ArticleThe EMBO journal2012
A DR4:tBID axis drives the p53 apoptotic response by promoting oligomerization of poised BAX.
Article in The EMBO journal, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
26 citing papers in PubMed, 35 citations in OpenAlex.
- Article
- Role and clinical significance of the DNA methylation of 14-3-3σ in cancer (Review).Oncology letters · 2025Review
- Pleiotropic Effects of Metformin on the Chemotherapy Response of HPV-Positive Cancer Cells.Journal of medical virology · 2025Article
- Anticancer activity mechanism of novelly synthesized and characterized benzofuran ring-linked 3-nitrophenyl chalcone derivative on colon cancer cells.Open medicine (Warsaw, Poland) · 2025Article
- FAM193A is a positive regulator of p53 activity.Cell reports · 2023Article
- P-TEFb promotes cell survival upon p53 activation by suppressing intrinsic apoptosis pathway.Nucleic acids research · 2023Article
- Cordycepin Induces Apoptosis through JNK-Mediated Caspase Activation in Human OEC-M1 Oral Cancer Cells.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Role of JNK activation in paclitaxel-induced apoptosis in human head and neck squamous cell carcinoma.Oncology letters · 2021Article
- Gasdermin E-mediated programmed cell death: An unpaved path to tumor suppression.Journal of Cancer · 2021Review
- The NKL-code for innate lymphoid cells reveals deregulated expression of NKL homeobox genes HHEX and HLX in anaplastic large cell lymphoma (ALCL).Oncotarget · 2020Article
- CDK8 Kinase Activity Promotes Glycolysis.Cell reports · 2017Article
- Activation of the p53 Transcriptional Program Sensitizes Cancer Cells to Cdk7 Inhibitors.Cell reports · 2017Article
- Identification of a core TP53 transcriptional program with highly distributed tumor suppressive activity.Genome research · 2017Article
- Cardiac-specific ablation of the E3 ubiquitin ligase Mdm2 leads to oxidative stress, broad mitochondrial deficiency and early death.PloS one · 2017Article
- ATM regulates cell fate choice upon p53 activation by modulating mitochondrial turnover and ROS levels.Cell cycle (Georgetown, Tex.) · 2015Article
- Article
- Drugging the p53 pathway: understanding the route to clinical efficacy.Nature reviews. Drug discovery · 2014Review
- Human embryonic and induced pluripotent stem cells express TRAIL receptors and can be sensitized to TRAIL-induced apoptosis.Stem cells and development · 2013Article
- Article
- Up-regulation of Smurf1 after spinal cord injury in adult rats.Journal of molecular histology · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The cellular response to p53 activation varies greatly in a stimulus- and cell type-specific manner. Dissecting the molecular mechanisms defining these cell fate choices will assist the development of effective p53-based cancer therapies and also illuminate fundamental processes by which gene networks control cellular behaviour. Using an experimental system wherein stimulus-specific p53 responses are elicited by non-genotoxic versus genotoxic agents, we discovered a novel mechanism that determines whether cells undergo proliferation arrest or cell death. Strikingly, we observe that key mediators of cell-cycle arrest (p21, 14-3-3σ) and apoptosis (PUMA, BAX) are equally activated regardless of outcome. In fact, arresting cells display strong translocation of PUMA and BAX to the mitochondria, yet fail to release cytochrome C or activate caspases. Surprisingly, the key differential events in apoptotic cells are p53-dependent activation of the DR4 death receptor pathway, caspase 8-mediated cleavage of BID, and BID-dependent activation of poised BAX at the mitochondria. These results reveal a previously unappreciated role for DR4 and the extrinsic apoptotic pathway in cell fate choice following p53 activation.
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.