ArticleMolecular and cellular biology2003
Nucleocytoplasmic shuttling of p53 is essential for MDM2-mediated cytoplasmic degradation but not ubiquitination.
Article in Molecular and cellular biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.
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Who cites it
72 citing papers in PubMed, 133 citations in OpenAlex.
- Identification and characterization of BRAF⇔TP53 interactions in melanoma.Cell reports · 2026Article
- Uncovering cancer dependencies in peptide-interacting protein pockets.bioRxiv : the preprint server for biology · 2026Article
- E2F1-autophagy-ALDH1A1 axis enhances self-renewal and drug resistance of lung cancer stem-like cells in a p53-dependent manner.Journal of experimental & clinical cancer research : CR · 2025Article
- Lipid Droplet-Organized MDM2-Mediated P53 Degradation: A Metabolic Switch Governing Diet-Driven Tumor Progression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- PIPKIγ promotes non-homologous end joining through LIG4 to enhance radiotherapy resistance in triple-negative breast cancer.Cell death & disease · 2025Article
- Article
- Correlation of p53 oligomeric status and its subcellular localization in the presence of the AML-associated NPM mutant.PloS one · 2025Article
- Unlocking the Gateway: The Spatio-Temporal Dynamics of the p53 Family Driven by the Nuclear Pores and Its Implication for the Therapeutic Approach in Cancer.International journal of molecular sciences · 2024Review
- Myospreader improves gene editing in skeletal muscle by myonuclear propagation.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Characterization of p53/p63/p73 and Myc expressions during embryogenesis of the sea urchin.Developmental dynamics : an official publication of the American Association of Anatomists · 2024Article
- Zinc Oxide and Magnesium-Doped Zinc Oxide Nanoparticles Ameliorate Murine Chronic Toxoplasmosis.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Myospreader improves gene editing in skeletal muscle by myonuclear propagation.bioRxiv : the preprint server for biology · 2023Article
- Role of p53 suppression in the pathogenesis of hepatocellular carcinoma.World journal of gastrointestinal pathophysiology · 2023Review
- Phosphoproteomics of primary AML patient samples reveals rationale for AKT combination therapy and p53 context to overcome selinexor resistance.Cell reports · 2022Article
- Complementary omics strategies to dissect p53 signaling networks under nutrient stress.Cellular and molecular life sciences : CMLS · 2022Article
- MDMX is essential for the regulation of p53 protein levels in the absence of a functional MDM2 C-terminal tail.BMC molecular and cell biology · 2021Article
- TP53 in Biology and Treatment of Osteosarcoma.Cancers · 2021Review
- PSPC1 is a new contextual determinant of aberrant subcellular translocation of oncogenes in tumor progression.Journal of biomedical science · 2021Review
- An anterograde pathway for sensory axon degeneration gated by a cytoplasmic action of the transcriptional regulator P53.Developmental cell · 2021Article
- Role of RUNX Family Transcription Factors in DNA Damage Response.Molecules and cells · 2020Review
12 more citing papers are in PubMed but not listed here.
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
As a shuttling protein, p53 is constantly transported through the nuclear pore complex. p53 nucleocytoplasmic transport is carried out by a bipartite nuclear localization signal (NLS) located at its C-terminal domain and two nuclear export signals (NES) located in its N- and C-terminal regions, respectively. The role of nucleocytoplasmic shuttling in p53 ubiquitination and degradation has been a subject of debate. Here we show that the two basic amino acid groups in the p53 bipartite NLS function collaboratively to import p53. Mutations disrupting individual amino acids in the NLS, although causing accumulation of p53 in the cytoplasm to various degrees, reduce but do not eliminate the NLS activity, and these mutants remain sensitive to MDM2 degradation. However, disrupting both parts of the bipartite NLS completely blocks p53 from entering the nucleus and causes p53 to become resistant to MDM2-mediated degradation. Similarly, mutations disrupting four conserved hydrophobic amino acids in the p53 C-terminal NES block p53 export and prohibit it from MDM2 degradation. We also show that colocalization of a nonshuttling p53 with MDM2 either in the nucleus or in the cytoplasm is sufficient for MDM2-induced p53 polyubiquitination but not degradation. Our data provide new insight into the mechanism and regulation of p53 nucleocytoplasmic shuttling and degradation.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.