archive-com.com » COM » C » CELL-RESEARCH.COM

Total: 1754

Choose link from "Titles, links and description words view":

Or switch to "Titles and links view".
  • Cell Research
    of Medicine Shanghai 200025 China 2 Laboratory of Clinical Immunology the Ninth People s Hospital School of Medicine Shanghai Jiao Tong University Shanghai 200011 China 3 Key Laboratory of Molecular Virology and Immunology Institut Pasteur of Shanghai Chinese Academy of Sciences Shanghai 200025 China 4 The State Key Laboratory of Cell Biology Institute of Biochemistry and Cell Biology Shanghai Institutes for Biological Sciences Chinese Academy of Sciences Shanghai 200031 China Correspondence Youcun Qian Tel 86 21 63852804 E mail ycqian sibs ac cn NOD like receptors NLRs are a family of intracellular proteins that play critical roles in innate immunity against microbial infection NLRC5 the largest member of the NLR family has recently attracted much attention However in vitro studies have reported inconsistent results about the roles of NLRC5 in host defense and in regulating immune signaling pathways The in vivo function of NLRC5 remains unknown Here we report that NLRC5 is a critical regulator of host defense against intracellular pathogens in vivo NLRC5 was specifically required for the expression of genes involved in MHC class I antigen presentation NLRC5 deficient mice showed a profound defect in the expression of MHC class I genes and a concomitant failure to activate

    Original URL path: http://www.cell-research.com/arts.asp?id=164 (2016-02-14)
    Open archived version from archive


  • Cell Research
    1 Kara M Foshay 1 1 Department of Human Genetics University of Chicago Howard Hughes Medical Institute Chicago IL 60637 USA 2 Center for Stem Cell Biology and Tissue Engineering Sun Yat sen University Guangzhou 510080 China Correspondence Bruce T Lahn E mail blahn bsd uchicago edu The progressive restriction of cell fate during lineage differentiation is a poorly understood phenomenon despite its ubiquity in multicellular organisms We recently used a cell fusion assay to define a mode of epigenetic silencing that we termed occlusion wherein affected genes are silenced by cis acting chromatin mechanisms irrespective of whether trans acting transcriptional activators are present We hypothesized that occlusion of lineage inappropriate genes could contribute to cell fate restriction Here we test this hypothesis by introducing bacterial artificial chromosomes BACs which are devoid of chromatin modifications necessary for occlusion into mouse fibroblasts We found that BAC transgenes corresponding to occluded endogenous genes are expressed in most cases whereas BAC transgenes corresponding to silent but non occluded endogenous genes are not expressed This indicates that the cellular milieu in trans supports the expression of most occluded genes in fibroblasts and that the silent state of these genes is solely the consequence of

    Original URL path: http://www.cell-research.com/arts.asp?id=165 (2016-02-14)
    Open archived version from archive

  • Cell Research
    Sciences Chinese Academy of Medical Sciences Peking Union Medical College PUMC 5 Dong Dan San Tiao Beijing 100005 China 2 Genome Structure Stability Group Disease Genomics and Individualized Medicine Laboratory Beijing Institute of Genomics Chinese Academy of Sciences Beijing 100029 China 3 Leibniz Institute for Age Research Fritz Lipmann Institute Friedrich Schiller University Jena 07745 Jena Germany 4 Faculty of Biology Pharmacy Friedrich Schiller University Jena 07745 Jena Germany Correspondence Wei Min Tong Tel 86 10 6529 5942 E mail wmtong ibms pumc edu cn Microcephaly is a clinical characteristic for human nijmegen breakage syndrome NBS mutated in NBS1 gene a chromosomal instability syndrome However the underlying molecular pathogenesis remains elusive In the present study we demonstrate that neuronal disruption of NBS Nbn in mice causes microcephaly characterized by the reduction of cerebral cortex and corpus callosum recapitulating neuronal anomalies in human NBS Nbs1 deficient neocortex shows accumulative endogenous DNA damage and defective activation of Ataxia telangiectasia and Rad3 related ATR Chk1 pathway upon DNA damage Notably in contrast to massive apoptotic cell death in Nbs1 deficient cerebella activation of p53 leads to a defective neuroprogenitor proliferation in neocortex likely via specific persistent induction of hematopoietic zinc finger Hzf that

    Original URL path: http://www.cell-research.com/arts.asp?id=166 (2016-02-14)
    Open archived version from archive

  • Cell Research
    In Sook An 1 Jongdoo Kim 1 Functional Genoproteome Research Centre Konkuk University Seoul 143 701 Korea 2 LIFEnGENE Inc Konkuk University Seoul 143 701 Korea 3 Laboratory of Radiation Tumor Physiology Korea Institute of Radiological and Medical Sciences Seoul 139 706 Korea 4 Laboratory of Functional Genomics Korea Institute of Radiological and Medical Sciences Seoul 139 706 Korea 5 Department of Chemistry Hanyang University Seoul 133 791 Korea 6 Division of Radiation Effect Research Radiation Health Research Institute of KHNP Seoul 132 703 Korea 7 Laboratory of Molecular Oncology Cheil General Hospital and Women s Healthcare Center Kwandong University College of Medicine Seoul 100 380 Korea Correspondence Sungkwan An Tel 82 2 450 4054 E mail ansfgrc konkuk ac kr The serine threonine kinase Akt functions in multiple cellular processes including cell survival and tumor development Studies of the mechanisms that negatively regulate Akt have focused on dephosphorylation mediated inactivation In this study we identified a negative regulator of Akt MULAN which possesses both a RING finger domain and E3 ubiquitin ligase activity Akt was found to directly interact with MULAN and to be ubiquitinated by MULAN in vitro and in vivo Other molecular assays demonstrated that phosphorylated Akt

