ArticleOncogene2013
Activation of p53 following ionizing radiation, but not other stressors, is dependent on the proline-rich domain (PRD).
Article in Oncogene, 2013. 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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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.
The trial behind it
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
11 citing papers in PubMed, 16 citations in OpenAlex.
- Unveiling the Mechanisms of EGCG-p53 Interactions through Molecular Dynamics Simulations.ACS omega · 2024Article
- Deregulation and Targeting of TP53 Pathway in Multiple Myeloma.Frontiers in oncology · 2018Review
- Chromatin remodeling protein MORC2 promotes breast cancer invasion and metastasis through a PRD domain-mediated interaction with CTNND1.Oncotarget · 2017Article
- The proline rich domain of p53 is dispensable for MGMT-dependent DNA repair and cell survival following alkylation damage.Cell death and differentiation · 2017Article
- The Trp53 delta proline (Trp53ΔP) mouse exhibits increased genome instability and susceptibility to radiation-induced, but not spontaneous, tumor development.Molecular carcinogenesis · 2016Article
- Δ122p53, a mouse model of Δ133p53α, enhances the tumor-suppressor activities of an attenuated p53 mutant.Cell death & disease · 2015Article
- Alpha-enolase is upregulated on the cell surface and responds to plasminogen activation in mice expressing a ∆133p53α mimic.PloS one · 2015Article
- Illuminating p53 function in cancer with genetically engineered mouse models.Seminars in cell & developmental biology · 2014Review
- Targeting the ubiquitin-mediated proteasome degradation of p53 for cancer therapy.Current pharmaceutical design · 2013Review
- Molecular dynamic simulation insights into the normal state and restoration of p53 function.International journal of molecular sciences · 2012Review
- Chromosome Translocation t(10;19)(q26;q13) in a CIC-sarcoma.In vivo (Athens, Greece)Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The tumor suppressor protein, p53 is one of the most important cellular defences against malignant transformation. In response to cellular stressors p53 can induce apoptosis, cell cycle arrest or senescence as well as aid in DNA repair. Which p53 function is required for tumor suppression is unclear. The proline-rich domain (PRD) of p53 (residues 58-101) has been reported to be essential for the induction of apoptosis. To determine the importance of the PRD in tumor suppression in vivo we previously generated a mouse containing a 33-amino-acid deletion (residues 55-88) in p53 (mΔpro). We showed that mΔpro mice are protected from T-cell tumors but not late-onset B-cell tumors. Here, we characterize the functionality of the PRD and show that it is important for mediating the p53 response to DNA damage induced by γ-radiation, but not the p53-mediated responses to Ha-Ras expression or oxidative stress. We conclude that the PRD is important for receiving incoming activating signals. Failure of PRD mutants to respond to the activating signaling produced by DNA damage leads to impaired downstream signaling, accumulation of mutations, which potentially leads to late-onset tumors.
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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.