Functional Interaction Between ß-Catenin and FOXO in Oxidative Stress Signaling

By M. Essers, Lydia M M de Vries-Smits, Nick Barker, Paulien E. Polderman, B. Burgering, H. Korswagen. Science, 2005

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Loss of FBP1 by Snail-mediated Repression Provides Metabolic Advantages in Basal-like Breast Cancer (2013, neutral): “In the cellular aging process, ROS antagonizes b-catenin activity by shifting the interaction of b-catenin with TCF4 toward FOXO3a (Figure 7D) (Bowerman, 2005; Essers et al., 2005; Manolagas and Almeida, 2007).”
FoxOs are critical mediators of hematopoietic stem cell resistance to physiologic oxidative stress. (2007, background): “In addition, increased levels of ROS have been reported to mediate association of b-catenin and FoxO; b-catenin is purported to enhance FoxO’s role in inhibiting cell cycle progression (Essers et al., 2005).”
FOXO transcription factors at the interface between longevity and tumor suppression (2005, background): “The binding of b-catenin to FOXO factors enhances the ability of FOXO proteins to inhibit cell cycle progression (Essers et al., 2005).”
Osteocytes, mechanosensing and Wnt signaling. (2008, background): “Evidence has also been presented for an interaction with the FOXO family of transcription factors that are important in cellular responses to oxidative stress (33)(4).”
The many faces and functions of β‐catenin (2012, positive): “This mechanism is evolutionarily conserved (Essers et al , 2005).”