作者: Yan-Lin Guo , Baobin Kang , Jiahuai Han , John R. Williamson
DOI: 10.1002/JCB.1180
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摘要: p38 MAP kinases (p38) and c-Jun N-terminal protein (JNK) have been associated with TNF-α-induced apoptosis. However, recent studies indicate that an early but brief activation of JNK and/or may actually protect some cells from Whether the provides a pro- or anti-apoptotic signal for TNF-α has controversial. In this study, we investigated role in regulation cytotoxicity rat mesangial cells. Treatment alone had little effect on their viability, they became very sensitive to apoptosis when treated presence inhibitor SB 203580. These results suggested pathway is critical survive toxic TNF-α. Using adenovirus-mediated gene transfer technique, further demonstrated p38β, not p38α, essential toxicity. It speculated there synergetic interaction between nuclear factor-κB (NF-κB) pathways protecting certain expression neither p38β nor its dominant negative mutant interfered translocation NF-κB, initial step NF-κB activation. While it unclear whether regulates transcription activity at other steps, apparent does affect stage translocation. J. Cell. Biochem. 82: 556–565, 2001. © 2001 Wiley-Liss, Inc.