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摘要:
Interleukin I receptor associated kinase 1 (IRAK1) is a downstream signal molecule of activated MyD88 recruitment, which can activate Fas associated death domain protein (FADD) to induce apoptosis. IRAK1 can also activate tumor necrosis factor-related factor 6 (TRAF6) and induce the expression of a series of downstream specific genes. IRAK1 is an essential factor in the induction of mitochondrial division and necroptosis. In the current study, RNAi technique was used to silence IRAK1, and the apoptosis and necroptosis rate of SK-Hep1 cells were detected by flow cytometry. The apoptosis and the necroptosis pathway of hepatoma SK-Hep1 cells were blocked separately, and the expressions of FADD, RIP1 and TRAF6 genes were silenced separately. The results showed when the expression of IRAK1 was down-regulated, the apoptosis and necroptosis rate of SK-Hep1 cells were significantly increased. With silenced FADD, RIP1 and TRAF6, respectively, the expression of IRAK1 protein had no significant change. However, the expression of IRAK1 mRNA decreased significantly (p < 0.01) after the silencing of RIP1 and TRAF6 genes, while the IRAK1 mRNA did not change significantly after the silencing of FADD genes;when z-VAD-FMK was interfered, the expression of IRAK1 mRNA decreased significantly after the silencing of TRAF6 genes, while the IRAK1 mRNA did not change significantly after the silencing of FADD and RIP1genes. The study shows that RAK1 gene inhibits apoptosis and necroptosis in SK-Hep1 cells. TRAF6 gene affected the role of IRAK1 in apoptosis and necroptosis, RIP1 gene affected the role of IRAK1 in apoptosis, while FADD gene did not affect the role of IRAK1 in apoptosis and necroptosis.
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篇名 Effect of IRAK1 on Apoptosis and Necroptosis of Hepatoma Cell Line SK-Hep1
来源期刊 中医(英文) 学科 医学
关键词 IRAK1 APOPTOSIS NECROPTOSIS FADD RIP1 TRAF6
年,卷(期) zyyw_2019,(1) 所属期刊栏目
研究方向 页码范围 19-29
页数 11页 分类号 R73
字数 语种
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研究主题发展历程
节点文献
IRAK1
APOPTOSIS
NECROPTOSIS
FADD
RIP1
TRAF6
研究起点
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研究分支
研究去脉
引文网络交叉学科
相关学者/机构
期刊影响力
中医(英文)
季刊
2151-1918
武汉市江夏区汤逊湖北路38号光谷总部空间
出版文献量(篇)
35
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0
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