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首页> 外文期刊>Diabetes >Glycogen Synthase Kinase-3 and Mammalian Target of Rapamycin Pathways Contribute to DNA Synthesis, Cell Cycle Progression, and Proliferation in Human Islets
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Glycogen Synthase Kinase-3 and Mammalian Target of Rapamycin Pathways Contribute to DNA Synthesis, Cell Cycle Progression, and Proliferation in Human Islets

机译:糖原合酶激酶3和雷帕霉素途径的哺乳动物目标有助于人类胰岛的DNA合成,细胞周期进程和增殖。

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摘要

Our previous studies demonstrated that nutrient regulation of mammalian target of rapamycin (mTOR) signaling promotes regenerative processes in rodent islets but rarely in human islets. Our objective was to extend these findings by using therapeutic agents to determine whether the regulation of glycogen synthase kinase-3 (GSK-3)/beta-catenin and mTOR signaling represent key components necessary for effecting a positive impact on human beta-cell mass relevant to type 1 and 2 diabetes.
机译:我们以前的研究表明,哺乳动物雷帕霉素靶标(mTOR)信号的营养调节可促进啮齿动物胰岛的再生过程,而在人类胰岛则很少。我们的目标是通过使用治疗剂确定糖原合酶激酶3(GSK-3)/β-catenin和mTOR信号传导的调节是否代表对人类β细胞质量相关产生积极影响所必需的关键成分来扩展这些发现。 1型和2型糖尿病。

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  • 来源
    《Diabetes 》 |2009年第3期| p.663-672| 共10页
  • 作者单位

    Hui Liu,1 Maria S. Remedi,2 Kirk L. Pappan,1 Guim Kwon,3 Nidhi Rohatgi,1 Connie A. Marshall,1 and Michael L. McDaniel1From the 1Department of Pathology and Immunology, Washington University, St. Louis, Missouri, the 2 Department of Cell Biology and Physiology, Washington University, St. Louis, Missouri, and the 3 Department of Pharmaceutical Sciences, School of Pharmacy, Southern Illinois University, Edwardsville, Illinois.Corresponding author Michael L. McDaniel, mmcdaniel@wustl.edu.Received 27 August 2007 and accepted 30 November 2008.Published ahead of print at http://diabetes.diabetesjournals.org on 10 December 2008. DOI: 10.2337/db07-1208.H.L., M.S.R., and K.L.P. contributed equally to this work.The contents of this work are solely the responsibility of the authors and do not necessarily represent the official views of the National Institutes of Health (NIH) or American Diabetes Association (ADA).© 2009 by the American Diabetes Association. Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. See http://creativecommons.org/licenses/by -nc-nd/3.0/ for details.The costs of publication of this article were defrayed in pari by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section i734 solely to indicate this fact.,;

  • 收录信息 美国《科学引文索引》(SCI);美国《化学文摘》(CA);
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  • 正文语种 eng
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