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Xaf1通过胱冬肽酶非依赖机制释放细胞色素C诱导凋亡 被引量:2

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摘要 【目的】利用基因开关调节Xaf1-Saos诱导细胞株,检测Xaf1对肿瘤坏死因子受体(TNFR)(外源性)以及线粒体(内源性)凋亡信号通路的影响,研究Xaf1诱导肿瘤细胞凋亡的机制。【方法】流式细胞术DNA含量检测Xaf1诱导的细胞凋亡和Bcl2对Xaf1-Saos细胞凋亡的影响,Gel Mobility Shift Assay检测NFkB的DNA结合活性,激酶分析法检测SAPK/ JNK激酶的活性,细胞色素C流式细胞术检测Xaf1对细胞色素C释放的调节。【结果】Xaf1与TNFα显著协同诱导细胞凋亡,凋亡峰值49%,Xaf1的表达抑制TNFα介导的NFkB的DNA结合活性(50%)和JNK/SAPK的活性,Xaf1可释放细胞色素C,而且不被胱冬肽酶抑制剂所抑制(Z-VAD)。【结论】Xaf1通过胱冬肽酶非依赖机制释放细胞色素C而诱导肿瘤细胞凋亡。
出处 《中山大学学报(医学科学版)》 CAS CSCD 北大核心 2006年第B03期54-56,共3页 Journal of Sun Yat-Sen University:Medical Sciences
基金 国家中医药管理局基金资助项目(2005LHR08)
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共引文献4

同被引文献32

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