ArticleCell research2008
p53's mitochondrial translocation and MOMP action is independent of Puma and Bax and severely disrupts mitochondrial membrane integrity.
Article in Cell research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It carries an expression of concern. Cited by 81 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
81 citing papers in PubMed, 184 citations in OpenAlex.
- miR-125b Attenuates Sepsis-Induced Hippocampal Mitochondrial Fission and Cognitive Impairment via the ROS/p53 Pathway.Molecular neurobiology · 2026Article
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- p53 Interacts with VDAC1, Modulating Its Expression Level and Oligomeric State to Activate Apoptosis.Biomolecules · 2026Article
- VDAC1-interacting proteins: binding site mapping and their derived peptides induce apoptosis and multifaceted cellular effects.Apoptosis : an international journal on programmed cell death · 2025Article
- Bridging Inflammation and Repair: The Promise of MFG-E8 in Ischemic Stroke Therapy.International journal of molecular sciences · 2025Review
- Article
- Etoposide-induced cancer cell death: roles of mitochondrial VDAC1 and calpain, and resistance mechanisms.Molecular oncology · 2025Article
- ATM and p53 in aging and cancer: a double-edged sword in genomic integrity.Biogerontology · 2025Review
- MicroRNA, Myostatin, and Metabolic Rate Depression: Skeletal Muscle Atrophy Resistance in HibernatingCells · 2024Article
- Cell fate regulation governed by p53: Friends or reversible foes in cancer therapy.Cancer communications (London, England) · 2024Review
- Li-Fraumeni Syndrome-Associated Dimer-Forming Mutant p53 Promotes Transactivation-Independent Mitochondrial Cell Death.Cancer discovery · 2023Article
- Article
- Quercetin Is An Active Agent in Berries against Neurodegenerative Diseases Progression through Modulation of Nrf2/HO1.Nutrients · 2022Review
- Mutant p53 in cancer: from molecular mechanism to therapeutic modulation.Cell death & disease · 2022Review
- Resveratrol as a modulatory of apoptosis and autophagy in cancer therapy.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022Review
- Targeting Apoptosis in Cancer.Current oncology reports · 2022Review
- Cyclophilin D: Guardian or Executioner for Tumor Cells?Frontiers in oncology · 2022Review
- Burn Injury: Mechanisms of Keratinocyte Cell Death.Medical sciences (Basel, Switzerland) · 2021Review
- TMEM166 inhibits cell proliferation, migration and invasion in hepatocellular carcinoma via upregulating TP53.Molecular and cellular biochemistry · 2021Article
- O-GlcNAc Transferase Inhibitor Synergistically Enhances Doxorubicin-Induced Apoptosis in HepG2 Cells.Cancers · 2020Article
21 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
- Expression of concern
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
p53's apoptotic program consists of transcription-dependent and transcription-independent pathways. In the latter, physical interactions between mitochondrial p53 and anti- and pro-apoptotic members of the Bcl2 family of mitochondrial permeability regulators are central. Using isogenic cell systems with defined deficiencies, we characterize in detail how mitochondrial p53 contributes to mitochondrial permeabilization, to what extent its action depends on other key Bcl2 family members and define its release activity. We show that mitochondrial p53 is highly efficient in inducing the release of soluble and insoluble apoptogenic factors by severely disrupting outer and inner mitochondrial membrane integrity. This action is associated with wild-type p53-induced oligomerization of Bax, Bak and VDAC and the formation of a stress-induced endogenous complex between p53 and cyclophilin D, normally located at the inner membrane. Tumor-derived p53 mutants are deficient in activating the Bax/Bak lipid pore. These actions are independent of Puma and Bax. Importantly, the latter distinguishes the mitochondrial from the cytosolic p53 death pathway.
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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.