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Mutant TP53 Posttranslational Modifications: Challenges and Opportunities
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“In the case of mutant p53, these modifications may further alter its functional and kinetic properties, thereby affecting its behavior in tumorigenesis and progression.170”
From p53: from understanding its structure to advances in therapeutic targeting (2026) · cites this paper as [170]
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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
Crystal Structure of a p53 Tumor Suppressor-DNA Complex: Understanding Tumorigenic Mutations
Cho, Y., Gorina, S., Jeffrey, P. D., & Pavletich, N. P. (1994) · Science · doi:10.1126/science.8023157 · Cited by 2,551 · cited 1×
“Among the mutations in this domain, about 30% locate within six “hotspot” residues that are frequent in almost all cancer types [Hollstein et al., 1991; Cho et al., 1994], for example, Arg175, Gly245, Arg248, Arg249, Arg273, and Arg282, but which are not known to be posttranslationally modified.”
BackgroundDNA damage-induced phosphorylation of p53 alleviates inhibition by MDM2
Shieh, S.-Y., Ikeda, M., Taya, Y., & Prives, C. (1997) · Cell · doi:10.1016/s0092-8674(00)80416-x · Cited by 2,100
Transcriptional control of human p53-regulated genes
Riley, T., Sontag, E., Chen, P., & Levine, A. (2008) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm2395 · Cited by 1,921
Kruse, J.-P., & Gu, W. (2009) · Cell · doi:10.1016/j.cell.2009.04.050 · Cited by 1,610 · cited 4×
“Most of the lysine residues subject to acetylation can also be modified by methylation, Ub, and neddylation, all of which have inhibitory effects on a variety of TP53 functions [Kruse and Gu, 2009b].”
BackgroundInfluentialPetitjean, A., Mathe, E., Kato, S., Ishioka, C., Tavtigian, S. V., Hainaut, P., & Olivier, M. (2007) · Human Mutation · doi:10.1002/humu.20495 · Cited by 1,598 · cited 3×
“Alteration of the TP53 gene itself or perturbations in TP53 signaling pathways are the most frequent events in tumorigenesis [Petitjean et al., 2007] and can be considered hallmarks of cancer cells [Pfeifer and Hainaut, 2011].”
BackgroundMutant p53 gain of function in two mouse models of Li-Fraumeni syndrome
Olive, K. P., Tuveson, D. A., Ruhe, Z. C., Yin, B., Willis, N. A., Bronson, R. T., Crowley, D., & Jacks, T. (2004) · Cell · doi:10.1016/j.cell.2004.11.004 · Cited by 1,308
Regulating the p53 pathway: in vitro hypotheses, in vivo veritas
Toledo, F., & Wahl, G. M. (2006) · Nature reviews. Cancer · doi:10.1038/nrc2012 · Cited by 1,286
MDM2, MDMX and p53 in oncogenesis and cancer therapy
Wade, M., Li, Y.-C., & Wahl, G. M. (2013) · Nature Reviews Cancer · doi:10.1038/nrc3430 · Cited by 1,279
Post-translational modification of p53 in tumorigenesis
Bode, A. M., & Dong, Z. (2004) · Nature Reviews Cancer · doi:10.1038/nrc1455 · Cited by 1,270
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Metadata
- Authors
- Nguyen, T.-A., Menendez, D., Resnick, M. A., & Anderson, C. W.
- Venue
- Human Mutation
- Publisher
- Wiley
- Published
- 2014-02-11
- Volume
- 35
- Issue
- 6
- Pages
- 738-755
- ISSN
- 1059-7794
- Cited by
- 69
- References
- 29
- Language
- en
- Licence
- doi.wiley.com/10.1002/tdm_license_1.1 (tdm, 567 d)
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- CoChat. (2026). Citation check: Mutant TP53 Posttranslational Modifications: Challenges and Opportunities. https://app.cochat.ai/papers/10.1002/humu.22506
- The paper
- Nguyen, T.-A., Menendez, D., Resnick, M. A., & Anderson, C. W. (2014). Mutant TP53 Posttranslational Modifications: Challenges and Opportunities. Human Mutation. https://doi.org/10.1002/humu.22506
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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