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TRAF2 plays a dual role in NF‐κB‐dependent gene activation by mediating the TNF‐induced activation of p38 MAPK and IκB kinase pathways
Author(s) -
Carpentier Isabelle,
Declercq Wim,
Malinin Nikolai L,
Wallach David,
Fiers Walter,
Beyaert Rudi
Publication year - 1998
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(98)00226-9
Subject(s) - traf2 , mapk/erk pathway , p38 mitogen activated protein kinases , kinase , microbiology and biotechnology , fadd , mediator , map kinase kinase kinase , tumor necrosis factor alpha , protein kinase a , signal transduction , nf κb , chemistry , biology , caspase , cancer research , apoptosis , biochemistry , tumor necrosis factor receptor , immunology , programmed cell death
We previously demonstrated that p38 MAPK is a crucial mediator in the NF‐κB‐dependent gene activation induced by TNF. Here, we have studied the role of several TNF receptor‐associated proteins and caspases in p38 MAPK activation by TNF. The latter appears to be dependent on TRAF2, but independent of FADD or caspases. Remarkably, p38 MAPK activation by TNF proceeds independently of the TRAF2‐associated NF‐κB‐inducing kinase NIK, which is known to bind and activate two recently identified IκB kinases. These results demonstrate that two kinase pathways involved in NF‐κB regulation, viz. NIK and p38 MAPK‐mediated, diverge at the level of TRAF2.