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首页> 外文期刊>Radiation Protection Dosimetry >INFLUENCES OF TP53 EXPRESSION ON CELLULAR RADIATION RESPONSE AND ITS RELEVANCE TO DIAGNOSTIC BIODOSIMETRY FOR MISSION ENVIRONMENTAL MONITORING
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INFLUENCES OF TP53 EXPRESSION ON CELLULAR RADIATION RESPONSE AND ITS RELEVANCE TO DIAGNOSTIC BIODOSIMETRY FOR MISSION ENVIRONMENTAL MONITORING

机译:TP53表达对细胞辐射响应及其与诊断生物剂量学相关性的监测

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摘要

TP53 is a transcriptional activator and regulates genomic instability and cellular responses to DNA damage in response to ionising radiation. The molecular mechanism behind p53-mediated responses, such as, apoptosis and genomic instability remains unclear. An in vitro model of biological effects to irradiation was established. In order to elucidate the functional role of TPS3 under different stress-reaction pathways and identify possible biological indicators, p53 was stably transfected into HL-60 cells, which provides a p53 minus background. Significantly enhanced radiosensitivity and growth suppression were observed. G_2 accumulation was obtained. Radiation-induced apoptosis of HL-60 cells was significantly inhibited by TP53, indicating that, in the event of DNA damage, TP53 is able to prevent cell death of HL-60 leukaemia cells by sustaining an arrest of the cell cycle at G_2 phase. Further evidence will be presented to identify specific radiation-targeted genes or signals as possible biomarkers for early diagnosis of radiation damage as well as mission environmental monitoring.
机译:TP53是一种转录激活因子,可调节基因组不稳定和细胞对电离辐射对DNA损伤的反应。 p53介导的反应,如细胞凋亡和基因组不稳定性背后的分子机制仍不清楚。建立了对辐射的生物学效应的体外模型。为了阐明TPS3在不同应激反应途径下的功能作用并鉴定可能的生物学指标,将p53稳定转染到HL-60细胞中,该细胞提供了一个p53负背景。观察到显着增强的放射敏感性和生长抑制。获得了G_2积累。辐射诱导的HL-60细胞凋亡被TP53显着抑制,表明在DNA损伤的情况下,TP53能够通过维持细胞周期在G_2期的停滞来预防HL-60白血病细胞的细胞死亡。将提供进一步的证据来鉴定特定的辐射靶向基因或信号,作为可能的生物标志物,以进行辐射损伤的早期诊断以及任务环境监测。

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