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TRAF6 deficiency promotes TNF-induced cell death through inactivation of GSK3β

Title
TRAF6 deficiency promotes TNF-induced cell death through inactivation of GSK3β
Authors
Yoon K.Jung E.J.Lee S.R.Kim J.Choi Y.Lee S.Y.
Ewha Authors
이수영김재상
SCOPUS Author ID
이수영scopus; 김재상scopus
Issue Date
2008
Journal Title
Cell Death and Differentiation
ISSN
1350-9047JCR Link
Citation
vol. 15, no. 4, pp. 730 - 738
Indexed
SCI; SCIE; SCOPUS WOS scopus
Abstract
TNF receptor-associated factor 6 (TRAF6) plays a key role in the regulation of innate immune responses by mediating signals from both TNF receptors (TNFRs) and interleukin-1 receptors (IL-1Rs)/Toll-like receptors (TLRs). Here, we define a new role for TRAF6 in antagonizing cell death during TNF signaling. In TRAF6-deficient 3T3 (T6 -/- 3T3) cells, TNF stimulation leads to the accumulation of reactive oxygen species (ROS), which in turn results in prolonged c-Jun N-terminal kinase (JNK) activation and accelerated cell death. Furthermore, TNF-induced p65/RelA phosphorylation as well as transcriptional activity of nuclear factor-κB (NF-κB) was significantly downregulated in T6 -/- 3T3 cells. Interestingly, TRAF6 deficiency leads to constitutive phosphorylation and inactivation of glycogen synthase kinase 3β (GSK3β). Restoration of GSK3β activity through exogenous expression of a GSK3β constitutive active form rescued cell death in TRAF6-null 3T3 cells. These data suggest a role for TRAF6 in the maintenance of cell survival by regulating GSK3β activity in TNF signaling.
DOI
10.1038/sj.cdd.4402304
Appears in Collections:
자연과학대학 > 생명과학전공 > Journal papers
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