicine Here we show that human induced mesenchymal stem cells iMSCs can be efficiently generated from cord blood CB or adult peripheral blood PB CD34 cells by direct reprogramming with a single factor OCT4 In the presence of a GSK3 inhibitor 16 of the OCT4 transduced CD34 cells are converted into iMSCs within 2 weeks Efficient direct reprogramming is achieved with both episomal vector mediated transient OCT4 expression and lentiviral vector mediated OCT4 transduction The iMSCs express MSC markers resemble bone marrow BM MSCs in morphology and possess in vitro multilineage differentiation capacity yet have a greater proliferative capacity compared with BM MSCs Similar to BM MSCs the implanted iMSCs form bone and connective tissues and are non tumorigenic in mice However BM MSCs do not whereas iMSCs do form muscle fibers indicating a potential functional advantage of iMSCs In addition we observed that a high level of OCT4

    Original URL path: http://www.cell-research.com/arts.asp?id=1663 (2016-02-14)
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  • Cell Research
    Chartier 1 Xavier De Deken 3 Emmanuelle Brochiero 1 4 Françoise Miot 3 and Nathalie Grandvaux 1 2 1 Centre de Recherche du CHUM CRCHUM Montréal Québec Canada H2X 1P1 2 Department of Biochemistry Faculty of Medicine Université de Montréal Québec Canada H3T 1J4 3 Institut de Recherche Interdisciplinaire en Biologie Humaine et Moléculaire Université Libre de Bruxelles Campus Erasme 1070 Brussels Belgium 4 Department of Medicine Faculty of Medicine Université de Montréal Montréal Québec Canada H3T 1J4 Correspondence Nathalie Grandvaux Tel 1 514 890 8000 ext 35292 E mail nathalie grandvaux umontreal ca Airway epithelial cells are key initial innate immune responders in the fight against respiratory viruses primarily via the secretion of antiviral and proinflammatory cytokines that act in an autocrine paracrine fashion to trigger the establishment of an antiviral state It is currently thought that the early antiviral state in airway epithelial cells primarily relies on IFNβ secretion and the subsequent activation of the interferon stimulated gene factor 3 ISGF3 transcription factor complex composed of STAT1 STAT2 and IRF9 which regulates the expression of a panoply of interferon stimulated genes encoding proteins with antiviral activities However the specific pathways engaged by the synergistic action of different cytokines during viral infections and the resulting physiological outcomes are still ill defined Here we unveil a novel delayed antiviral response in the airways which is initiated by the synergistic autocrine paracrine action of IFNβ and TNFα and signals through a non canonical STAT2 and IRF9 dependent but STAT1 independent cascade This pathway ultimately leads to the late induction of the DUOX2 NADPH oxidase expression Importantly our study uncovers that the development of the antiviral state relies on DUOX2 dependent H2O2 production Key antiviral pathways are often targeted by evasion strategies evolved by various pathogenic viruses In this regard the importance

    Original URL path: http://www.cell-research.com/arts.asp?id=1664 (2016-02-14)
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  • Cell Research
    Zhang 4 Fei Sun 6 Shuang Huang 4 and Honglin Li 4 1 Cancer Center University of Illinois at Chicago Chicago IL 60612 USA 2 Shanghai Institute of Biochemistry and Cell Biology Shanghai 200031 China 3 Cambridge Institute for Medical Research Department of Medical Genetics University of Cambridge Cambridge CB2 0XY UK 4 Department of Biochemistry and Molecular Biology Cancer Center Georgia Health Sciences University Augusta GA 30912 USA 5 Department of Oncology Tongji Hospital Tongji Medical College Huazhong University of Science Technology Wuhan 430030 China 6 Department of Physiology Wayne State University Detroit MI 48202 USA Correspondence Honglin Li Tel 1 706 721 6143 E mail hli gru edu Apoptotic nucleus undergoes distinct morphological and biochemical changes including nuclear shrinkage chromatin condensation and DNA fragmentation which are attributed to caspase mediated cleavage of several nuclear substrates such as lamins As most of active caspases reside in the cytoplasm disruption of the nuclear cytoplasmic barrier is essential for caspases to reach their nuclear targets The prevailing proposed mechanism is that the increase in the permeability of nuclear pores induced by caspases allows the caspases and other apoptotic factors to diffuse into the nucleus thereby resulting in the nuclear destruction Here we report a novel observation that physical rupture of the nuclear envelope NE occurs in the early stage of apoptosis We found that the NE rupture was caused by caspase mediated cleavage of C53 LZAP a protein that has been implicated in various signaling pathways including NF κB signaling and DNA damage response as well as tumorigenesis and metastasis We also demonstrated that C53 LZAP bound indirectly to the microtubule MT and expression of the C53 LZAP cleavage product caused abnormal MT bundling and NE rupture Taken together our findings suggest a novel role of C53 LZAP in the regulation

    Original URL path: http://www.cell-research.com/arts.asp?id=1665 (2016-02-14)
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