Signaling to p53: ribosomal proteins find their way
Open accessAbstract
Inherently disparate cell growth and division, which are intimately coupled through a delicate network of intracellular and extracellular signaling, require ribosomal biogenesis. A number of events imparting instability to ribosomal biogenesis can cause nucleolar stress. In response to this stress, several ribosomal proteins bind to MDM2 and block MDM2-mediated p53 ubiquitination and degradation, resulting in p53-dependent cell cycle arrest. By doing so, the ribosomal proteins play a crucial role in connecting deregulated cell growth with inhibition of cell division. The ribosomal protein-MDM2-p53 signaling pathway provides a molecular switch that may constitute a surveillance network monitoring the integrity of ribosomal biogenesis.
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Mdm2 and Mdmx bind many other proteins, including proteins involved in development, morphogenesis, and tumorigenesis.
“However, both Mdm2 and Mdmx interact with many other proteins, including those involved in development, morphogenesis and tumorigenesis (Table 2; [81–92]).”
From The p53 orchestra: Mdm2 and Mdmx set the tone (2010) · cites this paper as [82]
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- Authors
- Zhang, Y., & Lu, H.
- Affiliations
- University of North Carolina at Chapel Hill (US)
- Indiana University School of Medicine (US)
- Corresponding author
- Zhang, Yanping
- Lu, Hua
- Venue
- Cancer Cell
- Publisher
- Elsevier BV
- Published
- 2009-11
- Volume
- 16
- Issue
- 5
- Pages
- 369-377
- ISSN
- 1535-6108 (ISSN-L)
- PMC
- PMC4369769
- OpenAlex
- W1992307025
- Cited by
- 591
- References
- 125
- Citations by year
- 2026: 20 · 2025: 26 · 2024: 25 · 2023: 28 · 2022: 31 · 2021: 29 · 2020: 32 · 2019: 26 · 2018: 45 · 2017: 31 · 2016: 41 · 2015: 39 · 2014: 63 · 2013: 39 · 2012: 39
- FWCI
- 3.39
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cancer Cell (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Carolina Digital Repository (University of North Carolina at Chapel Hill) (submittedVersion)
- Purdue University Indianapolis (Indiana University) (submittedVersion)
- UNC Libraries
- Funders
- American Cancer Society
- National Cancer Institute (R01CA155235, K01CA087580, R01CA100302, R01CA127770)
- 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 › PI3K/AKT/mTOR signaling in cancer
- Keywords
- ribosomal proteins, p53, MDM2, ribosome biogenesis, nucleolar stress, p53 ubiquitination, p53 degradation, cell cycle arrest, cell growth regulation, cell division, tumor suppressor signaling
- MeSH terms
- Animals, Cell Cycle, Humans, Ribosomal Proteins, Signal Transduction, Tumor Suppressor Protein p53, Proto-Oncogene Proteins c-mdm2, Ubiquitination
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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