    Original URL path: http://www.cell-research.com/arts.asp?id=167 (2016-02-14)
    Open archived version from archive

  • Cell Research
    of Molecular and Developmental Biology Chinese Academy of Sciences Beijing 100101 China 2 State Key Laboratory of Plant Genomics Institute of Genetics and Developmental Biology Chinese Academy of Sciences Beijing 100101 China 3 Graduate School Chinese Academy of Sciences Beijing 100309 China Correspondence Chonglin Yang E mail clyang genetics ac cn During meiotic cell division proper chromosome synapsis and accurate repair of DNA double strand breaks DSBs are required to maintain genomic integrity loss of which leads to apoptosis or meiotic defects The mechanisms underlying meiotic chromosome synapsis DSB repair and apoptosis are not fully understood Here we report that the chromodomain containing protein MRG 1 is an important factor for genomic integrity in meiosis in Caenorhabditis elegans Loss of mrg 1 function resulted in a significant increase in germ cell apoptosis that was partially inhibited by mutations affecting DNA damage checkpoint genes Consistently mrg 1 mutant germ lines exhibited SPO 11 generated DSBs and elevated exogenous DNA damage induced chromosome fragmentation at diakinesis In addition the excessive apoptosis in mrg 1 mutants was partially suppressed by loss of the synapsis checkpoint gene pch 2 and a significant number of meiotic nuclei accumulated at the leptotene zygotene stages with an

    Original URL path: http://www.cell-research.com/arts.asp?id=168 (2016-02-14)
    Open archived version from archive

  • Cell Research
    Zhen Liu 1 Quanbi Zhao 1 1 State Key Laboratory for Infectious Disease Prevention and Control National Center for AIDS STD Control and Prevention Chinese Center for Disease Control and Prevention Beijing 102206 China 2 Henan Center for Disease Control and Prevention Zhengzhou Henan 450016 China 3 Anhui Center for Disease Control and Prevention Hefei Anhui 230061 China 4 Ragon Institute of MGH MIT and Harvard Charlestown MA 02129 USA Correspondence Yiming Shao Tel 86 10 58900981 E mail yshao08 gmail com It is generally believed that CD8 cytotoxic T lymphocytes CTLs play a critical role in limiting the replication of human immunodeficiency virus type 1 HIV 1 and in determining the outcome of the infection and this effect may partly depend on which HIV product is preferentially targeted To address the correlation between HIV 1 specific CTL responses and virus replication in a cohort of former plasma donors FPDs 143 antiretroviral therapy naive FPDs infected with HIV 1 clade B strains were assessed for HIV 1 specific CTL responses with an IFN γ Elispot assay at single peptide level by using overlapping peptides OLPs covering the whole consensus clade B proteome By using a Spearman s rank correlation analysis we found that the proportion of Gag specific CTL responses among the total virus specific CTL activity was inversely correlated with viral loads while being positively correlated to CD4 counts as opposed to Pol and Env specific responses that were associated with increased viral loads and decreased CD4 counts In addition Vpr specifc CTL responses showed a similar protective effect with Gag responses but with a much lower frequency of recognition Significantly we also observed an association between HLA A 30 B 13 Cw 06 haplotype and lower viral loads that was probably due to restricted Gag specific CTL responses

    Original URL path: http://www.cell-research.com/arts.asp?id=169 (2016-02-14)
    Open archived version from archive

  • Cell Research
    Sciences Beijing 100871 China Correspondence Hongwei Guo Fengying An E mail hongweig pku edu cn fyan1204 gmail com Dark grown Arabidopsis seedlings develop an apical hook when germinating in soil which protects the cotyledons and apical meristematic tissues when protruding through the soil Several hormones are reported to distinctly modulate this process Previous studies have shown that ethylene and gibberellins GAs coordinately regulate the hook development although the underlying molecular mechanism is largely unknown Here we showed that GA3 enhanced while paclobutrazol repressed ethylene and EIN3 overexpression EIN3ox induced hook curvature and della mutant exhibited exaggerated hook curvature which required an intact ethylene signaling pathway Genetic study revealed that GA enhanced hook development was dependent on HOOKLESS 1 HLS1 a central regulator mediating the input of the multiple signaling pathways during apical hook development We further found that GA3 induced and DELLA proteins repressed HLS1 expression in an ETHYLENE INSENSITIVE 3 EIN3 LIKE 1 EIN3 EIL1 dependent manner whereby EIN3 EIL1 activated HLS1 transcription by directly binding to its promoter Additionally DELLA proteins were found to interact with the DNA binding domains of EIN3 EIL1 and repress EIN3 EIL1 regulated HLS1 expression Treatment with naphthylphthalamic acid a polar auxin transport

    Original URL path: http://www.cell-research.com/arts.asp?id=170 (2016-02-14)
    Open archived version from archive

  • Cell Research
    Rong Fang 1 Zhaoyuan Fang 1 Jufeng Xia 1 Xiangkun Han 1 Xin Yuan Liu 1 Haiquan Chen 2 3 Hongyan Liu 1 and Hongbin Ji 1 1 State Key Laboratory of Cell Biology Institute of Biochemistry and Cell Biology Shanghai Institutes for Biological Sciences Chinese Academy of Sciences Shanghai 200031 China 2 Department of Thoracic Surgery Fudan University Shanghai Cancer Center Shanghai 200032 China 3 Department of Oncology Shanghai

    Original URL path: http://www.cell-research.com/arts.asp?id=171 (2016-02-14)
    Open archived version from archive



  •