葡萄孢霉素
蛋白酵素
半胱氨酸蛋白酶
细胞生物学
细胞凋亡
激酶
化学
蛋白激酶A
蛋白激酶C
半胱氨酸蛋白酶3
分子生物学
生物化学
生物
酶
程序性细胞死亡
作者
Han‐Jung Chae,Jian Kang,Jong-Ook Byun,Kyung-Soo Han,Dae-Up Kim,Sang-Woo Oh,Hyung-Min Kim,Soo‐Wan Chae,Hyung‐Ryong Kim
标识
DOI:10.1006/phrs.2000.0700
摘要
Staurosporine, a microbial alkaloid, is a strong inhibitor of protein kinases. We induced apoptosis in murine osteoblast MC3T3E-1 cells by exposure to the staurosporine. Staurosporine transiently increased the phosphotransferase activity of c-Jun N-terminal kinase-1 (JNK1), which in turn may activate the transcriptional activity of activating protein-1 (AP-1). We then prepared extracts from staurosporine-treated MC3T3E-1 cells and monitored the cleavage of acetyl-YVAD-AMC and acetyl-DEVD-AMC, fluorogenic substrates of caspase-1-like and caspase-3-like proteases, respectively. Staurosporine caused a significant increase in the proteolytic activity of caspase-3-like proteases, but not in the activity of caspase-1-like proteases. Furthermore, staurosporine increased the transcriptional activity of nuclear factor- kappa B (NF- kappa B). These data suggest that staurosporine-induced apoptosis in osteoblasts may occur via activation of JNK1, caspase-3-like proteases, and transcriptional factors including AP-1 and NF- kappa B.
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