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  • Cell Research
    507 Survive an innate immune response through XBP1 Arthur Kaser 1 and Richard S Blumberg 2 1 Department of Medicine II Innsbruck Medical University Anichstrasse 35 A 6020 Innsbruck Austria 2 Division of Gastroenterology Hepatology and Endoscopy Department of Medicine Brigham and Women s Hospital Harvard Medical School 75 Francis Street Boston MA 02115 USA Correspondence Arthur Kaser Richard S Blumberg Tel 43 512 504 81996 1 617 732 6917

    Original URL path: http://www.cell-research.com/arts.asp?id=530 (2016-02-14)
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  • Cell Research
    Online Publication Current Issue Top 10 VOLUME 20 ISSUE 5 5 2010 508 509 Decoding the dual coding region key factors influencing the translational potential of a two ORF containing transcript Han Liang Department of Bioinformatics and Computational Biology The University of Texas M D Anderson Cancer Center 1515 Holcombe Blvd Houston TX 77030 USA Correspondence Han Liang Tel 1 713 745 9815 E mail hliang1 mdanderson org Cell Research

    Original URL path: http://www.cell-research.com/arts.asp?id=531 (2016-02-14)
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  • Cell Research
    for Biological Sciences Chinese Academy of Sciences Shanghai Jiao Tong University School of Medicine Shanghai 200025 China 2 Department of Molecular Genetics Microbiology and Immunology Robert Wood Johnson Medical School University of Medicine and Dentistry of New Jersey Piscataway NJ 08854 USA Correspondence Yufang Shi Tel 86 21 63848329 E mail shiyufang2 gmail com Mesenchymal stem cells MSCs have great potential for treating various diseases especially those related to tissue damage involving immune reactions Various studies have demonstrated that MSCs are strongly immunosuppressive in vitro and in vivo Our recent studies have shown that un stimulated MSCs are indeed incapable of immunosuppression they become potently immunosuppressive upon stimulation with the supernatant of activated lymphocytes or with combinations of IFN γ with TNF α IL 1α or IL 1β This observation revealed that under certain circumstances inflammatory cytokines can actually become immunosuppressive We showed that there is a species variation in the mechanisms of MSC mediated immunosuppression immunosuppression by cytokine primed mouse MSCs is mediated by nitric oxide NO whereas immunosuppression by cytokine primed human MSCs is executed through indoleamine 2 3 dioxygenase IDO Additionally upon stimulation with the inflammatory cytokines both mouse and human MSCs secrete several leukocyte chemokines that

    Original URL path: http://www.cell-research.com/arts.asp?id=532 (2016-02-14)
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  • Cell Research
    Hansen 1 1 Department of Biochemistry and Molecular Biology Colorado State University Fort Collins CO 80523 USA 2 Van Andel Institute Grand Rapids MI 49503 USA Correspondence Steven J McBryant Jeffrey C Hansen Tel 1 970 491 5440 1 970 491 5440 E mail Steven Mcbryant colostate edu Jeffrey c hansen colostate edu Linker histones e g H1 are best known for their ability to bind to nucleosomes and stabilize both nucleosome structure and condensed higher order chromatin structures However over the years many investigators have reported specific interactions between linker histones and proteins involved in important cellular processes The purpose of this review is to highlight evidence indicating an important alternative mode of action for H1 namely protein protein interactions We first review key aspects of the traditional view of linker histone action including the importance of the H1 C terminal domain We then discuss the current state of knowledge of linker histone interactions with other proteins and where possible highlight the mechanism of linker histone mediated protein protein interactions Taken together the data suggest a combinatorial role for the linker histones functioning both as primary chromatin architectural proteins and simultaneously as recruitment hubs for proteins involved in accessing

    Original URL path: http://www.cell-research.com/arts.asp?id=533 (2016-02-14)
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  • Cell Research
    2010 529 538 Structural insights into selective histone H3 recognition by the human Polybromo bromodomain 2 Zachary Charlop Powers Lei Zeng Qiang Zhang and Ming Ming Zhou Department of Structural and Chemical Biology Mount Sinai School of Medicine 1425 Madison Avenue Box 1677 New York NY 10029 USA Correspondence Ming Ming Zhou Tel 212 659 8652 E mail ming ming zhou mssm edu The Polybromo PB protein functions as a key component of the human PBAF chromatin remodeling complex in regulation of gene transcription PB is made up of modular domains including six bromodomains that are known as acetyl lysine binding domains However histone binding specificity of the bromodomains of PB has remained elusive In this study we report biochemical characterization of all six PB bromodomains binding to a suite of lysine acetylated peptides derived from known acetylation sites on human core histones We demonstrate that bromodomain 2 of PB preferentially recognizes acetylated lysine 14 of histone H3 H3K14ac a post translational mark known for gene transcriptional activation We further describe the molecular basis of the selective H3K14ac recognition of bromodomain 2 by solving the protein structures in both the free and bound forms using X ray crystallography and NMR

