ArticleCell cycle (Georgetown, Tex.)2010
Life or death: p53-induced apoptosis requires DNA binding cooperativity.
Article in Cell cycle (Georgetown, Tex.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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.
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
30 citing papers in PubMed, 52 citations in OpenAlex.
- P53 Inhibition Diminishes IGSF9 Gene Activity to Promote DNA Repair and Exacerbate the Progression of Colon Cancer.Journal of biochemical and molecular toxicology · 2026Article
- Ashwagandha-Induced Programmed Cell Death in the Treatment of Breast Cancer.Current issues in molecular biology · 2024Review
- Targeted Radium Alpha Therapy in the Era of Nanomedicine: In Vivo Results.International journal of molecular sciences · 2024Review
- Rely on Each Other: DNA Binding Cooperativity Shapes p53 Functions in Tumor Suppression and Cancer Therapy.Cancers · 2021Review
- Salmonella enterica serovar Typhimurium inhibits the innate immune response and promotes apoptosis in a ribosomal/TRP53-dependent manner in swine neutrophils.Veterinary research · 2020Article
- p53's Extended Reach: The Mutant p53 Secretome.Biomolecules · 2020Review
- Inactivation of Mdm2 restores apoptosis proficiency of cooperativity mutant p53 in vivo.Cell cycle (Georgetown, Tex.) · 2020Article
- Metformin Synergistically Enhanced the Antitumor Activity of Celecoxib in Human Non-Small Cell Lung Cancer Cells.Frontiers in pharmacology · 2020Article
- Residual apoptotic activity of a tumorigenic p53 mutant improves cancer therapy responses.The EMBO journal · 2019Article
- Regulators of Salmonella-host interaction identified by peripheral blood transcriptome profiling: roles of TGFB1 and TRP53 in intracellular Salmonella replication in pigs.Veterinary research · 2018Article
- Pro-metastatic p53 mutants control folding of N-glycoproteins.Cell cycle (Georgetown, Tex.) · 2017Article
- Solution structure and binding specificity of the p63 DNA binding domain.Scientific reports · 2016Article
- Inhibition of Wild-Type p53-Expressing AML by the Novel Small Molecule HDM2 Inhibitor CGM097.Molecular cancer therapeutics · 2015Article
- Gradual reduction in rRNA transcription triggers p53 acetylation and apoptosis via MYBBP1A.Scientific reports · 2015Article
- Article
- Senescence and apoptosis: dueling or complementary cell fates?EMBO reports · 2014Review
- ∆N-P63α and TA-P63α exhibit intrinsic differences in transactivation specificities that depend on distinct features of DNA target sites.Oncotarget · 2014Article
- Drugging the p53 pathway: understanding the route to clinical efficacy.Nature reviews. Drug discovery · 2014Review
- Transactivation specificity is conserved among p53 family proteins and depends on a response element sequence code.Nucleic acids research · 2013Article
- Role of p53 in regulating tissue response to radiation by mechanisms independent of apoptosis.Translational cancer research · 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
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The tumor suppressor p53 provides exquisite protection from cancer by balancing cell survival and death in response to stress. Sustained stress or irreparable damage trigger p53's killer functions to permanently eliminate genetically-altered cells as a potential source of cancer. To prevent the unnecessary loss of cells that could cause premature aging as a result of stem cell attrition, the killer functions of p53 are tightly regulated and balanced against protector functions that promote damage repair and support survival in response to low stress or mild damage. In molecular terms these p53-based cell fate decisions involve protein interactions with cofactors and modifying enzymes, which modulate the activation of distinct sets of p53 target genes. In addition, we demonstrate that part of this regulation occurs at the level of DNA binding. We show that the killer function of p53 requires the four DNA binding domains within the p53 tetramer to interact with one another. These intermolecular interactions enable cooperative binding of p53 to less perfect response elements in the genome, which are present in many target genes essential for apoptosis. Modulating p53 interactions within the tetramer could therefore present a novel promising strategy to fine-tune p53-based cell fate decisions.
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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.