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J Clin Invest. 2011 Apr;121(4):1263-5. doi: 10.1172/JCI57080. Epub 2011 Mar 14.

Good COP1 or bad COP1? In vivo veritas.

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1
Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA.

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.

PMID:
21403396
PMCID:
PMC3069793
DOI:
10.1172/JCI57080
[Indexed for MEDLINE]
Free PMC Article
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