Hsp90-mediated inhibition of FKBP38 regulates apoptosis in neuroblastoma cells
摘要：Abstract The FK506-binding protein 38 (FKBP38) is a pro-apoptotic regulator of Bcl-2 in neuroblastoma cells. Hsp90 inhibits the pro-apoptotic FKBP38/CaM/Ca2+ complex and thus prevents interactions between FKBP38 and Bcl-2. Here we show that Hsp90 increases cell survival rates of neuroblastoma cells after apoptosis induction. Depletion of FKBP38 by short interference RNA significantly decreased the anti-apoptotic effect of Hsp90 expression. In addition, the influence of high cellular Hsp90 levels was only observed in post-stimulation apoptosis that is sensitive to selective FKBP38 active site inhibition. Similar anti-apoptotic effects in neuroblastoma cells were observed after stimulation of endogenous Hsp90 expression. Hence, the inhibition of FKBP38 by Hsp90 participates in programmed cell death control of neuroblastoma cells.
关键词：FKBP FK506-binding protein; FK506-binding protein; PPIase peptidyl–prolyl cis/trans isomerases; peptidyl–prolyl cis/trans isomerases; siRNA short interference RNA; short interference RNA; TPR tetratricopeptide repeat; tetratricopeptide repeat; IAA iodoacetic acid; iodoacetic acid; Apoptosis; Bcl-2; PPIase; FK506-binding protein; FKBP38
论文方向：[{"id":13,"name":"细胞生物学"},{"id":879,"name":"生物化学"}]
发表期刊：FEBS Letters Volume 581, Issue 29
发表时间：Tue Dec 11 00:00:00 CST 2007
数字识别码：10.1016/j.febslet.2007.11.037
是否作者本人： 否
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