ArticleCell death and differentiation2011
Serine 312 phosphorylation is dispensable for wild-type p53 functions in vivo.
Article in Cell death and differentiation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
9 citing papers in PubMed, 17 citations in OpenAlex.
- DUSP26 protects against acute kidney injury by dephosphorylating p53 at serine 312.Nature communications · 2026Article
- Regulating tumor suppressor genes: post-translational modifications.Signal transduction and targeted therapy · 2020Review
- Understanding p53 functions through p53 antibodies.Journal of molecular cell biology · 2019Review
- 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
- Dynamics of re-constitution of the human nuclear proteome after cell division is regulated by NLS-adjacent phosphorylation.Cell cycle (Georgetown, Tex.) · 2014Article
- p63 the guardian of human reproduction.Cell cycle (Georgetown, Tex.) · 2012Review
- NRF2 and p53: Januses in cancer?Oncotarget · 2012Review
- Regulation of p73 activity by post-translational modifications.Cell death & disease · 2012Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cellular stimulation results in phosphorylation of the tumor suppressor p53 on multiple residues, though the functional relevance is not always clear. It is noteworthy that the serine (S) 315 residue is unique, as it has been suggested to be phosphorylated not only by genotoxic signals, but also during cell-cycle progression and by endoplasmic-reticulum stress. However, in vitro data have been conflicting as phosphorylation at this site was shown to both positively and negatively regulate p53 functions. We have thus generated knock-in mice expressing an unphosphorylable S312 (equivalent to human S315), by substitution with an alanine (A) residue, to clarify the conflicting observations and to evaluate its functional relevance in vivo. Born at Mendelian ratios, the p53(S312A/S312A) mice show no anomalies during development and adulthood. p53 activation, stability, localization and ability to induce apoptosis, cell-cycle arrest and prevent centrosome amplification are not compromised in p53(S312A/S312A) cells. p53(S312A/S312A) mice are unable to rescue mdm2(-/-) lethality, and tumorigenesis--both spontaneous and irradiation/oncogene-induced--is not accentuated. Taken together, the results show that the S312 phosphorylation site is not in itself necessary for efficient p53 function, and advocates the possibility that it is neither relevant in the mouse context nor important for p53 functions in vivo.
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Registered trials
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.