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  • Cell Research
    adaptive immunity This function has been widely attributed to its role as the central activator of the NF κB family of transcription factors However another important consequence of IKK activation is the regulation of TPL 2 a MEK kinase that is required for activation of ERK 1 2 MAP kinases in myeloid cells following Toll like receptor and TNF receptor stimulation In unstimulated cells TPL 2 is stoichiometrically complexed with the NF κB inhibitory protein NF κB1 p105 which blocks TPL 2 access to its substrate MEK and the ubiquitin binding protein ABIN 2 A20 binding inhibitor of NF κB 2 both of which are required to maintain TPL 2 protein stability Following agonist stimulation the IKK complex phosphorylates p105 triggering its K48 linked ubiquitination and degradation by the proteasome This releases TPL 2 from p105 mediated inhibition facilitating activation of MEK in addition to modulating NF κB activation by liberating associated Rel subunits for translocation into the nucleus IKK induced proteolysis of p105 therefore can directly regulate both NF κB and ERK MAP kinase activation via NF κB1 p105 TPL 2 is critical for production of the proinflammatory cytokine TNF during inflammatory responses Consequently there has been considerable interest

    Original URL path: http://www.cell-research.com/arts.asp?id=426 (2016-02-14)
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  • Cell Research
    kinase NF κB signaling pathway has been implicated in the pathogenesis of several inflammatory diseases Increased activation of NF κB is often detected in both immune and non immune cells in tissues affected by chronic inflammation where it is believed to exert detrimental functions by inducing the expression of proinflammatory mediators that orchestrate and sustain the inflammatory response and cause tissue damage Thus increased NF κB activation is considered an important pathogenic factor in many acute and chronic inflammatory disorders raising hopes that NF κB inhibitors could be effective for the treatment of inflammatory diseases However ample evidence has accumulated that NF κB inhibition can also be harmful for the organism and in some cases trigger the development of inflammation and disease These findings suggested that NF κB signaling has important functions for the maintenance of physiological immune homeostasis and for the prevention of inflammatory diseases in many tissues This beneficial function of NF κB has been predominantly observed in epithelial cells indicating that NF κB signaling has a particularly important role for the maintenance of immune homeostasis in epithelial tissues It seems therefore that NF κB displays two faces in chronic inflammation on the one hand increased and sustained

    Original URL path: http://www.cell-research.com/arts.asp?id=427 (2016-02-14)
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  • Cell Research
    Medicine University of California at San Diego 9500 Gilman Drive MC 0723 La Jolla CA 92093 0723 USA 2 Current address Isis Pharmaceuticals Inc 1896 Rutherford Road Carlsbad CA 92008 326 E mail ghe isisph com Correspondence Michael Karin Tel 858 534 1361 E mail karinoffice ucsd edu Hepatocellular carcinoma HCC the major form of primary liver cancer is one of the most deadly human cancers The pathogenesis of HCC is frequently linked with continuous hepatocyte death inflammatory cell infiltration and compensatory liver regeneration Understanding the molecular signaling pathways driving or mediating these processes during liver tumorigenesis is important for the identification of novel therapeutic targets for this dreadful disease The classical IKKβ dependent NF κB signaling pathway has been shown to promote hepatocyte survival in both developing and adult livers In addition it also plays a crucial role in liver inflammatory responses by controlling the expression of an array of growth factors and cytokines One of these cytokines is IL 6 which is best known for its role in the liver acute phase response IL 6 exerts many of its functions via activation of STAT3 a transcription factor found to be important for HCC development This review will focus

    Original URL path: http://www.cell-research.com/arts.asp?id=428 (2016-02-14)
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  • Cell Research
    1 314 454 8472 E mail novack wustl edu Since the discovery that deletion of the NF κB subunits p50 and p52 causes osteopetrosis in mice there has been considerable interest in the role of NF κB signaling in bone NF κB controls the differentiation or activity of the major skeletal cell types osteoclasts osteoblasts osteocytes and chondrocytes However with five NF κB subunits and two distinct activation pathways not

