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  • Cell Research
    Kimberly S Schluns 1 Mary Hall 1 Huiyuan 1 Department of Immunology Unit 902 The University of Texas MD Anderson Cancer Center 7455 Fannin Street Houston TX 77054 USA 2 Immune Regulation Laboratory Institut de Recherches Cliniques de Montr閍l IRCM Montr閍l QC Canada H2W 1R7 3 The Campbell Family Institute for Breast Cancer Research University Health Network Toronto ON Canada M5G 2C1 4 Department of Biochemistry and Molecular Biology The University of Texas Houston Medical School Houston TX 77030 USA Correspondence Hector Martinez Valdez Tel 1 713 563 3212 E mail hmartine mdanderson org Gene expression can be regulated by chromatin modifiers transcription factors and proteins that modulate DNA architecture Among the latter AT hook transcription factors have emerged as multifaceted regulators that can activate or repress broad A T rich gene networks Thus alterations of AT hook genes could affect the transcription of multiple genes causing global cell dysfunction Here we report that targeted deletions of mouse AKNA a hypothetical AT hook like transcription factor sensitize mice to pathogen induced inflammation and cause sudden neonatal death Compared with wild type littermates AKNA KO mice appeared weak failed to thrive and most died by postnatal day 10 Systemic inflammation predominantly in the lungs was accompanied by enhanced leukocyte infiltration and alveolar destruction Cytologic immunohistochemical and molecular analyses revealed CD11b Gr1 neutrophils as major tissue infiltrators neutrophilic granule protein cathelin related antimicrobial peptide and S100A8 9 as neutrophil specific chemoattracting factors interleukin 1β and interferon γ as proinflammatory mediators and matrix metalloprotease 9 as a plausible proteolytic trigger of alveolar damage AKNA KO bone marrow transplants in wild type recipients reproduced the severe pathogen induced reactions and confirmed the involvement of neutrophils in acute inflammation Moreover promoter reporter experiments showed that AKNA could act as a gene repressor Our results support

    Original URL path: http://www.cell-research.com/arts.asp?id=271 (2016-02-14)
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  • Cell Research
    0192 Japan 2 Department of Pathology and Applied Neurobiology Graduate School of Medical Sciences Kyoto Prefectural University of Medicine Kawaramachi Hirokoji Kajii cho Kamigyo ku Kyoto 602 8566 Japan Correspondence Eishou Matsuda Tel 81 743 72 5537 E mail ematsuda bs naist jp Postnatal growth and regeneration of skeletal muscle are carried out mainly by satellite cells which upon stimulation begin to express myogenin Myog the critical determinant of myogenic differentiation DNA methylation status has been associated with the expression of Myog but the causative mechanism remains almost unknown Here we report that the level of CIBZ a methyl CpG binding protein decreases upon myogenic differentiation of satellite derived C2C12 cells and during skeletal muscle regeneration in mice We present data showing that the loss of CIBZ promotes myogenic differentiation whereas exogenous expression of CIBZ impairs it in cultured cells CIBZ binds to a Myog promoter proximal region and inhibits Myog transcription in a methylation dependent manner These data suggest that the suppression of myogenic differentiation by CIBZ is dependent at least in part on the regulation of Myog Our data show that the methylation status of this proximal Myog promoter inversely correlates with Myog transcription in cells and tissues

    Original URL path: http://www.cell-research.com/arts.asp?id=272 (2016-02-14)
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  • Cell Research
    STAR Brenner Centre for Molecular Medicine 30 Medical Drive Singapore 117609 3 Center for Integrative Genomics NCCR Frontiers in Genetics University of Lausanne Lausanne Switzerland 4 Department of Biochemistry Yong Loo Lin School of Medicine National University of Singapore Singapore Correspondence Ravi Kambadur Tel 65 6513 8043 E mail KRavi ntu eud sg TGF β and myostatin are the two most important regulators of muscle growth Both growth factors have been shown to signal through a Smad3 dependent pathway However to date the role of Smad3 in muscle growth and differentiation is not investigated Here we demonstrate that Smad3 null mice have decreased muscle mass and pronounced skeletal muscle atrophy Consistent with this we also find increased protein ubiquitination and elevated levels of the ubiquitin E3 ligase MuRF1 in muscle tissue isolated from Smad3 null mice Loss of Smad3 also led to defective satellite cell SC functionality Smad3 null SCs showed reduced propensity for self renewal which may lead to a progressive loss of SC number Indeed decreased SC number was observed in skeletal muscle from Smad3 null mice showing signs of severe muscle wasting Further in vitro analysis of primary myoblast cultures identified that Smad3 null myoblasts exhibit impaired

