DC Field | Value | Language |
---|---|---|
dc.contributor.author | Kim, Jin Woo | - |
dc.contributor.author | Joe, Cheol O. | - |
dc.contributor.author | Choi, Eui-Ju | - |
dc.date.accessioned | 2011-09-19T01:31:51Z | - |
dc.date.available | 2011-09-19T01:31:51Z | - |
dc.date.issued | 2001-05-21 | - |
dc.identifier.citation | Journal of Biological Chemistry, Vol.276, No.29, pp.27064-27070 | en |
dc.identifier.uri | http://hdl.handle.net/10203/25219 | - |
dc.description.abstract | Receptor-interacting protein (RIP), a death domain serine/threonine kinase, has been shown to play a critical role in tumor necrosis factor- (TNF-)-induced activation of the nuclear factor-B signaling pathway. We demonstrate here that ectopically expressed RIP induces I-B kinase- (IKK) activation in intact cells and that RIP-induced IKK activation can be blocked by a kinase-inactive form of MEKK1, MEKK1(K1253M). Interestingly, RIP physically associated with MEKK1 both in vitro and in vivo. RIP phosphorylated MEKK1 at Ser-957 and Ser-994. Our data also indicate that RIP induced the stimulation of MEKK1 but not MEKK1(S957A/S994A) in transfected cells. Furthermore, overexpressed MEKK1(S957A/S994A) inhibited the RIP-induced activation of both IKK and nuclear factor-B. We also demonstrated that the TNF--induced MEKK1 activation was defective in RIP-deficient Jurkat cells. Taken together, our results suggest that RIP phosphorylates and activates MEKK1 and that RIP is involved in TNF--induced MEKK1 activation. | en |
dc.description.sponsorship | We thank Dr. D. Goeddel (Tularik Inc.) and Dr. G. Johnson (University of Colorado) for kindly providing cDNA clones and Dr. B. Seed (Harvard Medical School) for the RIP-deficient Jurkat cells. | en |
dc.language.iso | en_US | en |
dc.publisher | American Society for Biochemistry and Molecular Biology | en |
dc.title | Role of receptor-interacting protein in tumor necrosis factor-α dependent MEKK1 activation. | en |
dc.type | Book | en |
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