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Title: IKKβ programs to turn on the GADD45α-MKK4-JNK apoptotic cascade specifically via p50 NF-κB in arsenite response
Authors: Song, L.
Li, J.
Zhang, D.
Liu, Z.-G.
Ye, J.
Zhan, Q.
Shen, H.-M. 
Whiteman, M.
Huang, C.
Issue Date: 20-Nov-2006
Citation: Song, L., Li, J., Zhang, D., Liu, Z.-G., Ye, J., Zhan, Q., Shen, H.-M., Whiteman, M., Huang, C. (2006-11-20). IKKβ programs to turn on the GADD45α-MKK4-JNK apoptotic cascade specifically via p50 NF-κB in arsenite response. Journal of Cell Biology 175 (4) : 607-617. ScholarBank@NUS Repository.
Abstract: Cross talk between NF-κB and c-Jun N-terminal kinases (JNKs) has been implicated in the cell life and death decision under various stresses. Functional suppression of JNK activation by NF-κB has recently been proposed as a key cellular survival mechanism and contributes to cancer cells escaping from apoptosis. We provide a novel scenario of the proapoptotic role of IκB kinase β (IKKβ)-NF-κB, which can act as the activator of the JNK pathway through the induction of GADD45α for triggering MKK4/JNK activation, in response to the stimulation of arsenite, a cancer therapeutic reagent. This effect of IKKβ-NF-κB is dependent on p50 but not the p65/relA NF-κB subunit, which can increase the stability of GADD45α protein through suppressing its ubiquitination and proteasome-dependent degradation. IKKβ-NF-κB can therefore either activate or suppress the JNK cascade and consequently mediate pro- or antiapoptotic effects, depending on the manner of its induction. Furthermore, the NF-κB p50 subunit can exert a novel regulatory function on protein modification independent of the classical NF-κB transcriptional activity. © The Rockefeller University Press.
Source Title: Journal of Cell Biology
ISSN: 00219525
DOI: 10.1083/jcb.200602149
Appears in Collections:Staff Publications

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