The DOI matches its Crossref record; 7 of the 7 references it cites were found in a registry or an index.
Genetic determinants of p53-induced apoptosis and growth arrest.
Open accessAbstract
Previous studies have suggested that expression of p53 in cancer cells can result in either growth arrest or apoptosis. Accordingly, expression of p53 in a series of colorectal cancer cell lines yielded growth arrest in some lines (A-lines) and apoptosis in others (D-lines). To investigate the basis of this difference, we evaluated the role of p21WAF1/Cip1, a known mediator of p53-induced growth arrest. Inactivation of p21 by homologous recombination converted an A-line to a D-line, suggesting that p21 could protect cells from apoptosis. However, examination of p53-induced p21 expression in naturally occurring D-lines and A-lines demonstrated that the induction of p21 could not account for the differential response to p53. Moreover, when a D-line was fused to an A-line, the resulting hybrid cells underwent apoptosis in response to p53, indicating that the apoptosis pathway was dominant over the growth arrest pathway. Therefore, the apoptotic response to p53 in colorectal cancer cells is modulated by at least two factors: p21-mediated growth arrest that can protect cells from apoptosis in A-cells, and trans-acting factors in D-cells that can overcome this protection, resulting in cell death.
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Cites
p53 Mutations in Human Cancers
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Self-citationTumor suppressor p53 is a direct transcriptional activator of the human bax gene
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p53 is required for radiation-induced apoptosis in mouse thymocytes
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Mice Lacking p21CIP1/WAF1 undergo normal development, but are defective in G1 checkpoint control
Deng, C., Zhang, P., Wade Harper, J., Elledge, S. J., & Leder, P. (1995) · Cell · doi:10.1016/0092-8674(95)90039-x · Cited by 2,113
Radiation-induced cell cycle arrest compromised by p21 deficiency
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p53-Dependent apoptosis suppresses tumor growth and progression in vivo
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Uncoupling of S phase and mitosis induced by anticancer agents in cells lacking p21
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Cited by
p53, the cellular gatekeeper for growth and division
Levine, A. J. (1997) · Cell · doi:10.1016/s0092-8674(00)81871-1 · Cited by 7,693
A model for p53-induced apoptosis
Polyak, K., Xia, Y., Zweier, J. L., Kinzler, K. W., & Vogelstein, B. (1997) · Nature · doi:10.1038/38525 · Cited by 2,500
Self-citationTIGAR, a p53-Inducible Regulator of Glycolysis and Apoptosis
Bensaad, K., Tsuruta, A., Selak, M. A., Vidal, M. N. C., Nakano, K., Bartrons, R., Gottlieb, E., & Vousden, K. H. (2006) · Cell · doi:10.1016/j.cell.2006.05.036 · Cited by 2,019
Autophagy, mitochondria and oxidative stress: cross-talk and redox signalling.
Lee, J., Giordano, S., & Zhang, J. (2012) · Biochemical Journal · doi:10.1042/bj20111451 · Cited by 1,438
Is a p53-Regulated Inhibitor of G2/M Progression
Hermeking, H., Lengauer, C., Polyak, K., He, T.-C., Zhang, L., Thiagalingam, S., Kinzler, K. W., & Vogelstein, B. (1997) · Molecular Cell · doi:10.1016/s1097-2765(00)80002-7 · Cited by 1,251
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Metadata
- Authors
- Polyak, K., Waldman, T., He, T. C., Kinzler, K. W., & Vogelstein, B.
- Venue
- Genes & Development
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 1996-08-01
- Volume
- 10
- Issue
- 15
- Pages
- 1945-1952
- ISSN
- 0890-9369 (ISSN-L)
- 1549-5477
- OpenAlex
- W2076940668
- Cited by
- 459
- References
- 7
- Type
- posted content
- Language
- en
- Open access
- diamond
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- Polyak, K., Waldman, T., He, T. C., Kinzler, K. W., & Vogelstein, B. (1996). Genetic determinants of p53-induced apoptosis and growth arrest. Genes & Development. https://doi.org/10.1101/gad.10.15.1945
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