The DOI matches its Crossref record; 25 of the 25 references it cites were found in a registry or an index.
The p53 family and programmed cell death
Open accessAbstract
The p53 tumor suppressor continues to hold distinction as the most frequently mutated gene in human cancer. The ability of p53 to induce programmed cell death, or apoptosis, of cells exposed to environmental or oncogenic stress constitutes a major pathway whereby p53 exerts its tumor suppressor function. In the past decade, we have discovered that p53 is not alone in its mission to destroy damaged or aberrantly proliferating cells: it has two homologs, p63 and p73, that in various cellular contexts and stresses contribute to this process. In this review, the mechanisms whereby p53, and in some cases p63 and p73, induce apoptosis are discussed. Other reviews have focused more extensively on the contribution of individual p53-regulated genes to apoptosis induction by this protein, whereas in this review, we focus more on those factors that mediate the decision between growth arrest and apoptosis by p53, p63 and p73, and on the post-translational modifications and protein–protein interactions that influence this decision.
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BackgroundDefinition of a consensus binding site for p53
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DNA damage and the balance between survival and death in cancer biology
Roos, W. P., Thomas, A. D., & Kaina, B. (2016) · Nature Reviews Cancer · doi:10.1038/nrc.2015.2 · Cited by 1,189
Molecular Profiles of Pyramidal Neurons in the Superior Temporal Cortex in Schizophrenia
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NFκB/p53 crosstalk—a promising new therapeutic target
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Metadata
- Authors
- Pietsch, E. C., Sykes, S. M., McMahon, S. B., & Murphy, M. E.
- Venue
- Oncogene
- Published
- 2008-10-27
- Volume
- 27
- Issue
- 50
- Pages
- 6507-6521
- ISSN
- 0950-9232 (ISSN-L)
- 1476-5594
- OpenAlex
- W2063131548
- Cited by
- 315
- References
- 25
- FWCI
- 15.40
- Type
- journal article
- Language
- en
- Open access
- green
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