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The role of the death‐domain kinase RIP in tumour‐necrosis‐factor‐induced activation of mitogen‐activated protein kinases
Author(s) -
Devin Anne,
Lin Yong,
Liu Zhenggang
Publication year - 2003
Publication title -
embo reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.584
H-Index - 184
eISSN - 1469-3178
pISSN - 1469-221X
DOI - 10.1038/sj.embor.embor854
Subject(s) - kinase , p38 mitogen activated protein kinases , mapk/erk pathway , microbiology and biotechnology , mitogen activated protein kinase , mitogen activated protein kinase kinase , map kinase kinase kinase , ask1 , protein kinase a , mitogen activated protein kinase 3 , biology , chemistry , cancer research
The death‐domain kinase RIP (receptor‐interacting protein) is an important effector of tumour necrosis factor (TNF) signalling and is essential for TNF‐induced nuclear factor‐κB activation. However, the function of RIP in the TNF‐induced activation of mitogen‐activated protein kinases (MAPKs) has not been fully investigated. In this report, using Rip null ( Rip −/− ) mouse fibroblast cells, we investigated whether RIP is required for TNF‐induced activation of the MAPKs extracellular‐signal‐related kinase (ERK), p38 and c‐Jun amino‐terminal kinase (JNK). We found that TNF‐induced activation of ERK, p38 and JNK is decreased in Rip −/− cells. The activation of these kinases by interleukin‐1 is normal in Rip −/− cells. More importantly, we showed that the kinase activity of RIP is needed for ERK activation.