Epitranscriptomic control of ROS

ROS的表观转录组控制

基本信息

  • 批准号:
    10792216
  • 负责人:
  • 金额:
    $ 29.69万
  • 依托单位:
  • 依托单位国家:
    美国
  • 项目类别:
  • 财政年份:
    2023
  • 资助国家:
    美国
  • 起止时间:
    2023-08-01 至 2025-07-31
  • 项目状态:
    未结题

项目摘要

Maintenance of the GSH redox cycle is reliant on the activities of selenocysteine-containing GSH metabolizing enzymes which play fundamental roles in chemoprevention. Selenocysteine is the 21st amino acid and does not contain a dedicated codon. Selenocysteine incorporation during translation requires UGA-stop-codon recoding, which uses specifically modified tRNA for accurate decoding. Dynamic changes in tRNA modification are an epitranscriptomic signal because they regulate gene expression post-transcriptionally. We have shown that the stress-induced translation of many selenocysteine containing ROS detoxifying enzymes is dependent on the Alkbh8 tRNA methyltransferase. Alkbh8 enzymatically methylates the uridine wobble base on tRNASelenocysteine to promote UGA-stop codon decoding. We have developed an Alkbh8 deficient mouse and have used molecular, biochemical, and genomic approaches to demonstrate that Alkbh8Def mouse embryonic fibroblasts (MEFs) and some organs display markers of senescence and a senescence gene signature. Using human cells and our new Alkbh8Def/p16-3MR mice we propose to test the hypothesis that senescence occurs in vitro and in vivo because of defective epitranscriptomic signals that controls selenocysteine utilization. To achieve this, two aims will: 1. determine if Alkbh8 and other epitranscriptomic writers that limit selenocysteine utilization restrict the senescence program and 2. determine if Alkbh8-deficiency drives senescence in vivo and whether senescence ablation accelerates or tempers pathologies that accompany selenoprotein loss. Our proposal is being submitted with significant preliminary data supporting the idea that Alkbh8 and epitranscriptomic signals are key to chemoprevention by limiting senescent activity.
谷胱甘肽氧化还原循环的维持依赖于含硒半胱氨酸的谷胱甘肽的活性

项目成果

期刊论文数量(2)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Arsenite toxicity is regulated by queuine availability and oxidation-induced reprogramming of the human tRNA epitranscriptome.
The therapeutic bionanoscience interface.
治疗生物纳米科学界面。
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JUAN Andres MELENDEZ其他文献

JUAN Andres MELENDEZ的其他文献

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{{ truncateString('JUAN Andres MELENDEZ', 18)}}的其他基金

Redox-Control of MMP-1 and Senescence
MMP-1 和衰老的氧化还原控制
  • 批准号:
    7886232
  • 财政年份:
    2009
  • 资助金额:
    $ 29.69万
  • 项目类别:
Redox-Control of MMP-1 and Senescence
MMP-1 和衰老的氧化还原控制
  • 批准号:
    7476689
  • 财政年份:
    2008
  • 资助金额:
    $ 29.69万
  • 项目类别:
Redox-Control of MMP-1 and Senescence
MMP-1 和衰老的氧化还原控制
  • 批准号:
    7849359
  • 财政年份:
    2008
  • 资助金额:
    $ 29.69万
  • 项目类别:
Redox-Control of MMP-1 and Senescence
MMP-1 和衰老的氧化还原控制
  • 批准号:
    7585314
  • 财政年份:
    2008
  • 资助金额:
    $ 29.69万
  • 项目类别:
Redox-Control of MMP-1 and Senescence
MMP-1 和衰老的氧化还原控制
  • 批准号:
    8049150
  • 财政年份:
    2008
  • 资助金额:
    $ 29.69万
  • 项目类别:
Redox-Control of MMP-1 and Senescence
MMP-1 和衰老的氧化还原控制
  • 批准号:
    7798968
  • 财政年份:
    2008
  • 资助金额:
    $ 29.69万
  • 项目类别:
Redox-Control of MMP-1 and Senescence
MMP-1 和衰老的氧化还原控制
  • 批准号:
    8415608
  • 财政年份:
    2008
  • 资助金额:
    $ 29.69万
  • 项目类别:
Redox Regulation of Metastasis by Sod2
Sod2 对转移的氧化还原调节
  • 批准号:
    6460443
  • 财政年份:
    2002
  • 资助金额:
    $ 29.69万
  • 项目类别:
Redox Regulation of Metastasis by Sod2
Sod2 对转移的氧化还原调节
  • 批准号:
    6755946
  • 财政年份:
    2002
  • 资助金额:
    $ 29.69万
  • 项目类别:
Redox Regulation of Metastasis by Sod2
Sod2 对转移的氧化还原调节
  • 批准号:
    6623036
  • 财政年份:
    2002
  • 资助金额:
    $ 29.69万
  • 项目类别:

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