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Title 

Cytosolic peroxiredoxin attenuates the activation of JNK and p38 but potentiates that of ERK in HeLa cells stimulated with tumor necrosis factor-α

Authors 

S W KangT S ChangT H LeeE S KimDae Yeul YuS G Rhee

Publisher 

American Society for Biochemistry and Molecular Biology

Issue Date 

2004

Citation 

Journal of Biological Chemistry, vol. 279, no. 4, pp. 2535-2543

Keywords 

cellstumorsperoxiredoxintumor necrosis factor alphacell deathcell functioncell stimulationcell survivalenzyme activationhuman cell

Abstract 

Tumor necrosis factor-α (TNF-α) induces the activation of all three types of mitogen-activated protein kinase (MAPK): c-Jun NH 2-terminal kinase (JNK), p38, and extracellular signal-regulated kinase (ERK). This cytokine also induces the production of several types of reactive oxygen species, including H2O2. With the use both of HeLa cells expressing wild-type or dominant negative forms of the cytosolic peroxidase peroxiredoxin II and of mouse embryonic fibroblasts deficient in this protein, we evaluated the roles of H2O2 in the activation of MAPKs by TNF-α. In vitro kinase assays as well as immunoblot analysis with antibodies specific for activated MAPKs indicated that H2O2 produced in response to TNF-α potentiates the activation of JNK and p38 induced by this cytokine but inhibits that of ERK. Our results also suggest that cytosolic peroxiredoxins are important regulators of TNF signaling pathways.

ISSN 

0021-9258

Link 

http://dx.doi.org/10.1074/jbc.M307698200

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2019-05-02


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