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Publication : Cell-autonomous beta-catenin signaling regulates cortical precursor proliferation.

First Author  Woodhead GJ Year  2006
Journal  J Neurosci Volume  26
Issue  48 Pages  12620-30
PubMed ID  17135424 Mgi Jnum  J:116183
Mgi Id  MGI:3693144 Doi  10.1523/JNEUROSCI.3180-06.2006
Citation  Woodhead GJ, et al. (2006) Cell-autonomous beta-catenin signaling regulates cortical precursor proliferation. J Neurosci 26(48):12620-30
abstractText  Overexpression of beta-catenin, a protein that functions in both cell adhesion and signaling, causes expansion of the cerebral cortical precursor population and cortical surface area enlargement. Here, we find that focal elimination of beta-catenin from cortical neural precursors in vivo causes premature neuronal differentiation. Precursors within the cerebral cortical ventricular zone exhibit robust beta-catenin-mediated transcriptional activation, which is downregulated as cells exit the ventricular zone. Targeted inhibition of beta-catenin signaling during embryonic development causes cortical precursor cells to prematurely exit the cell cycle, differentiate into neurons, and migrate to the cortical plate. These results show that beta-catenin-mediated transcriptional activation functions in the decision of cortical ventricular zone precursors to proliferate or differentiate during development, and suggest that the cell-autonomous signaling activity of beta-catenin can control the production of cortical neurons and thus regulate cerebral cortical size.
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