ArticleProceedings of the National Academy of Sciences of the United States of America2021
MDM2, MDMX, and p73 regulate cell-cycle progression in the absence of wild-type p53.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.
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
32 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.
- Hyperprogressive disease in carcinoma induced by immune checkpoint inhibitor therapy: a systematic review.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Pooled it
- Evaluation of novel targeted small-molecule therapeutics in desmoplastic small round cell tumor (DSRCT) cells.Journal of cancer research and clinical oncology · 2026Article
- Opportunities in cancer gene therapy: inhibiting MDM2 and restoring p14ARF as a means to activate p53.Molecular and cellular biochemistry · 2026Review
- The PIDDosome controls cardiomyocyte polyploidization during postnatal heart development.Cell death and differentiation · 2026Article
- Article
- MDM4 at the Crossroads: Beyond p53 and MDM2.Cancers · 2026Review
- Senescence-associated LncRNAs TRMP and TRMP-S promote gastric cancer by activating IGFL4.Scientific reports · 2026Article
- NFATc1-mediated activation of the pentose phosphate pathway and cell cycle dysregulation collectively drive tumor progression.Oncogenesis · 2025Article
- Mutant p53 regulates cancer cell invasion in complex three-dimensional environments through mevalonate pathway-dependent Rho/ROCK signaling.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Targeting MDM2 homodimer and heterodimer disruption with DRx-098D inMolecular therapy. Oncology · 2025Article
- Discovery of a Phenylalanine-Derived Natural Compound as a Potential Dual Inhibitor of MDM2 and MDMX.ChemMedChem · 2025Article
- Ribosomal RNA transcription regulates splicing through ribosomal protein RPL22.Cell chemical biology · 2025Article
- The novel piperine derivative MHJ-LN inhibits breast cancer by inducing apoptosis via p53 activation.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Article
- Analysis of p53-Independent Functions of the Mdm2-MdmX Complex Using Data-Independent Acquisition-Based Profiling.Proteomes · 2025Article
- Review
- A novel TAp73-inhibitory compound counteracts stemness features of glioblastoma stem cells.Molecular oncology · 2025Article
- Dual inhibitor of MDM2 and NFAT1 for experimental therapy of breast cancer:Frontiers in pharmacology · 2025Article
- Targeting MDM2-p53 interaction for breast cancer therapy.Oncology research · 2025Review
- TAp73 regulates mitochondrial dynamics and multiciliated cell homeostasis through an OPA1 axis.Cell death & disease · 2024Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
The p53 tumor suppressor protein, known to be critically important in several processes including cell-cycle arrest and apoptosis, is highly regulated by multiple mechanisms, most certifiably the Murine Double Minute 2-Murine Double Minute X (MDM2-MDMX) heterodimer. The role of MDM2-MDMX in cell-cycle regulation through inhibition of p53 has been well established. Here we report that in cells either lacking p53 or expressing certain tumor-derived mutant forms of p53, loss of endogenous MDM2 or MDMX, or inhibition of E3 ligase activity of the heterocomplex, causes cell-cycle arrest. This arrest is correlated with a reduction in E2F1, E2F3, and p73 levels. Remarkably, direct ablation of endogenous p73 produces a similar effect on the cell cycle and the expression of certain E2F family members at both protein and messenger RNA levels. These data suggest that MDM2 and MDMX, working at least in part as a heterocomplex, may play a p53-independent role in maintaining cell-cycle progression by promoting the activity of E2F family members as well as p73, making them a potential target of interest in cancers lacking wild-type p53.
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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 Socratic graph.