Jab1降解9-1-1引發(fā)DNA損傷修復(fù)障礙的機(jī)制研究
發(fā)布時(shí)間:2018-10-11 12:51
【摘要】:DNA損傷是細(xì)胞生命中的常見現(xiàn)象。各種各樣的環(huán)境因素均可持續(xù)損害細(xì)胞內(nèi)的遺傳物質(zhì)。這些因素包括來自太陽光的紫外線、電離輻射等外源因素,和來自體內(nèi)物質(zhì)代謝的氧化劑等內(nèi)源因素。在長期的進(jìn)化過程中,,針對各種代謝和外界來源的DNA損傷的因素,地球上的生物逐漸發(fā)展出一套完整的修復(fù)DNA損傷的機(jī)制,那就是高度保守的DNA損傷檢控點(diǎn)和DNA修復(fù)。 DNA損傷檢控點(diǎn)是指當(dāng)DNA損傷時(shí),延遲或阻滯細(xì)胞周期的生化過程。當(dāng)DNA損傷時(shí),該檢控點(diǎn)途徑的激活,能防止損傷的或復(fù)制不完全的遺傳物質(zhì)的傳播,給細(xì)胞以足夠的時(shí)間在細(xì)胞周期重新開始前,修復(fù)DNA損傷;或損傷過大時(shí),啟動(dòng)凋亡或細(xì)胞衰老程序。DNA損傷檢控點(diǎn)途徑的缺陷,可引起突變的傳播,導(dǎo)致其在體內(nèi)的積累。而突變在體內(nèi)的積累目前被認(rèn)為可能是腫瘤發(fā)生最主要的原因。因此,DNA損傷時(shí),DNA損傷檢控點(diǎn)途徑的激活,是維持遺傳物質(zhì)(染色體)的穩(wěn)定性、抑制腫瘤發(fā)生所必需的。 Rad9-Rad1-Hus1(9-1-1)復(fù)合體是DNA損傷檢控點(diǎn)途徑中重要的感受器,DNA損傷時(shí),該復(fù)合體在RFC-Rad17的幫助下,與損傷
[Abstract]:DNA damage is a common phenomenon in cell life. A variety of environmental factors can continue to damage the cell's genetic material. These factors include external factors such as ultraviolet radiation and ionizing radiation from the sun, and endogenous factors such as oxidizer from substance metabolism in the body. Over the course of a long evolutionary process, organisms on Earth have developed a complete mechanism for repairing DNA damage in response to various metabolic and external sources of DNA damage. That is the highly conserved DNA damage prosecution point and DNA repair. The DNA damage prosecution point is the biochemical process that delays or blocks the cell cycle when DNA is damaged. When DNA is damaged, the activation of the prosecution point pathway prevents the spread of damaged or incomplete genetic material, giving cells sufficient time to repair the DNA damage before the cell cycle restarts; or when the damage is excessive, To initiate the process of apoptosis or cell senescence. The defect of DNA damage control point pathway can cause the transmission of mutation and lead to its accumulation in vivo. The accumulation of mutations in the body is now thought to be the main cause of tumorigenesis. Therefore, during DNA damage, the activation of DNA damage checkpoint pathway is to maintain the stability of genetic material (chromosomes). Rad9-Rad1-Hus1 (9-1-1) complex is an important receptor in the pathway of DNA damage control point. When DNA is damaged, the complex is associated with injury with the help of RFC-Rad17.
【學(xué)位授予單位】:新疆醫(yī)科大學(xué)
【學(xué)位級別】:博士
【學(xué)位授予年份】:2006
【分類號(hào)】:R346
本文編號(hào):2264257
[Abstract]:DNA damage is a common phenomenon in cell life. A variety of environmental factors can continue to damage the cell's genetic material. These factors include external factors such as ultraviolet radiation and ionizing radiation from the sun, and endogenous factors such as oxidizer from substance metabolism in the body. Over the course of a long evolutionary process, organisms on Earth have developed a complete mechanism for repairing DNA damage in response to various metabolic and external sources of DNA damage. That is the highly conserved DNA damage prosecution point and DNA repair. The DNA damage prosecution point is the biochemical process that delays or blocks the cell cycle when DNA is damaged. When DNA is damaged, the activation of the prosecution point pathway prevents the spread of damaged or incomplete genetic material, giving cells sufficient time to repair the DNA damage before the cell cycle restarts; or when the damage is excessive, To initiate the process of apoptosis or cell senescence. The defect of DNA damage control point pathway can cause the transmission of mutation and lead to its accumulation in vivo. The accumulation of mutations in the body is now thought to be the main cause of tumorigenesis. Therefore, during DNA damage, the activation of DNA damage checkpoint pathway is to maintain the stability of genetic material (chromosomes). Rad9-Rad1-Hus1 (9-1-1) complex is an important receptor in the pathway of DNA damage control point. When DNA is damaged, the complex is associated with injury with the help of RFC-Rad17.
【學(xué)位授予單位】:新疆醫(yī)科大學(xué)
【學(xué)位級別】:博士
【學(xué)位授予年份】:2006
【分類號(hào)】:R346
【參考文獻(xiàn)】
相關(guān)期刊論文 前8條
1 王海燕,張連珍;輻射誘發(fā)細(xì)胞HPRT基因位點(diǎn)突變頻率的研究[J];輻射防護(hù);1999年06期
2 崔鳳梅,趙經(jīng)涌,勞勤華,王六一,洪承皎,寧萍;克隆法研究輻射誘發(fā)人外周血淋巴細(xì)胞HPRT基因突變[J];輻射防護(hù);2005年01期
3 張麗蘋,霍克克;蛋白質(zhì)相互作用研究技術(shù)進(jìn)展[J];高技術(shù)通訊;2003年11期
4 王曉;泛素-26s蛋白酶體途徑在凋亡中的作用[J];國外醫(yī)學(xué)(分子生物學(xué)分冊);2002年02期
5 張令強(qiáng),賀福初;c-Jun/激活蛋白-1活性調(diào)節(jié)研究進(jìn)展[J];生物化學(xué)與生物物理進(jìn)展;2002年06期
6 梁琳慧,韓忠朝;蛋白質(zhì)相互作用的研究方法[J];生命的化學(xué);2005年03期
7 燕飛,成卓敏;RNA干擾技術(shù)在幾項(xiàng)研究領(lǐng)域的應(yīng)用[J];中國生物工程雜志;2004年08期
8 王波,陳梅紅;反義技術(shù)研究進(jìn)展[J];中國生物工程雜志;2004年12期
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