Mice engineered for an obligatory Mdm4 exon skipping express higher levels of the Mdm4-S isoform but exhibit increased p53 activity-Reference-Cited by-同舟云学术

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Mice engineered for an obligatory Mdm4 exon skipping express higher levels of the Mdm4-S isoform but exhibit increased p53 activity

Published:2014-08-04 Issue:22 Volume:34 Page:2943-2948
ISSN:0950-9232
Container-title:Oncogene
language:en
Short-container-title:Oncogene

Author:

Bardot B,Bouarich-Bourimi R,Leemput J,Lejour V,Hamon A,Plancke L,Jochemsen A G,Simeonova I,Fang M,Toledo F

Publisher

Springer Science and Business Media LLC

Subject

Cancer Research,Genetics,Molecular Biology

Link

http://www.nature.com/articles/onc2014230.pdf

Reference38 articles.

1. Toledo F, Wahl GM . Regulating the p53 pathway: in vitro hypotheses, in vivo veritas. Nat Rev Cancer 2006; 6: 909–923.

2. Marine JC . MDM2 and MDMX in cancer and development. Curr Top Dev Biol 2011; 94: 45–75.

3. Toledo F, Krummel KA, Lee CJ, Liu CW, Rodewald LW, Tang M et al. A mouse p53 mutant lacking the proline rich domain rescues Mdm4 deficiency and provides insight into the Mdm2-Mdm4-p53 regulatory network. Cancer Cell 2006; 9: 273–285.

4. Laurie NA, Donovan SL, Shih CS, Zhang J, Mills N, Fuller C et al. Inactivation of the p53 pathway in retinoblastoma. Nature 2006; 444: 61–66.

5. Bernal F, Wade M, Godes M, Davis TN, Whitehead DG, Kung AL et al. A stapled p53 helix overcomes HDMX-mediated suppression of p53. Cancer Cell 2010; 18: 411–422.

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