Format

Send to

Choose Destination
J Biol Chem. 2003 Nov 28;278(48):48137-45. Epub 2003 Sep 12.

Trans-repression of beta-catenin activity by nuclear receptors.

Author information

1
The Lombardi Cancer Center and the Department of Oncology, Georgetown University School of Medicine, Washington, DC 20057, USA.

Abstract

The signaling/oncogenic activity of beta-catenin can be repressed by the activation of nuclear receptors such as the vitamin A, vitamin D, and androgen receptors. Although these receptors directly interact with beta-catenin and can sequester it away from its transcription factor partner T-cell factor, it is not known if this is the mechanism of trans-repression. Using several different promoter constructs and nuclear receptors and mammalian two-hybrid and mutation analyses we now show that interaction with the co-activator, p300, underlies the trans-repression of beta-catenin signaling by nuclear receptors and their ligands.

PMID:
12972427
DOI:
10.1074/jbc.M307154200
[Indexed for MEDLINE]
Free full text

Supplemental Content

Full text links

Icon for HighWire
Loading ...
Support Center