ArticleProceedings of the National Academy of Sciences of the United States of America2010
Phosphorylation of Ser312 contributes to tumor suppression by p53 in vivo.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- DUSP26 protects against acute kidney injury by dephosphorylating p53 at serine 312.Nature communications · 2026Article
- Development of Novel Phosphonodifluoromethyl-Containing Phosphotyrosine Mimetics and a First-In-Class, Potent, Selective, and Bioavailable Inhibitor of Human CDC14 Phosphatases.Journal of medicinal chemistry · 2024Article
- Residual apoptotic activity of a tumorigenic p53 mutant improves cancer therapy responses.The EMBO journal · 2019Article
- Tumor suppressive role for kinases phosphorylating p53 in DNA damage-induced apoptosis.Cancer science · 2018Review
- Mutant TP53 posttranslational modifications: challenges and opportunities.Human mutation · 2014Review
- Illuminating p53 function in cancer with genetically engineered mouse models.Seminars in cell & developmental biology · 2014Review
- Exploiting unique structural and functional properties of malarial glycolytic enzymes for antimalarial drug development.Malaria research and treatment · 2014Review
- Requirement for phosphorylation of P53 at Ser312 in suppression of chemical carcinogenesis.Scientific reports · 2013Article
- Transcriptional and translational regulation of C/EBPβ-HDAC1 protein complexes controls different levels of p53, SIRT1, and PGC1α proteins at the early and late stages of liver cancer.The Journal of biological chemistry · 2013Article
- A minimally invasive assay for individual assessment of the ATM/CHEK2/p53 pathway activity.Cell cycle (Georgetown, Tex.) · 2011Article
- Small changes huge impact: the role of protein posttranslational modifications in cellular homeostasis and disease.Journal of amino acids · 2011Article
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The tumor suppressor p53 is a master sensor of stress, and posttranslational modifications are key in controlling its stability and transcriptional activities. p53 can be phosphorylated on at least 23 Ser/Thr residues, the majority of which are phosphorylated by stress-related kinases. An exception is Ser315 in human p53 (Ser312 in mouse), which is predominantly phosphorylated by cell cycle-related kinases. To understand the biological importance of Ser312 phosphorylation in vivo, we generated p53Ser312Ala knock-in mice. We show here that, although Ser312 is not essential for mouse life span under normal physiological conditions, Ser312Ala mutation dampens p53's activity during embryonic development. This is evident from its partial rescue of embryonic lethality caused by Mdm4 deletion. In agreement with the notion that Ser312 mutation weakens p53 function, Ser312Ala mice are also more susceptible to tumorigenesis following a sublethal ionizing radiation dose. Importantly, in the cohort studied, Ser312 mutation predisposes mice to develop thymic lymphomas and liver tumors, partly due to p53Ser312Ala's inability to fully induce a set of p53 target genes including p21 and cyclin G1. Thus, we demonstrate that phosphorylation of Ser312 is required for p53 to function fully as a tumor suppressor in vivo.
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