ArticleCell death & disease2016
Constitutive p53 heightens mitochondrial apoptotic priming and favors cell death induction by BH3 mimetic inhibitors of BCL-xL.
Article in Cell death & disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 26 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
26 citing papers in PubMed, 37 citations in OpenAlex.
- In Silico Isomerization Produces Apt Negative Data for VHTS Validation.Journal of chemical information and modeling · 2026Article
- UPR/ATF4/Noxa pathway overactivation through SERCA2 inhibition or ONC201 treatment combined with ABT-737 triggers apoptosis in chemoresistant ovarian cancer cells and patient-derived tumor organoids.Cell death & disease · 2026Article
- Integrated molecular and functional characterization of the intrinsic apoptotic machinery identifies therapeutic vulnerabilities in glioma.Nature communications · 2024Article
- AMPK/PGC-1α and p53 modulate VDAC1 expression mediated by reduced ATP level and metabolic oxidative stress in neuronal cells.Acta biochimica et biophysica Sinica · 2024Article
- Sensitization of cancer cells to ferroptosis coincident with cell cycle arrest.Cell chemical biology · 2024Article
- Article
- A Mesenchymal Tumor Cell State Confers Increased Dependency on the BCL-XL Antiapoptotic Protein in Kidney Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2022Article
- Keeping Cell Death Alive: An Introduction into the French Cell Death Research Network.Biomolecules · 2022Review
- Partial p53 reactivation is sufficient to induce cancer regression.Journal of experimental & clinical cancer research : CR · 2022Article
- Regulation of Bcl-2 Family Proteins in Estrogen Receptor-Positive Breast Cancer and Their Implications in Endocrine Therapy.Cancers · 2022Review
- Full-length transcriptome sequencing and comparative transcriptome analysis ofFrontiers in cellular and infection microbiology · 2022Article
- Dying to Survive-The p53 Paradox.Cancers · 2021Review
- Mitochondrial apoptotic priming is a key determinant of cell fate upon p53 restoration.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Intact TP-53 function is essential for sustaining durable responses to BH3-mimetic drugs in leukemias.Blood · 2021Article
- Rely on Each Other: DNA Binding Cooperativity Shapes p53 Functions in Tumor Suppression and Cancer Therapy.Cancers · 2021Review
- Targeting of BCL-2 Family Members during Anticancer Treatment: A Necessary Compromise between Individual Cell and Ecosystemic Responses?Biomolecules · 2020Review
- Bim, Puma and Noxa upregulation by Naftopidil sensitizes ovarian cancer to the BH3-mimetic ABT-737 and the MEK inhibitor Trametinib.Cell death & disease · 2020Article
- Inactivation of Mdm2 restores apoptosis proficiency of cooperativity mutant p53 in vivo.Cell cycle (Georgetown, Tex.) · 2020Article
- Residual apoptotic activity of a tumorigenic p53 mutant improves cancer therapy responses.The EMBO journal · 2019Article
- Detection of a novel, primate-specific 'kill switch' tumor suppression mechanism that may fundamentally control cancer risk in humans: an unexpected twist in the basic biology of TP53.Endocrine-related cancer · 2018Review
Corrections and comments
- Erratum issued
Authors and funding
10 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Proapoptotic molecules directly targeting the BCL-2 family network are promising anticancer therapeutics, but an understanding of the cellular stress signals that render them effective is still elusive. We show here that the tumor suppressor p53, at least in part by transcription independent mechanisms, contributes to cell death induction and full activation of BAX by BH3 mimetic inhibitors of BCL-xL. In addition to mildly facilitating the ability of compounds to derepress BAX from BCL-xL, p53 also provides a death signal downstream of anti-apoptotic proteins inhibition. This death signal cooperates with BH3-induced activation of BAX and it is independent from PUMA, as enhanced p53 can substitute for PUMA to promote BAX activation in response to BH3 mimetics. The acute sensitivity of mitochondrial priming to p53 revealed here is likely to be critical for the clinical use of BH3 mimetics.
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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 Socratic graph.