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https://doi.org/10.1083/jcb.200602149
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. https://doi.org/10.1083/jcb.200602149 | 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 | URI: | http://scholarbank.nus.edu.sg/handle/10635/109391 | ISSN: | 00219525 | DOI: | 10.1083/jcb.200602149 |
Appears in Collections: | Staff Publications |
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