转录因子作为慢性暴露致癌效应的潜在标记物。审查

E. A. Kodintseva
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引用次数: 0

摘要

人体长期暴露于电离辐射下,主要对红骨髓细胞造成损害,主要影响免疫系统的t细胞部分。长期以来,受影响人群的癌症和心血管疾病发病率有所上升。晚期辐射诱导免疫变化的机制尚未得到充分的研究。慢性暴露的后期效应的病理生理机制尚不清楚。本文综述了参与细胞电离辐射应答的NF-κB、JNK、Р38等转录因子的最新研究进展。主要的转录因子如STAT3、GATA3、T-BOX、FOXР3、RORС等控制t淋巴细胞的分化。本文简要介绍了几种转录因子的定位及其功能。综述了转录因子研究的最新方法,分析了它们的优缺点。辐射对细胞的影响主要是通过应力适应机制实现的,这使得研究细胞对电离辐射的响应和影响的实现机制,特别是延迟效应的研究变得困难。细胞内信号通路的复杂研究与遗传和受体细胞装置(Т-lymphocytes,执行调节功能,以及抗肿瘤免疫的细胞效应器)有关,将使未来的研究能够发现电离辐射长期暴露于人体的晚期效应机制,主要是致癌效应
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Transcription factors as potential markers of carcinogenic effects of chronic exposure. Review
Chronic human exposure to ionizing radiation causes mainly damage to red bone marrow cells, that primarily affects T-cell part of the immunity. Increased incidence of cancer and cardiovascular diseases in the affected people has been registered during long time. Mechanisms of the late radiation-induced immunity changes have not been sufficiently studied. Pathophysiological mechanisms of late effects of chronic exposure are unknown. The paper reviews the latest information on some transcription factors, among them NF-κB, JNK, Р38 and other, involved in cellular response to ionizing radiation. The main transcription factors, such as STAT3, GATA3, T-BOX, FOXР3, RORС and other, control T-lymphocytes differentiation. Location of some transcription factors and short description of their functions are given in the paper. The latest methods of the transcription factors research have been summarized, their advantages and disadvantages have been analyzed. Radiation effects on cells are mainly realized through stress-adaptive mechanism, this makes difficult to study cells response to ionizing radiation and mechanisms of the effects realization, especially delayed effects. Complex research of intracellular signal pathway in relation to genetic and receptor cells apparatus (Т-lymphocytes, performing regulatory functions, and cells effectors of antitumor immunity) will allow the future researches to find out mechanisms of late effects of ionizing radiation chronic exposure to a human, primarily carcinogenic effects
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