Journal
EMBO REPORTS
Volume 1, Issue 1, Pages 24-28Publisher
WILEY
DOI: 10.1093/embo-reports/kvd012
Keywords
-
Categories
Ask authors/readers for more resources
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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available