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
    1 Signal Transduction Cancer Research UK London Research Institute 44 Lincoln s Inn Fields London WC2A 3LY UK 2 Bioinformatics and Biostatistics Cancer Research UK London Research Institute 44 Lincoln s Inn Fields London WC2A 3LY UK 3 High Throughput Screening Laboratories Cancer Research UK London Research Institute 44 Lincoln s Inn Fields London WC2A 3LY UK Correspondence Julian Downward Tel 44 20 7269 3533 E mail julian downward cancer org uk Oncogenic mutations in RAS genes are very common in human cancer resulting in cells with well characterized selective advantages but also less well understood vulnerabilities We have carried out a large scale loss of function screen to identify genes that are required by KRAS transformed colon cancer cells but not by derivatives lacking this oncogene Top scoring genes were then tested in a larger panel of KRAS mutant and wild type cancer cells Cancer cells expressing oncogenic KRAS were found to be highly dependent on the transcription factor GATA2 and the DNA replication initiation regulator CDC6 Extending this analysis using a collection of drugs with known targets we found that cancer cells with mutant KRAS showed selective addiction to proteasome function as well as synthetic lethality with topoisomerase

    Original URL path: http://www.cell-research.com/arts.asp?id=125 (2016-02-14)
    Open archived version from archive

  • Cell Research
    Ye 1 Shu Yong L 1 State Key Laboratory of Stress Cell Biology School of Life Sciences Xiamen University Xiamen Fujian 361005 China 2 State Key Laboratory of Microbial Technology School of Life Sciences Shandong University Jinan Shandong 250100 China Correspondence Sheng Cai Lin Tel 86 592 2182993 E mail linsc xmu edu cn Insulin stimulated glucose uptake by the glucose transporter GLUT4 plays a central role in whole body glucose homeostasis dysregulation of which leads to type 2 diabetes However the molecular components and mechanisms regulating insulin stimulated glucose uptake remain largely unclear Here we demonstrate that Axin interacts with the ADP ribosylase tankyrase 2 TNKS2 and the kinesin motor protein KIF3A forming a ternary complex crucial for GLUT4 translocation in response to insulin Specific knockdown of the individual components of the complex attenuated insulin stimulated GLUT4 translocation to the plasma membrane Importantly TNKS2 mice exhibit reduced insulin sensitivity and higher blood glucose levels when re fed after fasting Mechanistically we demonstrate that in the absence of insulin Axin TNKS and KIF3A are co localized with GLUT4 on the trans Golgi network Insulin treatment suppresses the ADP ribosylase activity of TNKS leading to a reduction in ADP ribosylation and

    Original URL path: http://www.cell-research.com/arts.asp?id=126 (2016-02-14)
    Open archived version from archive

  • Cell Research
    Cell Biology Institute of Biochemistry and Cell Biology Shanghai Institutes for Biological Sciences Chinese Academy of Sciences 320 Yue Yang Road Shanghai 200031 China 2 State Key Laboratory of Molecular Biology Institute of Biochemistry and Cell Biology Shanghai Institutes for Biological Sciences Chinese Academy of Sciences 320 Yue Yang Road Shanghai 200031 China Correspondence Xueliang Zhu Tel 86 21 54921406 E mail xlzhu sibs ac cn The WAVE regulatory complex WRC consisting of WAVE Sra Nap Abi and HSPC300 activates the Arp2 3 complex to control branched actin polymerization in response to Rac activation How the WRC is assembled in vivo is not clear Here we show that Nudel a protein critical for lamellipodia formation dramatically stabilized the Sra1 Nap1 Abi1 complex against degradation in cells through a dynamic binding to Sra1 whereas its physical interaction with HSPC300 protected free HSPC300 from the proteasome mediated degradation and stimulated the HSPC300 WAVE2 complex formation By contrast Nudel showed little or no interactions with the Sra1 Nap1 Abi1 WAVE2 and the Sra1 Nap1 Abi1 HSPC300 complexes as well as the mature WRC Depletion of Nudel by RNAi led to general subunit degradation and markedly attenuated the levels of mature WRC It also

