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Investigation of synergism between mTOR and eEF2 kinase pathways

Investigation of synergism between mTOR and eEF2 kinase pathways
mTOR 和 eEF2 激酶通路之间的协同作用研究
批准号:
8729435
负责人:
ALEXEY G. RYAZANOV
金额:
$18.78万
依托单位国家:
美国
项目类别:
财政年份:
2012
资助国家:
美国
项目状态:
已结题
起止时间:
2012-09-30 至 2014-06-30

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中文摘要
翻译
项目主任/首席研究员(最后、第一、中):PI: Alexey G. Ryazanov, Ph.D。
英文摘要
Program Director/Principal Investigator (Last, First, Middle): PI: Alexey G. Ryazanov, Ph.D. Abstract The TOR pathway plays an important role in aging. It has been demonstrated that treatment with rapamycin leads to prolongation of life span in diverse organisms. One of the components of TOR pathway is eEF2 kinase (eEF2K) which regulates the global rate of protein synthesis through phosphorylation of elongation factor 2 (eEF2). Activation of TOR results in the inhibition of eEF2K as a part of the mechanism that increases the rate of protein synthesis. Recently, we generated mice with knockout of eEF2K and found that its inactivation protects stem cells from apoptosis and retards aging. Thus, there exists a paradox: on one hand inhibition of TOR slows down aging, on the other hand inhibition of TOR may accelerate aging through activation of eEF2K. Therefore, the inhibition of TOR by rapamycin results in two opposite signals: inhibition of the TOR pathway slows down aging and at the same time activates eEF2K, which may counteract the anti- aging effect of rapamycin. Thus, we hypothesize that simultaneous inhibition of TOR and eEF2K increases the effect of TOR inhibition on aging. We will test this hypothesis by determining whether inactivation of eEF2K can synergize with rapamycin in producing an anti-aging effect. PHS 398/2590 (Rev. 06/09) Page 1 Continuation Format Page
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Use of EF2K Inhibitors to Reduce Toxicity to Normal Tissues in Chemotherapy
  • 批准号:
    8782369
  • 项目类别:
  • 资助金额:
    $22.2万
  • 财政年份:
    2014
  • 负责人:
    ALEXEY G. RYAZANOV
  • 依托单位:
Investigation of synergism between mTOR and eEF2 kinase pathways
Investigation of synergism between mTOR and eEF2 kinase pathways
Translational Control of Radiation-Induced Apoptosis
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