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. 2015 Jun 9;6:92. doi: 10.3389/fendo.2015.00092

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Copyright © 2015 Rota and Wood.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Wnt/β-catenin pathway regulates stem cell pluripotency and cell fate decisions during development. The Wnt pathway is activated when Wnt ligand binds to a Frizzled receptor, which then is brought into complex with the co-receptor LRP5/6. The activation of the Wnt pathway leads to stabilization of β-catenin through inactivation of the destruction complex (containing Axin, CK1, Gsk3β, and Apc). β-catenin can then translocate to the nucleus and interact with LEF/TCF to regulate Wnt target genes. The stimulation of the insulin receptor isoform A (IR-A) in IGF-1R null (R-/IR-A) fibroblasts by insulin was shown to increase levels of β-catenin through a mechanism that is currently unknown.