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Signal Transduction of Thapsigargin-induced Apoptosis in Osteoblast
CHAE, H. J.,CHAE, S. W.,WEON, K. H.,KANG, J. S.,KIM, H. R. 원광대학교 생체재료·매식연구소 2000 원광생체재료·매식 Vol.9 No.1
The toxicity of thapsigargin, a selective inhibitor of endoplasmic reticular Ca^2+ -ATPase, was investigated in osteoblasts. We induced apoptosis in murine osteoblastic MC3T3E1 cells by exposure to the thapsigargin. Thapsigargin transiently increased the phosphotransferase activity of c-Jun N-terminal kinases 1(JNK1), which might in turn activate transcriptional activity of activation protein-1(AP-1) we then prepared extracts from thapsigargin-treated MC3T3E1 cells and monitored cleavage of acetyl-YVAD-AMC and acetyl-DEVD-AMC, fluorogenic substrates for caspase 1-like and caspase 3-like proteases, respectively. Thapsigargin significantly increased the proteolytic activity of caspase 3-like proteases, but not the activity of caspase 1-like proteases. Furthermore, thapsigargin increased the transcriptional activity of nuclear factor-κB(NF-κB). These data suggest that thapsigargin-induced apoptosis in osteoblasts may be via activation of JNK1, caspase 3-like family proteases, and transcripitional factors including AP-1 and NF-κB. (Bone 25: 453-458; 1999) ⓒ1999 by Elsevier Science Inc. All rights reserved.