    Original URL path: http://www.cell-research.com/arts.asp?id=128 (2016-02-14)
    Open archived version from archive

  • Cell Research
    Tian 2 3 Fuchu He 1 2 3 and Lingqiang Zhang 2 3 1 Department of Medical Genetics Institute of Basic Medical Sciences Chinese Academy of Medical Sciences Peking Union Medical College Beijing 100005 China 2 State Key Laboratory of Proteomics Beijing Proteome Research Center Beijing Institute of Radiation Medicine Beijing 100850 China 3 National Engineering Research Center for Protein Drugs Beijing 100850 China 4 Department of Pathology School of Basic Medical Sciences Peking University Beijing 100191 China Correspondence Fuchu He Lingqiang Zhang E mail hefc nic bmi ac cn zhanglq nic bmi ac cn Alkylating agents induce genome wide base damage which is repaired mainly by N methylpurine DNA glycosylase MPG An elevated expression of MPG in certain types of tumor cells confers higher sensitivity to alkylation agents because MPG induced apurinic apyrimidic AP sites trigger more strand breaks However the determinant of drug sensitivity or insensitivity still remains unclear Here we report that the p53 status coordinates with MPG to play a pivotal role in such process MPG expression is positive in breast lung and colon cancers 38 7 43 4 and 25 3 respectively but negative in all adjacent normal tissues MPG directly binds to the tumor suppressor p53 and represses p53 activity in unstressed cells The overexpression of MPG reduced whereas depletion of MPG increased the expression levels of pro arrest gene downstream of p53 including p21 14 3 3s and Gadd45 but not proapoptotic ones The N terminal region of MPG was specifically required for the interaction with the DNA binding domain of p53 Upon DNA alkylation stress in p53 wild type tumor cells p53 dissociated from MPG and induced cell growth arrest Then AP sites were repaired efficiently which led to insensitivity to alkylating agents By contrast in p53 mutated cells the AP sites

    Original URL path: http://www.cell-research.com/arts.asp?id=129 (2016-02-14)
    Open archived version from archive

  • Cell Research
    Wang 6 Wenqing Shui 1 Laboratory of Structural Biology and MOE Laboratory of Protein Science School of Medicine and Life Sciences Tsinghua University Beijing 100084 China 2 College of Life Sciences and Tianjin State Laboratory of Protein Science Nankai University Tianjin 300071 China 3 High throughput Molecular Drug Discovery Center Tianjin Joint Academy of Biotechnology and Medicine Tianjin 300457 China 4 National Laboratory of Macromolecules Institute of Biophysics Chinese Academy

    Original URL path: http://www.cell-research.com/arts.asp?id=130 (2016-02-14)
    Open archived version from archive

  • Cell Research

    (No additional info available in detailed archive for this subpage)
    Original URL path: /artsmore1.asp?id=10 (2016-02-14)


  • Cell Research
    Israel Deaconess Cancer Center Departments of Medicine and Pathology Beth Israel Deaconess Medical Center Harvard Medical School Boston MA 02215 USA Correspondence Pier Paolo Pandolfi Tel 617 735 2121 E mail ppandolf bidmc harvard edu The mammalian target of rapamycin mTOR protein kinase regulates a wide variety of cellular processes including protein synthesis yet the downstream translational program under the control of mTOR is poorly understood Two recent studies by

    Original URL path: http://www.cell-research.com/arts.asp?id=108 (2016-02-14)
    Open archived version from archive

  • Cell Research
    Fribourg Chemin du Musée 5 1700 Fribourg Switzerland Correspondence Urs Albrecht E mail urs albrecht unifr ch A hallmark of the mammalian circadian timing system is synchronization of physiology and behavior but when this synchronization is disturbed chronic diseases such as metabolic syndrome and depression may develop Three new studies show that nuclear receptors of the Rev Erb family impact the circadian oscillator and its metabolic output and this can

    Original URL path: http://www.cell-research.com/arts.asp?id=109 (2016-02-14)
    Open archived version from archive



  •