Abstract
Past Visits Present: TCF/LEFs Partner with ATFs for β-Catenin–Independent Activity
Highlights
TCF/LEF transcription factors are best known for their role as mediators of Wnt signaling, helping Wnt direct developmental transitions of stem cells in tissues or driving cell transformation and cancer when Wnt is aberrantly active
Knockdown of ATF2 reduced cell growth and lowered expression of TCF1 and LEF1 target genes, similar to effects from overexpression of a dominant negative form of TCF4. Observations such as these suggest that ATF2 is integral to the regulatory role that TCF1/LEF1 play in lymphocytes
One of the first interactions for LEF1 and, later, TCF1 was with proteins that bind an ATF/CREB element in the T-Cell Receptor alpha chain enhancer (Figure 1D; [4,5]); interestingly, ATF4 was first discovered on the basis of its binding to this element
Summary
TCF/LEF transcription factors are best known for their role as mediators of Wnt signaling, helping Wnt direct developmental transitions of stem cells in tissues or driving cell transformation and cancer when Wnt is aberrantly active. Very little stabilized b-catenin could be detected and reporter activity was recapitulated using truncated forms of TCF1 missing the Nterminal b-catenin–binding domain (isoforms labelled dominant negatives, or dnTCF/dnLEF [Figure 1A]). Grumolato et al report that ATF family members (especially ATF2) bind directly to TCF1 and LEF1, not TCF4, and that interactions primarily require the Context Dependent Regulatory domain (CRD; Figure 1A, B).
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