Abstract：
:Oncoproteins and tumor suppressors antagonistically converge on critical nodes governing neoplastic growth, invasion, and metastasis. We discovered that phosphorylation of the ETS1 and ETS2 transcriptional oncoproteins at specific serine or threonine residues creates binding sites for the COP1 tumor suppressor protein, which is an ubiquitin ligase component, leading to their destruction. In the case of ETS1, however, phosphorylation of a neighboring tyrosine residue by Src family kinases disrupts COP1 binding, thereby stabilizing ETS1. Src-dependent accumulation of ETS1 in breast cancer cells promotes anchorage-independent growth in vitro and tumor growth in vivo. These findings expand the list of potential COP1 substrates to include proteins whose COP1-binding sites are subject to regulatory phosphorylation and provide insights into transformation by Src family kinases.
journal_name
Cancer Celljournal_title
Cancer cellauthors
Lu G,Zhang Q,Huang Y,Song J,Tomaino R,Ehrenberger T,Lim E,Liu W,Bronson RT,Bowden M,Brock J,Krop IE,Dillon DA,Gygi SP,Mills GB,Richardson AL,Signoretti S,Yaffe MB,Kaelin WG Jrdoi
10.1016/j.ccr.2014.06.026subject
Has Abstractpub_date
2014-08-11 00:00:00pages
222-34issue
2eissn
1535-6108issn
1878-3686pii
S1535-6108(14)00276-1journal_volume
26pub_type
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