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  • Cell Research
    Advanced Online Publication Current Issue Top 10 VOLUME 11 ISSUE 1 1 2005 43 48 Nucleo cytoplasmic communication in apoptotic response to genotoxic and inflammatory stress Jean Y J WANG Division of Biological Sciences and Moores Cancer Center University of California San Diego La Jolla CA 92093 0322 USA Correspondence Jean Y J WANG Tel 858 534 6253 E mail jywang ucsd edu Genotoxic agents or inflammatory cytokines activate cellular stress responses and trigger programmed cell death We have identified a signal transduction module including three nuclear proteins that participate in the regulation of cell death induced by chemotherapeutic agents and tumor necrosis factor TNF In this nuclear signaling module retinoblastoma protein Rb functions as an inhibitor of apoptotic signal transduction Inactivation of Rb by phosphorylation or caspase dependent cleavage degradation is required for cell death to occur Rb inhibits the Abl tyrosine kinase Thus Rb inactivation is a pre requisite for Abl activation by DNA damage or TNF Activation of nuclear Abl and its downstream effector p73 induces mitochondriadependent cell death The involvement of these nuclear signal transducers in TNF induced apoptosis which does not require new gene expression indicates that nuclear events other than transcription can contribute to

    Original URL path: http://www.cell-research.com/arts.asp?id=1220 (2016-02-14)
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  • Cell Research
    Van Andel Research Institute 333 Bostwick Ave N E Grand Rapids MI 49503 USA Correspondence George F VANDE WOUDE Tel 616 234 5298 E mail george vandewoude vai org Tumor progression is a multi step process that requires a sequential selection of specific malignant phenotypes Met activation may induce different phenotypes depending on tumor stage inducing proliferation and angiogenesis in primary tumors stimulating motility to form micrometastases and regaining the

    Original URL path: http://www.cell-research.com/arts.asp?id=1221 (2016-02-14)
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  • Cell Research
    POLLOCK Kathleen KELLY Cell and Cancer Biology Branch NCI NIH Bethesda MD 20892 USA Correspondence Kathleen KELLY E mail kkelly helix nih gov Some of the most common human cancers including breast cancer prostate cancer and lung cancer metastasize with avidity to bone What is the basis for their preferential growth within the bone microenvironment Bidirectional interactions between tumor cells and cells that make up bone result in a selective

    Original URL path: http://www.cell-research.com/arts.asp?id=1223 (2016-02-14)
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  • Cell Research
    2013 Free Sample Issue Submission Advanced Online Publication Current Issue Top 10 VOLUME 11 ISSUE 1 1 2005 63 65 Nitric oxide orchestrating hypoxia regulation through mitochondrial respiration and the endoplasmic reticulum stress response Weiming XU Ian G CHARLES Salvador MONCADA Wolfson Institute for Biomedical Research University College London The Cruciform Building Gower Street London WC1E 6BT UK Correspondence Salvador MONCADA E mail s moncada ucl ac uk Mitochondria have long been considered to be the powerhouse of the living cell generating energy in the form of the molecule ATP via the process of oxidative phosphorylation In the past 20 years it has been recognised that they also play an important role in the implementation of apoptosis or programmed cell death More recently it has become evident that mitochondria also participate in the orchestration of cellular defence responses At physiological concentrations the gaseous molecule nitric oxide NO inhibits the mitochondrial enzyme cytochrome c oxidase complex IV in competition with oxygen This interaction underlies the mitochondrial actions of NO which range from the physiological regulation of cell respiration through mitochondrial signalling to the development of metabolic hypoxia a situation in which although oxygen is available the cell is unable to utilise

