p63 and p73 are required for p53-dependent apoptosis in response to DNA damage (original) (raw)
References
Levine, A. J. p53, the cellular gatekeeper for growth and division. Cell88, 323–331 (1997). Google Scholar
Evan, G. I. & Vousden, K. H. Proliferation, cell cycle and apoptosis in cancer. Nature411, 342–348 (2001). Google Scholar
Yang, A. et al. p63, a p53 homolog at 3q27–29, encodes multiple products with transactivating, death-inducing, and dominant-negative activities. Mol. Cell2, 305–316 (1998). Google Scholar
Irwin, M. S. & Kaelin, W. G. Jr Role of the newer p53 family proteins in malignancy. Apoptosis6, 17–29 (2001). Google Scholar
Stiewe, T. & Putzer, B. M. Role of the p53-homologue p73 in E2F1-induced apoptosis. Nature Genet.26, 464–469 (2000). Google Scholar
Agami, R., Blandino, G., Oren, M. & Shaul, Y. Interaction of c-Abl and p73α and their collaboration to induce apoptosis. Nature399, 809–813 (1999). Google Scholar
Gong, J. G. et al. The tyrosine kinase c-Abl regulates p73 in apoptotic response to cisplatin-induced DNA damage. Nature399, 806–809 (1999). Google Scholar
Jost, C. A., Marin, M. C. & Kaelin, W. G. Jr p73 is a simian [correction of human] p53-related protein that can induce apoptosis. Nature389, 191–194 (1997). Google Scholar
Yuan, Z. M. et al. p73 is regulated by tyrosine kinase c-Abl in the apoptotic response to DNA damage. Nature399, 814–817 (1999). Google Scholar
Di Como, C. J., Gaiddon, C. & Prives, C. p73 function is inhibited by tumor-derived p53 mutants in mammalian cells. Mol. Cell. Biol.19, 1438–1449 (1999). Google Scholar
Gaiddon, C., Lokshin, M., Ahn, J., Zhang, T. & Prives, C. A subset of tumor-derived mutant forms of p53 down-regulate p63 and p73 through a direct interaction with the p53 core domain. Mol. Cell. Biol.21, 1874–1887 (2001). Google Scholar
Lowe, S. W., Ruley, H. E., Jacks, T. & Housman, D. E. p53-dependent apoptosis modulates the cytotoxicity of anticancer agents. Cell74, 957–967 (1993). Google Scholar
Lowe, S. W. & Ruley, H. E. Stabilization of the p53 tumor suppressor is induced by adenovirus 5 E1A and accompanies apoptosis. Genes Dev.7, 535–545 (1993). Google Scholar
Lowe, S. W., Jacks, T., Housman, D. E. & Ruley, H. E. Abrogation of oncogene-associated apoptosis allows transformation of p53-deficient cells. Proc. Natl Acad. Sci. USA91, 2026–2030 (1994). Google Scholar
Lee, Y., Chong, M. J. & McKinnon, P. J. Ataxia telangiectasia mutated-dependent apoptosis after genotoxic stress in the developing nervous system is determined by cellular differentiation status. J. Neurosci.21, 6687–6693 (2001). Google Scholar
Herzog, K. H., Chong, M. J., Kapsetaki, M., Morgan, J. I. & McKinnon, P. J. Requirement for Atm in ionizing radiation-induced cell death in the developing central nervous system. Science280, 1089–1091 (1998). Google Scholar
Chong, M. J. et al. Atm and Bax cooperate in ionizing radiation-induced apoptosis in the central nervous system. Proc. Natl Acad. Sci. USA97, 889–894 (2000). Google Scholar
Zaika, A., Irwin, M., Sansome, C. & Moll, U. M. Oncogenes induce and activate endogenous p73 protein. J. Biol. Chem.276, 11310–11316 (2001). Google Scholar
Miyashita, T. et al. Tumor suppressor p53 is a regulator of bcl-2 and bax gene expression in vitro and in vivo. Oncogene9, 1799–1805 (1994). Google Scholar
Yin, C., Knudson, C. M., Korsmeyer, S. J. & Van Dyke, T. Bax suppresses tumorigenesis and stimulates apoptosis in vivo. Nature385, 637–640 (1997). Google Scholar
Attardi, L. D. et al. PERP, an apoptosis-associated target of p53, is a novel member of the PMP-22/gas3 family. Genes Dev.14, 704–718 (2000). Google Scholar
Oda, E. et al. Noxa, a BH3-only member of the Bcl-2 family and candidate mediator of p53-induced apoptosis. Science288, 1053–1058 (2000). Google Scholar
Jacks, T. et al. Tumor spectrum analysis in p53-mutant mice. Curr. Biol.4, 1–7 (1994). Google Scholar
Yang, A. et al. p63 is essential for regenerative proliferation in limb, craniofacial and epithelial development. Nature398, 714–718 (1999). Google Scholar
Yang, A. et al. p73-deficient mice have neurological, pheromonal and inflammatory defects but lack spontaneous tumours. Nature404, 99–103 (2000). Google Scholar
Kinsella, T. M. & Nolan, G. P. Episomal vectors rapidly and stably produce high-titer recombinant retrovirus. Hum. Gene Ther.7, 1405–1413 (1996). Google Scholar
Wells, J., Boyd, K. E., Fry, C. J., Bartley, S. M. & Farnham, P. J. Target gene specificity of E2F and pocket protein family members in living cells. Mol. Cell. Biol.20, 5797–5807 (2000). Google Scholar