    Original URL path: http://www.cell-research.com/arts.asp?id=273 (2016-02-14)
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  • Cell Research
    Cai 1 3 Ge Gao 2 Wenxia Zhang 1 Zuoyan Zhu 1 Dong Liu 1 and Qichang Fan 1 1 The Education Ministry Key Laboratory of Cell Proliferation and Differentiation and the State Key Laboratory of Bio membrane and Membrane Bio engineering Peking University 5 Summer Palace Road Beijing 100871 China 2 The Center for Bioinformatics School of Life Sciences Peking University 5 Summer Palace Road Beijing 100871 China 3 Current address Department of Obstetrics and Gynecology Indiana University School of Medicine Indianapolis Indianapolis IN 46202 USA Correspondence Dong Liu Qichang Fan E mail doliu pku edu cn qfan pku edu cn MicroRNA miRNA regulates gene expression in many cellular events yet functions of only a few miRNAs are known in C elegans We analyzed the function of mir 35 41 unique to the worm and show here that mir 35 regulates the G1 S transition of intestinal cells and germ cell proliferation Loss of mir 35 leads to a decrease of nuclei numbers in intestine and distal mitotic gonad while re introduction of mir 35 rescues the mutant phenotypes Genetic analysis indicates that mir 35 may act through Rb E2F and SCF pathways Further bioinformatic and functional analyses demonstrate

    Original URL path: http://www.cell-research.com/arts.asp?id=274 (2016-02-14)
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  • Cell Research
    Yang Zhao 1 Wei Li 1 5 Yi Bo Wu 2 Hai Jiang Zhang 1 Hua Jun Wu 3 5 1 State Key Laboratory of Reproductive Biology Institute of Zoology Chinese Academy of Sciences Beijing 100101 China 2 State Key Laboratory of Reproductive Medicine Nanjing Medical University Nanjing 210029 China 3 Institute of Genetics and Developmental Biology Chinese Academy of Sciences Beijing 100101 China 4 Shanghai Institute of Medical Genetics

    Original URL path: http://www.cell-research.com/arts.asp?id=276 (2016-02-14)
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  • Cell Research
    beta lactoglobulin BLG gene via zinc finger nucleases in cattle Shengli Yu 1 Junjie Luo 1 Zhiyuan Song 1 Fangrong Ding 2 Yunping Dai 1 2 and Ning Li 1 1 State Key Laboratory for Agrobiotechnology College of Biological Science China Agricultural University No 2 Yuanmingyuan West Road Haidian District Beijing 100193 China 2 Beijing GenProtein Biotechnology Co Ltd Room 306 Zhongding Building Malianwa North Road No 158 Haidian District

    Original URL path: http://www.cell-research.com/arts.asp?id=277 (2016-02-14)
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  • Cell Research
    Reuters 2013 Free Sample Issue Submission Advanced Online Publication Current Issue Top 10 VOLUME 21 ISSUE 11 11 2011 1642 1642 From the Gla domain to a novel small molecule detector of apoptosis Avi Cohen Anat Shirvan Galit Levin Hagit Grimberg Ayelet Reshef and Ilan Ziv Aposense Ltd 5 7 Ha Odem St Kiryat Matalon PO Box 7119 Petach Tikva Israel Cell Research 2011 21 1642 doi 10 1038 cr

    Original URL path: http://www.cell-research.com/arts.asp?id=279 (2016-02-14)
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  • Cell Research

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    Original URL path: /artsmore1.asp?id=19 (2016-02-14)




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