ArticleScientific reports2013
Requirement for phosphorylation of P53 at Ser312 in suppression of chemical carcinogenesis.
Article in Scientific reports, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- DUSP26 protects against acute kidney injury by dephosphorylating p53 at serine 312.Nature communications · 2026Article
- The Cyclin-dependent kinase 1: more than a cell cycle regulator.British journal of cancer · 2023Review
- New horizons from novel therapies in malignant pleural mesothelioma.Advances in respiratory medicine · 2020Review
- Drug repurposing in malignant pleural mesothelioma: a breath of fresh air?European respiratory review : an official journal of the European Respiratory Society · 2018Review
- Stabilization of the c-Myc Protein by CAMKIIγ Promotes T Cell Lymphoma.Cancer cell · 2017Article
- Genetic and functional analysis of a Li Fraumeni syndrome family in China.Scientific reports · 2016Article
- Heterogeneity of Li-Fraumeni syndrome links to unequal gain-of-function effects of p53 mutations.Scientific reports · 2014Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The p53 tumour suppressor is activated in response to a wide variety of genotoxic stresses, frequently via post-translational modification. Using a knock in mouse model with a Ser312 to Ala mutation, we show here that phosphorylation of p53 on Ser312 helps to prevent tumour induction by the alkylating agent MNU, which predominantly caused T cell lymphomas. This is consistent with our previous observation that p53(312A/A) mice are more susceptible to X-ray induced tumourigenesis. Phosphorylation on Ser312 aids p53's interaction with E2F1, and enhances p53-mediated apoptosis. Loss of E2F1 alone does not affect tumour susceptibility to MNU, but its absence partially rescues tumour formation in p53(312A/A) mice, thus reflecting the oncogenic properties of E2F1. Our data confirms the participation of Ser312 phosphorylation in tumour suppression by p53.
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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.