ArticleProceedings of the National Academy of Sciences of the United States of America2008
Inhibition of Thr-55 phosphorylation restores p53 nuclear localization and sensitizes cancer cells to DNA damage.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 74 citations in OpenAlex.
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- Proteasomal proteolysis in p62 condensates directs tumor suppression or growth depending on their subcellular localization.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- PROTAC-Mediated Degradation of TAF1 Induces Apoptosis in AML Cells and Inhibits Tumor Growth In Vivo.Molecular cancer therapeutics · 2025Article
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- 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
- Therapeutic targeting of nuclear export and import receptors in cancer and their potential in combination chemotherapy.IUBMB life · 2024Review
- NRF2 activators inhibit influenza A virus replication by interfering with nucleo-cytoplasmic export of viral RNPs in an NRF2-independent manner.PLoS pathogens · 2023Article
- Toward Accurate Coarse-Grained Simulations of Disordered Proteins and Their Dynamic Interactions.Journal of chemical information and modeling · 2022Article
- Methyl-Donors Can Induce Apoptosis and Attenuate Both the Akt and the Erk1/2 Mediated Proliferation Pathways in Breast and Lung Cancer Cell Lines.International journal of molecular sciences · 2021Article
- A phosphorylation-dependent switch in the disordered p53 transactivation domain regulates DNA binding.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Pathogenic SREK1 decrease in Huntington's disease lowers TAF1 mimicking X-linked dystonia parkinsonism.Brain : a journal of neurology · 2020Article
- Sphingolipids and the link between alcohol and cancer.Chemico-biological interactions · 2020Review
- The human DEPhOsphorylation Database DEPOD: 2019 update.Database : the journal of biological databases and curation · 2019Article
- The Rules and Functions of Nucleocytoplasmic Shuttling Proteins.International journal of molecular sciences · 2018Review
- Functional Genome-wide Screening Identifies Targets and Pathways Sensitizing Pancreatic Cancer Cells to Dasatinib.Journal of Cancer · 2018Article
- Trans-chalcone increases p53 activity via DNAJB1/HSP40 induction and CRM1 inhibition.PloS one · 2018Article
- Epigallocatechin-3-gallate augments the therapeutic effects of benzo[a]pyrene-mediated lung carcinogenesis.BioFactors (Oxford, England) · 2017Article
- Phosphorylation of p53 at threonine 155 is required for Jab1-mediated nuclear export of p53.BMB reports · 2017Article
- Article
- X-linked Dystonia-Parkinsonism patient cells exhibit altered signaling via nuclear factor-kappa B.Neurobiology of disease · 2017Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The p53 tumor suppressor induces cell growth arrest and apoptosis in response to DNA damage. Because these functions are achieved largely by the transcriptional properties of p53, nuclear localization of the protein is essential. Indeed, the tumors with aberrant cytoplasmic localization of wild-type p53 often exhibit an impaired response to DNA damage. In this study, we report that Thr-55 phosphorylation induces the association of p53 with the nuclear export factor CRM1, leading to p53 nuclear export. We further show that MDM2 also promotes the CRM1-p53 association and Thr-55 phosphorylation is required for this process. Interestingly, inhibition of Thr-55 phosphorylation by a dietary flavonoid, apigenin, specifically blocks the CRM1-p53 association, restores p53 nuclear localization, and sensitizes tumor cells with cytoplasm localized wild-type p53 to DNA damage. These data provide insights into the regulation of p53 nuclear localization by post-translational modification and suggest an avenue for targeted therapy for cancers caused by aberrant cytoplasm localization of wild-type p53.
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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.