| First Author | Kelly KF | Year | 2011 |
| Journal | Cell Stem Cell | Volume | 8 |
| Issue | 2 | Pages | 214-27 |
| PubMed ID | 21295277 | Mgi Jnum | J:168827 |
| Mgi Id | MGI:4939072 | Doi | 10.1016/j.stem.2010.12.010 |
| Citation | Kelly KF, et al. (2011) beta-Catenin Enhances Oct-4 Activity and Reinforces Pluripotency through a TCF-Independent Mechanism. Cell Stem Cell 8(2):214-27 |
| abstractText | Understanding the mechanisms regulating pluripotency in embryonic and induced pluripotent stem cells is required to ensure their safe use in clinical applications. Glycogen synthase kinase-3 (GSK-3) has emerged as an important regulator of pluripotency, based primarily on studies with small-molecule GSK-3 inhibitors. Here, we use mouse embryonic stem cells (ESCs) lacking GSK-3 to demonstrate that a single GSK-3 substrate, beta-catenin, controls the ability of ESCs to exit the pluripotent state and to differentiate into neurectoderm. Unexpectedly, the effects of beta-catenin on pluripotency do not appear to be dependent on TCF-mediated signaling, based on experiments utilizing a beta-catenin C-terminal truncation mutant or highly efficient dominant-negative TCF strategies. Alternatively, we find that stabilized beta-catenin forms a complex with and enhances the activity of Oct-4, a core component of the transcriptional network regulating pluripotency. Collectively, our data suggest previously underappreciated, divergent TCF-dependent and TCF-independent roles for beta-catenin in ESCs. |
