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Modes of p53 regulation.
Open accessAbstract
The traditional view of p53 activation includes three steps-p53 stabilization, DNA binding, and transcriptional activation. However, recent studies indicate that each step of p53 activation is more complex than originally anticipated. Moreover, both genetic studies in mice and in vitro studies with purified components suggest that the classical model may not be sufficient to explain all aspects of p53 activation in vivo. To reconcile these differences, we propose that antirepression, the release of p53 from repression by factors such as Mdm2 and MdmX, is a key step in the physiological activation of p53.
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“Activation of p53 is dependent on various post translational modifications such as phosphorylation, methylation, acetylation, sumoylation, ubiquitination, and neddylation (Kruse and Gu, 2009).”
From Mechanisms of Cellular Senescence: Cell Cycle Arrest and Senescence Associated Secretory Phenotype (2021) · cites this paper as Kruse and Gu, 2009
In the citing paper
“This transcriptional antagonism can take place within the nucleus, as Mdm2 and Mdmx have been detected at p53-responsive promoter elements in chromatin [2].”
From The p53 orchestra: Mdm2 and Mdmx set the tone (2010) · cites this paper as [2]
In the citing paper
“MDM2 is a known E3 ubiquitin ligase that acts as a powerful inhibitor of the tumor suppressor P53 [141].”
From Proteolysis targeting chimeras (PROTACs) are emerging therapeutics for hematologic malignancies (2020) · cites this paper as [141]
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Citations
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Ji, W., Shan, M., Liu, T., Shi, Q., Zhong, Z., Wei, W., & Pang, D. (2016) · Journal of Breast Cancer · doi:10.4048/jbc.2016.19.1.61 · Cited by 18
“The p53 protein has been shown to be an important tumor suppressor gene and acts as a key transcription factor in cellular stress response pathways [16,17].”
BackgroundLysines in the tetramerization domain of p53 selectively modulate G1 arrest
Beckerman, R., Yoh, K. E., Mattia-Sansobrino, M., Zupnick, A., Laptenko, O., Karni-Schmidt, O., Ahn, J., Byeon, I. L., Keezer, S. M., & Prives, C. L. (2016) · Cell Cycle · doi:10.1080/15384101.2016.1170270 · Cited by 19
Timofeev, O. N., & Stiewe, T. (2021) · Cancers · doi:10.3390/cancers13102422 · Cited by 18
“Being a substrate for numerous protein-modifying enzymes, the CTD is subject to multiple post-translational modifications, such as acetylation, phosphorylation, methylation, neddylation, sumoylation, and ubiquitination, which determine stability, cellular localization, interaction partners, and functional activity of…”
BackgroundReplication Stress Response Modifies Sarcomeric Cardiomyopathy Remodeling
Pal, S., Nixon, B. R., Glennon, M. S., Shridhar, P., Satterfield, S. L., Su, Y. R., & Becker, J. R. (2021) · Journal of the American Heart Association · doi:10.1161/jaha.121.021768 · Cited by 20
Wang, L., Zhang, L., Gong, X., Fu, J., Gan, Y., Hou, M., Nie, Q., Xiang, J., Xiao, Y., Wang, Y., et al. (2021) · Aging Cell · doi:10.1111/acel.13458 · Cited by 16
“For p53, 17 serine/ threonine phosphorylation residues have been identified to implicate its stability and activation status (Bode & Dong, 2004; Kruse & Gu, 2009).”
BackgroundCai, M., Xu, S., Jin, Y., Yu, J., Dai, S., Shi, X., & Guo, R. (2023) · Cell Death Discovery · doi:10.1038/s41420-023-01478-y · Cited by 18
Okuda, M., & Nishimura, Y. (2015) · Oncogenesis · doi:10.1038/oncsis.2015.13 · Cited by 18
CP-31398 prevents the growth of p53-mutated colorectal cancer cells in vitro and in vivo
He, X., Kong, X., Yan, J., Yan, J., Zhang, Y., Wu, Q., Chang, Y., Shang, H., Dou, Q., Song, Y., et al. (2015) · Tumor Biology · doi:10.1007/s13277-014-2389-8 · Cited by 17
Induction of ASAP (MAP9) contributes to p53 stabilization in response to DNA damage
Basbous, J., Knani, D., Bonneaud, N., Giorgi, D., Brondello, J., & Rouquier, S. (2012) · Cell Cycle · doi:10.4161/cc.20858 · Cited by 17
“p53 stabilization following DNA damage.(2) ASAP overexpression had no effect on S15 phosphorylation, excluding a DNA damageindirect effect, but it was sufficient to stimulate p53 acetylation at K382 (Fig.”
BackgroundInfluentialPrognostic significance of p53 expression in malignant bone tumors: a meta-analysis
Jiang, L., Cheng, T., & Ai-yong, H. (2013) · Tumor Biology · doi:10.1007/s13277-012-0643-5 · Cited by 18
Meta-analysis of Associations between the MDM2-T309G Polymorphism and Prostate Cancer Risk
Chen, T., Yi, S., Liu, X., & Liu, Z.-G. (2012) · Asian Pacific Journal of Cancer Prevention · doi:10.7314/apjcp.2012.13.9.4327 · Cited by 17
Measurement of the cellular deacetylase activity of SIRT1 on p53 via LanthaScreen® technology
Robers, M. B., Loh, C., Carlson, C. B., Yang, H., Frey, E. A., Hermanson, S., & Bi, K. (2010) · Molecular BioSystems · doi:10.1039/c0mb00026d · Cited by 17
Modulation of the p53 family network by RNA-binding proteins
Lucchesi, C. A., Zhang, J., & Chen, X. (2016) · Translational Cancer Research · doi:10.21037/tcr.2016.08.30 · Cited by 17
“Subsequent studies revealed that not only were acetylation and phosphorylation important for regulating p53 stability and function, but other posttranslational modifications such as methylation, sumoylation, neddylation and ubiquitination were also able to modulate p53’s function and stability (32).”
