JWA在K562和MCF-7細(xì)胞應(yīng)答氧化應(yīng)激中的作用及其分子機(jī)制
本文關(guān)鍵詞: JWA K562細(xì)胞 MCF-7細(xì)胞 氧化應(yīng)激 熱休克蛋白質(zhì) 熱休克因子 p53 procaspase-3 出處:《南京醫(yī)科大學(xué)》2005年碩士論文 論文類型:學(xué)位論文
【摘要】:人類許多疾病與接觸的環(huán)境因素有關(guān),各種物理的、化學(xué)的和生物的有害因素暴露后,機(jī)體細(xì)胞很快產(chǎn)生應(yīng)答,表現(xiàn)為一系列基因有序地發(fā)生表達(dá)水平的變化,使細(xì)胞盡快適應(yīng)變化的環(huán)境而維持內(nèi)平衡。有害環(huán)境因素可直接引起細(xì)胞基因組的損傷,或化學(xué)物在體內(nèi)特異性分布和代謝后損傷基因組結(jié)構(gòu),或干擾細(xì)胞內(nèi)的信號(hào)轉(zhuǎn)導(dǎo)通路,最后引起疾病。 JWA基因是周建偉等1998年發(fā)現(xiàn)并克隆的受維甲酸誘導(dǎo)的新基因,并獲得美國(guó)基因庫(kù)新基因編號(hào)(AF070523.1)。通過對(duì)其結(jié)構(gòu)分析發(fā)現(xiàn),JWA基因啟動(dòng)子序列中含有包括熱休克反應(yīng)元件(hRE)、應(yīng)激反應(yīng)元件(SRE)等多種反應(yīng)元件。近幾年本課題組研究表明,JWA是一種新的微管相關(guān)蛋白,不僅廣泛地參與調(diào)節(jié)多種分化誘導(dǎo)劑(如TPA、ATRA、4HPR和AS_2O_3)涉及的信號(hào)通路,而且活躍地參與細(xì)胞對(duì)應(yīng)激刺激(如氧化應(yīng)激和熱應(yīng)激)的應(yīng)答。但是JWA基因是如何參與調(diào)控細(xì)胞氧化應(yīng)激的信號(hào)通路尚不清楚。 本課題用不同濃度的過氧化氫(H_2O_2)處理K562(慢性骨髓性
[Abstract]:Many human diseases are related to environmental factors in contact. After exposure to various physical, chemical and biological harmful factors, the cells of the body quickly respond, which is manifested by a series of gene expression changes in an orderly manner. The harmful environmental factors can directly cause the damage of the cell genome, or the specific distribution of chemicals in the body and damage to the genome structure after metabolism. Or interfere with the intracellular signal transduction pathway, and finally cause disease. JWA gene is a novel gene induced by retinoic acid found and cloned by Zhou Jianwei in 1998. The new gene number AF070523.1in American gene bank was obtained. It was found that the promoter sequence of JWA gene contained heat shock response element (hREE). In recent years, our research has shown that JWA is a new microtubule-associated protein, which is not only involved in the regulation of various differentiation inducers (such as TPA). ATRA-4HPR and ASSP _ 2o _ 3) are involved in the signal pathway. But it is not clear how JWA gene is involved in the regulation of cellular oxidative stress signaling pathway. In this study, K562 (chronic bone marrow) was treated with different concentrations of H _ 2O _ 2 hydrogen peroxide.
【學(xué)位授予單位】:南京醫(yī)科大學(xué)
【學(xué)位級(jí)別】:碩士
【學(xué)位授予年份】:2005
【分類號(hào)】:R363
【共引文獻(xiàn)】
相關(guān)期刊論文 前5條
1 馬琳琳,孫文靖,傅松濱;p53基因網(wǎng)絡(luò)王國(guó)[J];國(guó)外醫(yī)學(xué).遺傳學(xué)分冊(cè);2005年01期
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相關(guān)碩士學(xué)位論文 前2條
1 趙晶;中國(guó)肝癌病人中四種p53突變體細(xì)胞功能的研究[D];西北農(nóng)林科技大學(xué);2007年
2 李向榮;不同劑量葛根素對(duì)腦缺血/再灌注大鼠腦皮質(zhì)區(qū)Bcl-2、P53的影響[D];遵義醫(yī)學(xué)院;2009年
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