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Abstract
The evolutionarily conserved protein COP1 has been shown to operate as an E3 ubiquitin ligase complex, and a number of putative substrates have been identified, including the c-JUN oncoprotein and p53 tumor suppressor protein. New work by Migliorini and colleagues described in the current issue of JCI demonstrates that COP1 acts as a tumor suppressor in vivo and does so, at least in part, by promoting the destruction of c-JUN. These findings challenge the view that COP1 regulates p53 stability and call into question the wisdom of developing COP1 inhibitors as potential anticancer agents.
Authors
Wenyi Wei, William G. Kaelin Jr.
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Citations to this article in year 2014 (2)
| Title and authors | Publication | Year |
|---|---|---|
|
Phosphorylation of ETS1 by Src Family Kinases Prevents Its Recognition by the COP1 Tumor Suppressor
G Lu, Q Zhang, Y Huang, J Song, R Tomaino, T Ehrenberger, E Lim, W Liu, RT Bronson, M Bowden, J Brock, IE Krop, DA Dillon, SP Gygi, GB Mills, AL Richardson, S Signoretti, MB Yaffe, WG Kaelin |
Cancer Cell | 2014 |
|
APCCdc20 Suppresses Apoptosis through Targeting Bim for Ubiquitination and Destruction
L Wan, M Tan, J Yang, H Inuzuka, X Dai, T Wu, J Liu, S Shaik, G Chen, J Deng, M Malumbres, A Letai, MW Kirschner, Y Sun, W Wei |
Developmental Cell | 2014 |
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