The DOI matches its Crossref record; 7 of the 7 references it cites were found in a registry or an index.
The nuclear function of p53 is required for PUMA-mediated apoptosis induced by DNA damage
Open accessAbstract
The tumor suppressor p53 can induce apoptosis by activating gene expression in the nucleus, or by directly permeabilizing mitochondria in the cytoplasm. It has been shown that PUMA, a downstream target of p53 and a BH3-only Bcl-2 family member, plays an essential role in apoptosis induced by both nuclear and cytoplasmic p53. To understand how PUMA does so, we used homologous recombination to delete the binding sites of p53 in the promoter of PUMA in human colorectal cancer cells. As a result, the induction of PUMA and apoptosis in response to p53 and DNA-damaging agents were abrogated. Transcription coactivator recruitment and histone modifications in the PUMA promoter were suppressed. However, induction of PUMA and apoptosis in response to non-DNA-damaging stimuli were unaffected. These results indicate that the binding of nuclear p53 to the specific sites within the PUMA promoter is essential for its ability to induce apoptosis and is likely to be required for its tumor suppressive capacity.
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Vogelstein, B., Lane, D., & Levine, A. J. (2000) · Nature · doi:10.1038/35042675 · Cited by 6,607
Definition of a consensus binding site for p53
El-Deiry, W. S., Kern, S. E., Pietenpol, J. A., Kinzler, K. W., & Vogelstein, B. (1992) · Nature Genetics · doi:10.1038/ng0492-45 · Cited by 1,985
p53- and Drug-Induced Apoptotic Responses Mediated by BH3-Only Proteins Puma and Noxa
Villunger, A., Michalak, E. M., Coultas, L., Müllauer, F., Böck, G., Ausserlechner, M. J., Adams, J. M., & Strasser, A. (2003) · Science · doi:10.1126/science.1090072 · Cited by 1,327
A Global Map of p53 Transcription-Factor Binding Sites in the Human Genome
Wei, C.-L., Wu, Q., Vega, V. B., Chiu, K. P., Ng, P., Zhang, T., Shahab, A., Yong, H. C., Fu, Y., Weng, Z., et al. (2006) · Cell · doi:10.1016/j.cell.2005.10.043 · Cited by 1,141
Disruption of p53 in human cancer cells alters the responses to therapeutic agents.
Bunz, F., Hwang, P. M., Torrance, C., Waldman, T., Zhang, Y., Dillehay, L., Williams, J., Lengauer, C., Kinzler, K. W., & Vogelstein, B. (1999) · Journal of Clinical Investigation · doi:10.1172/jci6863 · Cited by 1,044
p73 is a human p53-related protein that can induce apoptosis
Jost, C. A., Marin, M. C., & Jr, W. G. K. (1997) · Nature · doi:10.1038/38298 · Cited by 948
The p53 response: Emerging levels of co-factor complexity
Coutts, A. S., & La Thangue, N. B. (2005) · Biochemical and Biophysical Research Communications · doi:10.1016/j.bbrc.2005.03.150 · Cited by 72
Cited by
Blinded by the Light: The Growing Complexity of p53
Vousden, K. H., & Prives, C. (2009) · Cell · doi:10.1016/j.cell.2009.04.037 · Cited by 3,163
Senescence and apoptosis: dueling or complementary cell fates?
Childs, B. G., Baker, D. J., Kirkland, J. L., Campisi, J., & van Deursen, J. M. (2014) · The EMBO Reports · doi:10.15252/embr.201439245 · Cited by 915
HMGB1 release and redox regulates autophagy and apoptosis in cancer cells
Tang, D., Kang, R., Cheh, C.-W., Livesey, K. M., Liang, X., Schapiro, N. E., Benschop, R., Sparvero, L. J., Amoscato, A. A., Tracey, K. J., et al. (2010) · Oncogene · doi:10.1038/onc.2010.261 · Cited by 461
Principles for the post-GWAS functional characterization of cancer risk loci
Freedman, M. L., Monteiro, A. N. A., Gayther, S. A., Coetzee, G. A., Risch, A., Plass, C., Casey, G., De Biasi, M., Carlson, C., Duggan, D., et al. (2011) · Nature Genetics · doi:10.1038/ng.840 · Cited by 438
microRNA-21 negatively regulates Cdc25A and cell cycle progression in colon cancer cells
Wang, P., Zou, F., Zhang, X., Li, H., Dulak, A., Tomko, R. J., Lazo, J. S., Wang, Z., Zhang, L., & Yu, J. (2009) · Cancer Research · doi:10.1158/0008-5472.can-09-1996 · Cited by 308
Self-citation
Metadata
- Authors
- Wang, P., Yu, J., & Zhang, L.
- Venue
- Proceedings of the National Academy of Sciences
- Published
- 2007-03-06
- Volume
- 104
- Issue
- 10
- Pages
- 4054-4059
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- OpenAlex
- W2091879550
- Cited by
- 163
- References
- 7
- FWCI
- 7.55
- Type
- journal article
- Language
- en
- Open access
- green
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