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EMBO Rep. 2000 Jul;1(1):24-8.

Curbing the nuclear activities of beta-catenin. Control over Wnt target gene expression.

Author information

1
Max-Planck-Institute of Immunobiology, Freiburg, Germany. hecht@immunbio.mpg.de

Abstract

Wnt molecules control numerous developmental processes by altering specific gene expression patterns, and deregulation of Wnt signaling can lead to cancer. Many Wnt factors employ beta-catenin as a nuclear effector. Upon Wnt stimulation, beta-catenin heterodimerizes with T-cell factor (TCF) DNA-binding proteins to form a transcriptional activator complex. As the activating subunit of this complex, beta-catenin performs dual tasks: it alleviates repression of target gene promoters and subsequently it activates them. Beta-catenin orchestrates these effects by recruiting chromatin modifying cofactors and contacting components of the basal transcription machinery. Although beta-catenin and TCFs are universal activators in Wnt signaling, their target genes display distinct temporal and spatial expression patterns. Apparently, post-translational modifications modulate the interactions between TCFs and beta-catenin or DNA, and certain transcription factors can sequester beta-catenin from TCFs while others synergize with beta-catenin-TCF complexes in a promoter-specific manner. These mechanisms provide points of intersection with other signaling pathways, and contribute to the complexity and specificity of Wnt target gene regulation.

PMID:
11256619
PMCID:
PMC1083688
DOI:
10.1093/embo-reports/kvd012
[Indexed for MEDLINE]
Free PMC Article
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