BackgroundA Dual Role of P53 in Regulating Colistin-Induced Autophagy in PC-12 Cells
Lu, Z., Chen, C., Wu, Z., Miao, Y., Ishfaq, M., Ding, L., Tian, E., Hu, W., Ni, H., Li, R., et al. (2017) · Frontiers in Pharmacology · doi:10.3389/fphar.2017.00768 · Cited by 18
“It rapidly undergoes reversible post-translational modifications for its stabilization in response to hypoxic, genotoxic, and oncogenic stress (Kruse and Gu, 2009).”
BackgroundInhibition of Mdmx (Mdm4) in vivo induces anti-obesity effects
Kon, N., Wang, D., Li, T., Jiang, L., Qiang, L., & Gu, W. (2018) · Oncotarget · doi:10.18632/oncotarget.23837 · Cited by 17
Self-citationZawacka‐Pankau, J. (2020) · Cancers · doi:10.3390/cancers12092717 · Cited by 16
“MDM2 activity towards p53 is enhanced by its homolog, MDMX protein, which lacks the E3 ligase activity but binds to the N-terminus of p53 and MDM2 alike, inhibiting its transcription function [16].”
BackgroundA mini-review of the diffusion dynamics of DNA-binding proteins: experiments and models
Park, S., Lee, O.-C., Durang, X., & Jeon, J.-H. (2021) · Journal of the Korean Physical Society · doi:10.1007/s40042-021-00060-y · Cited by 17
Miyajima, C., Hayakawa, Y., Inoue, Y., Nagasaka, M., & Hayashi, H. (2022) · Pharmaceuticals · doi:10.3390/ph15081015 · Cited by 17
“The functions of p53 are tightly regulated by post-translational modifications, such as acetylation, phosphorylation, and methylation [9,27].”
BackgroundSnoN activates p53 directly to regulate aging and tumorigenesis
Pan, D., Zhu, Q., Conboy, M. J., Conboy, I. M., & Luo, K. (2012) · Aging Cell · doi:10.1111/j.1474-9726.2012.00857.x · Cited by 17
“SnoN competes with Mdm2 for binding to the p53 responsive promoter DNA Mdm2 not only regulates p53 degradation but also represses its transcriptional activity at the promoter DNA (Kruse & Gu, 2009).”
BackgroundInfluentialBenzo(a)pyrene induces p73 mRNA expression and necrosis in human lung adenocarcinoma H1299 cells
Jiang, Y., Rao, K., Yang, G., Chen, X., Wang, Q., Liu, A., Zheng, H., & Yuan, J. (2010) · Environmental Toxicology · doi:10.1002/tox.20631 · Cited by 17
“These modifications collectively protect p53 from MDM2-mediated ubiquitylation and degradation (Kruse and Gu, 2009). mdm2 can be transcriptionally induced by p53.”
BackgroundCharacterization of the tilapia p53 gene and its role in chemical-induced apoptosis
Mai, W., Liu, P., & Wang, W. (2012) · Biotechnology Letters · doi:10.1007/s10529-012-0980-x · Cited by 17
Structure of the Taz2 domain of p300: insights into ligand binding
Miller, M., Dauter, Z., Cherry, S., Tropea, J. E., & Wlodawer, A. (2009) · Acta Crystallographica Section D Biological Crystallography · doi:10.1107/s0907444909040153 · Cited by 18
BRIT1 regulates p53 stability and functions as a tumor suppressor in breast cancer
Zhang, B., Wang, E., Dai, H., Hu, R., Liang, Y., Li, K., Wang, G., Peng, G., & Lin, S. (2013) · Carcinogenesis · doi:10.1093/carcin/bgt190 · Cited by 17
Yin, X., Chen, B., He, M., & Hu, B. (2019) · Microchimica Acta · doi:10.1007/s00604-019-3540-4 · Cited by 17
A systems biology view of evolutionary genetics
Bard, J. (2010) · BioEssays · doi:10.1002/bies.200900166 · Cited by 17
“Similarly, the transcription factors pax6 and p53 respectively play key upstream roles in head development and the DNA repair/apoptosis pathways [30, 31].”
Background
Metadata
- Authors
- Kruse, J.-P., & Gu, W.
- Affiliations
- Columbia University (US)
- Corresponding author
- Gu, Wei
- ORCID
- Gu, Wei
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2009-05
- Volume
- 137
- Issue
- 4
- Pages
- 609-622
- ISSN
- 0092-8674 (ISSN-L)
- PMC
- PMC3737742
- OpenAlex
- W2025722611
- Cited by
- 1,610
- References
- 152
- Citations by year
- 2026: 31 · 2025: 49 · 2024: 52 · 2023: 57 · 2022: 81 · 2021: 98 · 2020: 75 · 2019: 73 · 2018: 100 · 2017: 98 · 2016: 102 · 2015: 108 · 2014: 142 · 2013: 127 · 2012: 128
- FWCI
- 12.22
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (2r01ca085533-16)
- National Cancer Institute (R01-CA085533, R01CA131439, P01CA097403, R01CA104843, P01CA080058, R01CA098821, R01CA129627)
- Topics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Heat shock proteins research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Keywords
- p53 activation, p53 regulation, MDM2, MDMX, p53 stabilization, DNA binding, transcriptional activation, tumor suppressor
- MeSH terms
- Animals, Humans, Protein Processing, Post-Translational, Gene Expression Regulation, Neoplastic, Tumor Suppressor Protein p53, Proto-Oncogene Proteins c-mdm2
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