Inactivation of Cdc42 in embryonic brain results in hydrocephalus with ependymal cell defects in mice-Reference-Cited by-同舟云学术

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Inactivation of Cdc42 in embryonic brain results in hydrocephalus with ependymal cell defects in mice

Published:2012-11-12 Issue:3 Volume:4 Page:231-242
ISSN:1674-800X
Container-title:Protein & Cell
language:en
Short-container-title:Protein Cell

Author:

Peng Xu,Lin Qiong,Liu Yang,Jin Yixin,Druso Joseph E.,Antonyak Marc A.,Guan Jun-Lin,Cerione Richard A.

Publisher

Springer Science and Business Media LLC

Subject

Cell Biology,Drug Discovery,Biochemistry,Biotechnology

Link

http://link.springer.com/content/pdf/10.1007/s13238-012-2098-2.pdf

Reference48 articles.

1. Aoki, K., Nakamura, T., and Matsuda, M. (2004). Spatio-temporal regulation of Rac1 and Cdc42 activity during nerve growth factorinduced neurite outgrowth in PC12 cells. J Biol Chem 279, 713–719.

2. Bokoch, G.M. (2003). Biology of the p21-activated kinases. Annu Rev Biochem 72, 743–781.

3. Cappello, S., Attardo, A., Wu, X., Iwasato, T., Itohara, S., Wilsch-Brauninger, M., Eilken, H.M., Rieger, M.A., Schroeder, T.T., Huttner, W.B., et al. (2006). The Rho-GTPase cdc42 regulates neural progenitor fate at the apical surface. Nat Neurosci 9, 1099–1107.

4. Cerione, R.A. (2004). Cdc42: new roads to travel. Trends Cell Biol 14, 127–132.

5. Chen, F., Ma, L., Parrini, M.C., Mao, X., Lopez, M., Wu, C., Marks, P.W., Davidson, L., Kwiatkowski, D.J., Kirchhausen, T., et al. (2000). Cdc42 is required for PIP(2)-induced actin polymerization and early development but not for cell viability. Curr Biol 10, 758–765.

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