    Original URL path: http://www.cell-research.com/arts.asp?id=429 (2016-02-14)
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  • Cell Research
    κBs are a family of transcription factors that control a number of essential cellular functions including immune responses cell proliferation and antiapoptosis NF κB activities are tightly regulated through upstream signaling molecules and downstream feedback loops In this review structural discoveries in the NF κB pathway are presented With the structure information the following questions may be addressed 1 How do NF κBs activate their target genes 2 How do

    Original URL path: http://www.cell-research.com/arts.asp?id=430 (2016-02-14)
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  • Cell Research
    Hou 1 Jian Ge 1 2 Chun Liu 1 2 Weiqi Zhang 1 Xu Zhang 1 2 Yetao Wu 1 2 Honggang Li 1 2 Kang Liu 1 Chen Wu 1 2 Zhihua Song 1 2 Yang Zhao 1 3 Yan Shi 2 and Hongkui Deng 1 2 1 Department of Cell Biology and Genetics College of Life Sciences Peking University Beijing 100871 China 2 Laboratory of Chemical Genomics School of Chemical Biology and Biotechnology Shenzhen Graduate School of Peking University Shenzhen 518055 China 3 Beijing Rui Pu Chen Chuang Biotech Inc China Correspondence Yang Zhao Yan Shi Hongkui Deng E mail yangel zhao gmail com shiyan szpku edu cn hongkui deng pku edu cn The introduction of four transcription factors Oct4 Klf4 Sox2 and c Myc by viral transduction can induce reprogramming of somatic cells into induced pluripotent stem cells iPSCs but the use of iPSCs is hindered by the use of viral delivery systems Chemical induced reprogramming offers a novel approach to generating iPSCs without any viral vector based genetic modification Previous reports showed that several small molecules could replace some of the reprogramming factors although at least two transcription factors Oct4 and Klf4 are still required to generate iPSCs from mouse embryonic fibroblasts Here we identify a specific chemical combination which is sufficient to permit reprogramming from mouse embryonic and adult fibroblasts in the presence of a single transcription factor Oct4 within 20 days replacing Sox2 Klf4 and c Myc The iPSCs generated using this treatment resembled mouse embryonic stem cells in terms of global gene expression profile epigenetic status and pluripotency both in vitro and in vivo We also found that 8 days of Oct4 induction was sufficient to enable Oct4 induced reprogramming in the presence of the small molecules which suggests that reprogramming was initiated

    Original URL path: http://www.cell-research.com/arts.asp?id=431 (2016-02-14)
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  • Cell Research
    1 1 2011 205 212 BMPs functionally replace Klf4 and support efficient reprogramming of mouse fibroblasts by Oct4 alone Jiekai Chen Jing Liu Jiaqi Yang You Chen Jing Chen Su Ni Hong Song Lingwen Zeng Ke Ding and Duanqing Pei Key Laboratory of Regenerative Biology South China Institute for Stem Cell Biology and Regenerative Medicine at Guangzhou Institutes of Biomedicine and Health Chinese Academy of Sciences Guangzhou 510530 China Correspondence Duanqing Pei Tel 86 20 3201 5201 E mail pei duanqing gibh ac cn Generation of induced pluripotent stem cells by defined factors has become a useful model to investigate the mechanism of reprogramming and cell fate determination However the precise mechanism of factor based reprogramming remains unclear Here we show that Klf4 mainly acts at the initial phase of reprogramming to initiate mesenchymal to epithelial transition and can be functionally replaced by bone morphogenetic proteins BMPs BMPs boosted the efficiency of Oct4 Sox2 mediated reprogramming of mouse embryonic fibroblasts MEFs to 1 BMPs also promoted single factor Oct4 based reprogramming of MEFs and tail tibial fibroblasts Our studies clarify the contribution of Klf4 in reprogramming and establish Oct4 as a singular setter of pluripotency in differentiated cells Cell Research

    Original URL path: http://www.cell-research.com/arts.asp?id=432 (2016-02-14)
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  • Cell Research

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    Original URL path: /artsmore1.asp?id=29 (2016-02-14)




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