Loss of HSF1 results in defective radiation-induced G(2) arrest and DNA repair.
Loss of HSF1 results in defective radiation-induced G(2) arrest and DNA repair.
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DOI：
10.1667/rr2393.1
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发表时间：
2011-07
影响因子：
3.4
通讯作者：
Martinez JD
中科院分区：
文献类型：
--
作者：
Li Q;Martinez JD
HSF1是一种转录因子，在对热应激的反应中起着关键作用，我们之前的研究表明，HSF1对于p53进入细胞核也至关重要。在这里，我们扩展了这些研究，并表明HSF1的丧失使细胞对电离辐射的杀伤更敏感。缺乏功能性HSF1的细胞在暴露于电离辐射后无法在G2中停滞，这表明HSF1活性对于激活该细胞周期检查点至关重要。此外，没有HSF1的细胞显示修复辐射诱导的双链DNA断裂的能力降低。我们发现，在这些细胞中，53BP1没有在DNA损伤部位积聚，这表明HSF1对于这种DNA损伤介质的功能也是必不可少的。综上所述，我们的研究结果表明HSF1在检查点激活和DNA修复中发挥重要作用，并表明热应激反应途径与电离辐射反应途径之间存在重叠。
HSF1 is a transcription factor that plays a key role in the response to heat stress and was previously shown by us to also be essential for importation of p53 into the nucleus. Here we extend these studies and show that loss of HSF1 renders cells more sensitive to killing by ionizing radiation. Cells that lack a functional HSF1 were unable to arrest in G2 after exposure to ionizing radiation, suggesting that HSF1 activity was essential for activation of this cell cycle checkpoint. In addition, cells with no HSF1 showed a reduced capacity to repair radiation-induced double-stranded DNA breaks. We found that in these cells 53BP1 did not accumulate at sites of DNA damage, suggesting that HSF1 was also essential for the functioning of this DNA damage mediator. Taken together our results indicate that HSF1 plays an important role in checkpoint activation and DNA repair and suggest that there is overlap between the heat stress response pathway and the pathway that responds to ionizing radiation.
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影响因子：
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作者：
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通讯作者：
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