The DOI matches its Crossref record; 28 of the 28 references it cites were found in a registry or an index.
Tumor Suppressive Functions of p53
Open accessAbstract
The majority of human cancers acquire mutations that abrogate the p53 tumor suppressor network and, as a consequence, p53 is one of the most extensively studied proteins in cancer research. Because of its potent tumor suppressive activity, it is widely assumed that a molecular understanding of p53 action will produce fundamental insights into natural processes that limit tumorigenesis and may identify key molecular targets for therapeutic intervention. p53 functions largely as a transcription factor, and can trigger a variety of antiproliferative programs by activating or repressing key effector genes. Despite a significant body of literature detailing the biochemical and biological functions of p53, much remains to be elucidated. Indeed, the p53 network is as complex and enigmatic as it is relevant. It is the goal of this article, written 30 years after the discovery of p53, to present a concise review of the tumor suppressor role of the p53 network and to highlight the context-dependent nature of p53 target-gene functions.
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“p53-triggered apoptosis involves the transcriptional induction of components of both the extrinsic and intrinsic death pathways, including BAX, FAS, NOXA and PUMA, among others, which collaboratively promote cell death (Riley et al., 2008; Zilfou and Lowe, 2009).”
From p53 at a glance (2010) · cites this paper as Zilfou and Lowe, 2009
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Cites
Oncogenic ras provokes premature cell senescence associated with accumulation of p53 and p16INK4a
Serrano, M., Lin, A. W., McCurrach, M. E., Beach, D., & Lowe, S. W. (1997) · Cell · doi:10.1016/s0092-8674(00)81902-9 · Cited by 5,218 · cited 1×
“Interestingly, because certain oncogenes can trigger senescence, mutations that bypass senescence, forexample in the p53 network, cooperate with these changes to promote full malignant transformation (Serrano et al. 1997).”
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Cellular senescence: when bad things happen to good cells
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p53 is required for radiation-induced apoptosis in mouse thymocytes
Lowe, S. W., Schmitt, E. M., Smith, S. W., Osborne, B. A., & Jacks, T. (1993) · Nature · doi:10.1038/362847a0 · Cited by 2,864
Self-citationA microRNA component of the p53 tumour suppressor network
He, L., He, X., Lim, L. P., de Stanchina, E., Xuan, Z., Liang, Y., Xue, W., Zender, L., Magnus, J., Ridzon, D., et al. (2007) · Nature · doi:10.1038/nature05939 · Cited by 2,692
Self-citationSenescence and tumour clearance is triggered by p53 restoration in murine liver carcinomas
Xue, W., Zender, L., Miething, C., Dickins, R. A., Hernando, E., Krizhanovsky, V., Cordon-Cardo, C., & Lowe, S. W. (2007) · Nature · doi:10.1038/nature05529 · Cited by 2,473
Self-citationRb-mediated heterochromatin formation and silencing of E2F target genes during cellular senescence
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“For example, the phosphorylation of p53 at serine 46 has been shown to correlate with apoptosis, and may be partially explained by the ability of this phosphorylation to regulate expression of at least one p53 apoptotic target, p53AIP1 (Oda et al. 2000).”
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Mice Lacking p21CIP1/WAF1 undergo normal development, but are defective in G1 checkpoint control
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Cited by
Matthews, H. K., Bertoli, C., & de Bruin, R. A. M. (2022) · Nature Reviews Molecular Cell Biology · doi:10.1038/s41580-021-00404-3 · Cited by 1,506
Rushing, B. R., & Selim, M. I. (2019) · Food and Chemical Toxicology · doi:10.1016/j.fct.2018.11.047 · Cited by 989
Mustafa, M., Ahmad, R., Tantry, I. Q., Ahmad, W., Siddiqui, S., Alam, M., Abbas, K., Moinuddin, Hassan, M. I., Habib, S., et al. (2024) · Cells · doi:10.3390/cells13221838 · Cited by 595
Therapeutic targeting of p53: all mutants are equal, but some mutants are more equal than others
Sabapathy, K., & Lane, D. P. (2018) · Nature Reviews Clinical Oncology · doi:10.1038/nrclinonc.2017.151 · Cited by 517
Ubiquitylation in apoptosis: a post-translational modification at the edge of life and death
Vucic, D., Dixit, V. M., & Wertz, I. E. (2011) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm3143 · Cited by 444
Metadata
- Authors
- Zilfou, J. T., & Lowe, S. W.
- Venue
- Cold Spring Harbor Perspectives in Biology
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 2009-10-21
- Volume
- 1
- Issue
- 5
- Pages
- a001883-a001883
- ISSN
- 1943-0264 (ISSN-L)
- OpenAlex
- W1965086052
- Cited by
- 575
- References
- 28
- Type
- posted content
- Language
- en
- Open access
- bronze
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