ArticleMolecular cancer2008
Resistance of mitochondrial p53 to dominant inhibition.
Article in Molecular cancer, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 26 citations in OpenAlex.
- Biology of PEST-containing nuclear proteins as potential targets in ovarian cancer (Review).Oncology letters · 2026Review
- Mitochondrially Targeted p53-Bad* Fusion Gene Therapy Promotes Apoptosis in Hepatocellular Carcinoma by Pan-Bcl-2 Inhibition.Molecular pharmaceutics · 2025Article
- The Ashkenazi-Centric G334R Variant ofMolecular and cellular biology · 2024Article
- The Challenges and Prospects of p53-Based Therapies in Ovarian Cancer.Biomolecules · 2023Review
- Regulation of p53 Function by Formation of Non-Nuclear Heterologous Protein Complexes.Biomolecules · 2022Review
- p53-Bad: A Novel Tumor Suppressor/Proapoptotic Factor Hybrid Directed to the Mitochondria for Ovarian Cancer Gene Therapy.Molecular pharmaceutics · 2019Article
- Mitochondrially targeted p53 or DBD subdomain is superior to wild type p53 in ovarian cancer cells even with strong dominant negative mutant p53.Journal of ovarian research · 2019Article
- p53 and mitochondrial function in neurons.Biochimica et biophysica acta · 2014Review
- Tumor suppressor p53 and estrogen receptors in nuclear-mitochondrial communication.Mitochondrion · 2014Review
- Merkel cell polyomavirus large T antigen disrupts host genomic integrity and inhibits cellular proliferation.Journal of virology · 2013Article
- Quercetin induces mitochondrial mediated apoptosis and protective autophagy in human glioblastoma U373MG cells.Oxidative medicine and cellular longevity · 2013Article
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- Mutant p53 exhibits trivial effects on mitochondrial functions which can be reactivated by ellipticine in lymphoma cells.Apoptosis : an international journal on programmed cell death · 2011Article
- Translocation of p53 to mitochondria is regulated by its lipid binding property to anionic phospholipids and it participates in cell death control.Neoplasia (New York, N.Y.) · 2010Article
- The mitochondrial p53 pathway.Biochimica et biophysica acta · 2009Review
- Loss of p53 causes mitochondrial DNA depletion and altered mitochondrial reactive oxygen species homeostasis.Biochimica et biophysica acta · 2009Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMutation of a tumor suppressor allele leaves the second as backup. Not necessarily so with p53. This homo-tetrameric transcription factor can become contaminated with mutant p53 through hetero-tetramerization. In addition, it can be out-competed by the binding to p53 DNA recognition motifs of transactivation-incompetent isoforms (DeltaN and DeltaTA-isoforms) of the p53/p63/p73 family of proteins. Countermeasures against such dominant-negative or dominant-inhibitory action might include the evolutionary gain of novel, transactivation-independent tumor suppressor functions by the wild-type monomer.
resultsHere we have studied, mostly in human HCT116 colon adenocarcinoma cells with an intact p53 pathway, the effects of dominant-inhibitory p53 mutants and of Deltaex2/3p73, a tumor-associated DeltaTA-competitor of wild-type p53, on the nuclear transactivation-dependent and extra-nuclear transactivation-independent functions of wild-type p53. We report that mutant p53 and Deltaex2/3p73, expressed from a single gene copy per cell, interfere with the stress-induced expression of p53-responsive genes but leave the extra-nuclear apoptosis by mitochondrial p53 largely unaffected, although both wild-type and mutant p53 associate with the mitochondria. In accord with these observations, we present evidence that in contrast to nuclear p53 the vast majority of mitochondrial p53, be it wild-type or mutant, is consisting of monomeric protein.
conclusionThe extra-nuclear p53-dependent apoptosis may constitute a fail-safe mechanism against dominant inhibition.
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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 OpenQuestion graph.