    Original URL path: http://www.cell-research.com/arts.asp?id=534 (2016-02-14)
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  • Cell Research
    Jerry D Cohen 2 and Chuanyou Li 1 1 State Key Laboratory of Plant Genomics National Centre for Plant Gene Research Institute of Genetics and Developmental Biology Chinese Academy of Sciences No 5 Datun Road Chaoyang District Beijing 100101 China 2 Department of Horticultural Science and Microbial and Plant Genomics Institute University of Minnesota Saint Paul MN 55108 USA 3 Department of Horticulture Zhejiang University Hangzhou 310029 China Correspondence Chuanyou Li Tel 86 10 64865313 E mail cyli genetics ac cn Jasmonic acid JA is a fatty acid derived signaling molecule that regulates a broad range of plant defense responses against herbivores and some microbial pathogens Molecular genetic studies have established that JA also performs a critical role in several aspects of plant development Here we describe the characterization of the Arabidopsis mutant jasmonic acid hypersensitive1 1 jah1 1 which is defective in several aspects of JA responses Although the mutant exhibits increased sensitivity to JA in root growth inhibition it shows decreased expression of JA inducible defense genes and reduced resistance to the necrotrophic fungus Botrytis cinerea Gene cloning studies indicate that these defects are caused by a mutation in the cytochrome P450 protein CYP82C2 We provide evidence showing that the compromised resistance of the jah1 1 mutant to B cinerea is accompanied by decreased expression of JA induced defense genes and reduced accumulation of JA induced indole glucosinolates IGs Conversely the enhanced resistance to B cinerea in CYP82C2 overexpressing plants is accompanied by increased expression of JA induced defense genes and elevated levels of JA induced IGs We demonstrate that CYP82C2 affects JA induced accumulation of the IG biosynthetic precursor tryptophan Trp but not the JA induced IAA or pathogen induced camalexin Together our results support a hypothesis that CYP82C2 may act in the metabolism of Trp derived

    Original URL path: http://www.cell-research.com/arts.asp?id=535 (2016-02-14)
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  • Cell Research
    Molecular Physiology Unit Laboratory of Experimental Physiology University of Ioannina Medical School 45 110 Ioannina Greece Correspondence Theodore Tzavaras Tel 0030 26510 07569 E mail thtzavar cc uoi gr The impact of long terminal repeat LTR retrotransposition on cell fate is unknown Here we investigated the effect of VL30 retrotransposition on cell death in SV40 transformed mouse SVTT1 cells Transfection of a VL30 retrotransposon decreased the clonogenicity of SVTT1 by 17 fold as compared to parental NIH3T3 cells Correlated levels of retrotransposition frequency and cell death rates were found in retrotransposition positive SVTT1 cloned cells exhibiting DNA fragmentation nuclear condensation multinucleation and cytoplasmic vacuolization Analysis of activation of effector caspases revealed a caspase independent cell death mechanism However cell death was associated with p53 induction and concomitant upregulation of PUMAα and Bax and downregulation of Bcl 2 and Hsp70 protein expression Moreover we found partial loss of colocalization of large T antigen LT p53 and p53 translocation to mitochondria leading to mitochondrial outer membrane permeabilization MOMP accompanied by lysosomal membrane permeabilization LMP Interestingly treatment with the antioxidant N acetylcysteine abolished cell death suggesting the involvement of mitochondrial derived reactive oxygen species and resulted in an increase of retrotransposition frequency Importantly

    Original URL path: http://www.cell-research.com/arts.asp?id=536 (2016-02-14)
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  • Cell Research
    Zheng 2 Lihong Ye 2 and Xiaodong Zhang 1 1 Department of Cancer Research Key Laboratory of Molecular Microbiology and Technology Ministry of Education Institute For Molecular Biology College of Life Sciences Nankai University Tianjin 300071 China 2 Department of Biochemistry The Key Laboratory of Bioactive Materials Ministry of Education College of Life Sciences Nankai University Tianjin 300071 China Correspondence Xiaodong Zhang Lihong Ye Tel 86 22 23506830 86 22 23501385 E mail zhangxd nankai edu cn yelihong nankai edu cn Hepatitis B virus X protein HBx plays a crucial role in the development of hepatocellular carcinoma Here we sought to identify the mechanisms by which HBx mediates liver cell proliferation We found that HBx upregulated the levels of cyclooxygenase 2 COX 2 5 lipoxygenase 5 LOX and phosphorylated extracellular signal regulated protein kinases 1 2 p ERK1 2 in liver cells HBx induced p ERK1 2 was abolished by inhibition of Gi o proteins COX or LOX In addition HBx increased the amounts of prostaglandin E2 PGE2 and leukotriene B4 LTB4 released from cell lines derived from hepatocytes Moreover these released arachidonic acid metabolites were able to activate ERK1 2 Interestingly activated ERK1 2 could upregulate the expression of

    Original URL path: http://www.cell-research.com/arts.asp?id=537 (2016-02-14)
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