ArticleBiophysical journal2010
Coordination of the nuclear and cytoplasmic activities of p53 in response to DNA damage.
Article in Biophysical journal, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
14 citing papers in PubMed, 31 citations in OpenAlex.
- The autophagy-senescence axis as a threshold model of aging and therapeutic targeting.Redox biology · 2026Review
- The multifaceted role of PUMA in cell death pathways: its therapeutic potential across cancer types.Cell communication and signaling : CCS · 2025Review
- Article
- The Interplay Between Autophagy and Apoptosis in the Mechanisms of Action of Stilbenes in Cancer Cells.Antioxidants (Basel, Switzerland) · 2025Review
- Review
- Dual roles of SIRT1 in the BAX switch through the P53 module: A mathematical modeling study.Computational and structural biotechnology journal · 2021Article
- Does p53 codon 72 polymorphism have a prognostic value in carcinoma of the vulva and vagina?Medical oncology (Northwood, London, England) · 2017Article
- A novel mathematical model of ATM/p53/NF- κB pathways points to the importance of the DDR switch-off mechanisms.BMC systems biology · 2016Article
- Significance of p53 dynamics in regulating apoptosis in response to ionizing radiation, and polypharmacological strategies.Scientific reports · 2014Article
- Interplay between Mdm2 and HIPK2 in the DNA damage response.Journal of the Royal Society, Interface · 2014Article
- Article
- Radiation/paclitaxel treatment of p53-abnormal non-small cell lung cancer xenograft tumor and associated mechanism.Cancer biotherapy & radiopharmaceuticals · 2012Article
- A two-step mechanism for cell fate decision by coordination of nuclear and mitochondrial p53 activities.PloS one · 2012Article
- Real-time monitoring of cisplatin-induced cell death.PloS one · 2011Article
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 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The tumor suppressor p53 plays a key role in the cellular response to various stresses. Most previous studies have focused on either the nuclear or cytoplasmic proapoptotic functions of p53, ignoring the combination of both functions. To explore how the two functions of p53 are coordinated in the DNA damage response via computer simulation, we construct a model for the p53 network comprising coupled positive and negative feedback loops involving p53, Mdm2, and Akt, as well as PUMA and Bax. In our model p53 is stabilized and accumulates in the nucleus and cytoplasm upon DNA damage. Nuclear p53 induces expression of Mdm2, PTEN, PUMA, and Bax. Cytoplasmic p53 is then released from the p53.Bcl-xL complex by PUMA to activate Bax directly. We find that the switching between low and high protein levels underlies the decision between cell survival and death. Moreover, a balance between the nuclear and cytoplasmic p53 levels and appropriate levels of Akt and PUMA are required for reliable cell fate decision. Our results indicate that coordination of the transcription-dependent and -independent activities of p53 is important in determining cellular outcomes. These findings advance our understanding of the mechanism for p53-mediated cellular responses and provide clues to p53-based cancer therapy.
Indexed as
Identifiers
What OpenQuestion holds
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.