    Original URL path: http://www.cell-research.com/arts.asp?id=1224 (2016-02-14)
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  • Cell Research
    66 71 Negative regulation of receptor tyrosine kinases unexpected links to c Cbl and receptor ubiquitylation Chanan RUBIN Gal GUR Yosef YARDEN Department of Biological Regulation The Weizmann Institute of Science Rehovot 76100 Israel Correspondence Yosef YARDEN Tel 972 8 9343974 E mail yosef yarden weizmann ac il Intracellular signals mediated by the family of receptor tyrosine kinases play pivotal roles in morphogenesis cell fate determination and pathogenesis Precise control of signal amplitude and duration is critical for the fidelity and robustness of these processes Activation of receptor tyrosine kinases by their cognate growth factors not only leads to propagation of the signal through various biochemical cascades but also sets in motion multiple attenuation mechanisms that ultimately terminate the active state Early attenuators pre exist prior to receptor activation and they act to limit signal propagation Subsequently late attenuators such as Lrig and Sprouty are transcriptionally induced and further act to dampen the signal Central to the process of signaling attenuation is the role of the E3 ubiquitin ligase c Cbl While Cbl mediated processes of receptor ubiquitylation and endocytosis are relatively well understood the links of Cbl to other negative regulators are just now beginning to be appreciated Here

    Original URL path: http://www.cell-research.com/arts.asp?id=1225 (2016-02-14)
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  • Cell Research
    Issue Top 10 VOLUME 11 ISSUE 1 1 2005 72 77 Chronic pancreatitis pancreatic adenocarcinoma and the black box in between Natalia JURA 1 2 Herbert ARCHER 1 2 Dafna BAR SAGI 1 1 Department of Molecular Genetics and Microbiology Stony Brook University Stony Brook NY 11794 5222 USA 2 Graduate Program in Molecular and Cellular Biology Stony Brook University Stony Brook NY 11794 5222 USA Correspondence Dafna BAR SAGI Tel 631 632 9737 or 631 632 8800 E mail barsagi pharm sunysb edu Pancreatic cancer is a challenging disease for patients doctors and researchers who for decades have searched for a cure for this deadly malignancy Although existing mouse models of pancreatic cancer have shed light on the mechanistic basis of the neoplastic conversion of the pancreas their impact in terms of offering new diagnostics and therapeutic modalities remains limited Chronic pancreatitis is an inflammatory disease of the pancreas that is associated with a gradual damage of the organ and an increased risk of developing neoplastic lesions In this review we propose that detailed studies of chronic inflammatory processes in the pancreas will provide insights into the evolution of pancreatic cancer This information may prove useful in the design

    Original URL path: http://www.cell-research.com/arts.asp?id=1226 (2016-02-14)
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  • Cell Research

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    Original URL path: /artsmore1.asp?id=102 (2016-02-14)


  • Cell Research
    91 Inositol 1 4 5 trisphosphate 3 kinases functions and regulations Hui Jun XIA Guang YANG Key Laboratory of MOE for Plant Developmental Biology College of Life Sciences Wuhan University Wuhan Hubei 430072 China Correspondence Hui Jun XIA Tel 86 27 68752112 E mail hjxia whu edu cn Inositol 1 4 5 trisphosphate 3 kinase IP 3 3 kinase IP3K plays an important role in signal transduction in animal cells by phosphorylating inositol 1 4 5 trisphosphate IP 3 to inositol 1 3 4 5 tetrakisphosphate IP 4 Both IP 3 and IP 4 are critical second messengers which regulate calcium Ca 2 homeostasis Mammalian IP3Ks are involved in many biological processes including brain development memory learning and so on It is widely reported that Ca 2 is a canonical second messenger in higher plants Therefore plant IP3K should also play a crucial role in plant development Recently we reported the identification of plant IP3K gene AtIpk2β AtIP3K from Arabidopsis thaliana and its characterization Here we summarize the molecular cloning biochemical properties and biological functions of IP3Ks from animal yeast and plant This review also discusses potential functions of IP3Ks in signaling crosstalk inositol phosphate metabolism gene transcriptional control and

    Original URL path: http://www.cell-research.com/arts.asp?id=1203 (2016-02-14)
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