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p53 post-translational modification: deregulated in tumorigenesis
Open accessAbstract
The p53 tumor suppressor protein has well-established roles in monitoring various types of stress signals by activating specific transcriptional targets that control cell cycle arrest and apoptosis although some activities are also mediated in a transcription-independent manner. Here, we review the recent advances in our understanding of the wide spectrum of post-translational modifications that act as epigenetic-like codes for modulating specific functions of p53 in vivo and how deregulation of these modifications might contribute to tumorigenesis. We also discuss future research priorities to further understand p53 post-translational modifications and the interpretation of genetic data in appreciation of the increasing evidence that p53 regulates cellular metabolism, autophagy and many unconventional tumor suppressor activities.
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“Timely expression of wild-type p53 is crucial in preventing deregulated or stressed cells from turning into cancer cells [62]. p53 does this by transactivating expressions of gene sets that initiate cell cycle arrest, DNA repair, senescence, or apoptosis.”
Metadata
- Authors
- Dai, C., & Gu, W.
- Venue
- Trends in Molecular Medicine
- Publisher
- Elsevier BV
- Published
- 2010-11
- Volume
- 16
- Issue
- 11
- Pages
- 528-536
- ISSN
- 1471-4914 (ISSN-L)
- OpenAlex
- W2010706742
- Cited by
- 523
- References
- 20
- FWCI
- 3.24
- Type
- journal article
- Language
- en
- Open access
- green
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
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