Trans-repression of β-Catenin Activity by Nuclear Receptors*
By Salimuddin Shah, A. Hecht, R. Pestell, S. Byers. Journal of Biological Chemistry, 2003
102 citations recorded by the source corpus.
The signaling/oncogenic activity of β-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 β-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 β-catenin signaling by nuclear receptors and their ligands.
Subfields: Molecular Biology
View Paper: https://www.semanticscholar.org/paper/70fa86f2c5555f4a73d73bc14ae7fece266ae3f1
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In Molecular Biology
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- The nonskeletal effects of vitamin D: an Endocrine Society scientific statement. (2012, background): “Studies directed at identifying molecular partners of the unliganded VDR that play a role in the regulation of keratinocyte stem cell function demonstrated that, in contrast to investigations demonstrating that the liganded VDR impairs canonical Wnt signaling (30, 78), the unliganded VDR is essentia”