Please use this identifier to cite or link to this item: http://hdl.handle.net/11455/69750
標題: CpG-B oligodeoxynucleotide promotes cell survival via up-regulation of Hsp70 to increase Bcl-x(L) and to decrease apoptosis-inducing factor translocation
作者: Kuo, C.C.
Liang, S.M.
Liang, C.M.
關鍵字: heat-shock proteins
negative regulation
apaf-1 apoptosome
leukemia-cells
dna
heat-shock-protein-70
death
activation
overexpression
downstream
期刊/報告no:: Journal of Biological Chemistry, Volume 281, Issue 50, Page(s) 38200-38207.
摘要: Unmethylated CpG oligodeoxynucleotides (ODNs) activate immune responses in a TLR9-dependent manner. In this study, stimulation of mouse macrophages with CpG-B ODN increased cellular Hsp70 expression and prevented apoptosis induced by serum starvation or staurosporine treatment. CpG-B ODN-induced Hsp70 expression depended on TLR9, MyD88, and phosphatidylinositol 3-kinase. Inhibition of Hsp70 synthesis by an inhibitor (quercetin) or antisense hsp70 attenuated not only Hsp70 expression but also the anti-apoptotic capacity of CpG-B ODN. Ectopic expression of Hsp70 rescued the inhibitory effect of quercetin on CpG-B ODN-induced anti-apoptosis. Additional experiments demonstrated that quercetin and antisense hsp70 modulated CpG-B ODN-induced anti-apoptosis via a caspase-3-independent pathway by down-regulating the survival gene bcl-x(L) and by increasing translocation of apoptosis-inducing factor. These findings suggest that CpG-B ODN may up-regulate Hsp70 via a TLR9/MyD88/phosphatidylinositol 3-kinase pathway to increase Bcl-x(L) and to decrease apoptosis-inducing factor nuclear translocation, resulting in anti-apoptosis.
URI: http://hdl.handle.net/11455/69750
ISSN: 0021-9258
文章連結: http://dx.doi.org/10.1074/jbc.M605439200
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