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Title 

2,3,7,8-Tetrachlorodibenzo-p-dioxin activates ERK and p38 mitogen-activated protein kinases in RAW 264.7 cells

Authors 

S J ParkWoon Kee YoonH J KimH Y SonS W ChoK S JeongT H KimS H KimS R KimS Y Ryu

Publisher 

International Institute of Anticancer Research (IIAR)

Issue Date 

2005

Citation 

Anticancer Research, vol. 25, no. 4, pp. 2831-2836

Keywords 

2,3,7,8-Tetrachlorodibenzo-p-dioxincaspase-3ERKJNKp38RAW 264.7 cells2,3,7,8 tetrachlorodibenzo para dioxincaspase 3mitogen activated protein kinasemitogen activated protein kinase p38

Abstract 

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a widespread environmental contaminant, exposure to it eliciting a broad spectrum of deleterious pathophysiological effects. Since mitogen-activated protein kinase (MAPK) pathways appear to play an important role in both cell survival and the apoptotic process, we assessed the effects of TCDD on the activation of extracellular signal-regulated kinase (ERK), Jun-N-terminal kinase (JNK), p38 MAPKs and caspase-3 in RAW 264.7 cells. TCDD treatment induced a transient upshift in ERK activity, followed by a decline, but a concomitant dramatic activation of p38. However, TCDD did not cause any apparent change in the activity of JNK, though it induced an up-regulation in caspase-3 activity. These results demonstrate that the equilibrium between the ERK and p38 pathways is critical to the fate of the cells, and that the activation of p38, upstream of caspase, plays an important role in the apoptotic process. The data obtained in this study also suggests that TCDD activates the MAPK pathway via an arylhydrocarbon receptor (AhR)-independent mechanism in RAW 264.7 murine macrophages.

ISSN 

0250-7005

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2019-05-02


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