Secondary interaction between MDMX and p53 core domain inhibits p53 DNA binding.
Open accessAbstract
Significance: MDMX is a critical regulator of p53 and a potential drug target. The mechanisms by which MDMX inhibit p53 are not fully understood. Results in this report suggest that MDMX inhibits p53 DNA-binding function. Using a protein fragment release assay, MDMX and p53 were found to engage in multiple strong secondary interactions following initial binding through the canonical binding domains. These secondary interactions are involved in blocking p53 DNA binding and stabilizing the MDMX–p53 complex. The results suggest that secondary interactions play important roles in regulating the function of multidomain protein complexes.
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Mdm4 directly interacts with p53 to disrupt its DNA-binding and transcriptional activation.
“Further, Mdm4 directly interacts with p53 to disrupts its DNA-binding and transcriptional activation (Francoz et al., 2006; Wei et al., 2016).”
From USP7 Is a Master Regulator of Genome Stability (2020) · cites this paper as Wei et al., 2016
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References 24 · Cited by 50
- Authors
- Wei, X., Wu, S., Song, T., Chen, L., Gao, M., Borcherds, W., Daughdrill, G. W., & Chen, J.
- Affiliations
- Tianjin Medical University Cancer Institute and Hospital (CN)
- The University of Texas MD Anderson Cancer Center (US)
- Moffitt Cancer Center (US)
- University of South Florida (US)
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2016-04-25
- Volume
- 113
- Issue
- 19
- Pages
- E2558-63
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC4868482
- OpenAlex
- W2345249791
- Cited by
- 50
- References
- 24
- Citations by year
- 2026: 2 · 2025: 3 · 2024: 4 · 2023: 3 · 2022: 11 · 2021: 3 · 2020: 8 · 2019: 6 · 2018: 6 · 2017: 1 · 2016: 3
- FWCI
- 2.87
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Digital Commons - University of South Florida (University of South Florida) (submittedVersion)
- Funders
- HHS | NIH | National Cancer Institute (CA109636, CA141244, CA186917)
- Topics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ubiquitin and proteasome pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Heat shock proteins research
- Keywords
- MDMX, p53, p53 DNA binding, CK1α, RING domain, p53 core domain, tumor suppressor regulation
- MeSH terms
- Protein Domains, Binding Sites, DNA, Neoplasm, Humans, Neoplasms, Nuclear Proteins, Protein Binding, Proto-Oncogene Proteins, Tumor Suppressor Protein p53, Cell Cycle Proteins, Protein Interaction Mapping, Cell Line, Tumor
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