Canonical wnt signaling involves stabilization of beta catenin in the cytoplasm and its subsequent translocation to the nucleus where it acts in concert with other transcription factors. Level of wnt signaling is often gauged with levels of its target genes, for example Axin2. Is it possible that in cell culture, there is nuclear translocation of beta catenin because of some treatment and at the same time target genes are down? The time frame between treatment and wnt signaling assessment is 16 h. Is there any negative feedback mechanism involved in the downregulation of wnt targets despite of abundant nuclear beta catenin?
Wnt signaling status revolves around its time and production of Wnt ligand, Wnt antagonist followed by the binding status of Wnt receptors, and co-receptors.
B-catenin is a central player of the Wnt signaling pathway but b-catenin itself is highly regulated by multiple genes as well as many other pathway components are there that trigger b-catenin. So, translocation of b-catenin into the nucleus could be mediated by other regulators also which may not be associated with the death complex destabilization formed by APC, GSK3b, Axin2, Dvl, CKl.
Article β-Catenin Can Be Transported into the Nucleus in a Ran-unass...
https://jcs.biologists.org/content/119/7/1453
In many studies, researchers focussed on Wnt inhibitors/antagonists (Dkk1 & sFRP) followed by stabilization of death complex (GSK3b, APC, Axin2) components only and assumed to be Wnt inhibition.
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