| First Author | Lien WH | Year | 2008 |
| Journal | J Cell Sci | Volume | 121 |
| Issue | Pt 9 | Pages | 1357-62 |
| PubMed ID | 18397997 | Mgi Jnum | J:139820 |
| Mgi Id | MGI:3810208 | Doi | 10.1242/jcs.020537 |
| Citation | Lien WH, et al. (2008) alphaE-catenin is not a significant regulator of beta-catenin signaling in the developing mammalian brain. J Cell Sci 121(Pt 9):1357-62 |
| abstractText | beta-Catenin is a crucial mediator of the canonical Wnt-signaling pathway. alpha-catenin is a major beta-catenin-binding protein, and overexpressed alpha-catenin can negatively regulate beta-catenin activity. Thus, alpha-catenin may be an important modulator of the Wnt pathway. We show here that endogenous alpha-catenin has little impact on the transcriptional activity of beta-catenin in developing mammalian organisms. We analyzed beta-catenin signaling in mice with conditional deletion of alphaE-catenin (Ctnna1) in the developing central nervous system. This mutation results in brain hyperplasia and we investigated whether activation of beta-catenin signaling may be at least partially responsible for this phenotype. To reveal potential quantitative or spatial changes in beta-catenin signaling, we used mice carrying a beta-catenin-signaling reporter transgene. In addition, we analyzed the expression of known endogenous targets of the beta-catenin pathway and the amount and localization of beta-catenin in mutant progenitor cells. We found that although loss of alphaE-catenin resulted in disruption of intercellular adhesion and hyperplasia in the developing brain, beta-catenin signaling was not altered. We conclude that endogenous alphaE-catenin has no significant impact on beta-catenin transcriptional activities in the developing mammalian brain. |
