ArticleTranslational cancer research2012
MDM2 and MDMX: Alone and together in regulation of p53.
Article in Translational cancer research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 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.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
90 citing papers in PubMed, 1 synthesis or guideline pooled it, 124 citations in OpenAlex.
- Cellular functions and molecular mechanisms of ubiquitination in osteosarcoma.Frontiers in oncology · 2022Pooled it
- Milademetan in Advanced Solid Tumors with MDM2 Amplification and Wild-type TP53: Preclinical and Phase II Clinical Trial Results.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025Trial
- The MDM2 antagonist idasanutlin in patients with polycythemia vera: results from a single-arm phase 2 study.Blood advances · 2022Trial
- Role of the MDM2/p53 axis in regulating cisplatin response in tumor cells.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Review
- Ubiquitin E3 Ligases and p53 in Doxorubicin-Induced Cardiotoxicity.International journal of molecular sciences · 2025Review
- Polyethylene glycol incorporation to reduce the cytotoxicity associated with cationic cell-penetrating-peptide conjugation.RSC medicinal chemistry · 2025Article
- Analysis of p53-Independent Functions of the Mdm2-MdmX Complex Using Data-Independent Acquisition-Based Profiling.Proteomes · 2025Article
- FLT4 activation promotes acute lymphoid leukemia survival through stabilization of MDM2/MDMX and inactivation of p53.Oncogenesis · 2025Article
- BH3-mimetics or DNA-damaging agents in combination with RG7388 overcome p53 mutation-induced resistance to MDM2 inhibition.Apoptosis : an international journal on programmed cell death · 2024Article
- First reported advanced pancreatic cancer with hyperprogression treated with PD-1 blockade combined with chemotherapy: a case report and literature review.Discover oncology · 2024Article
- Upregulation of YPEL3 expression and induction of human breast cancer cell death by microRNAs.Toxicological research · 2024Article
- An Anti-Invasive Role for Mdmx through the RhoA GTPase under the Control of the NEDD8 Pathway.Cells · 2024Article
- Article
- Targeting Hdm2 and Hdm4 in Anticancer Drug Discovery: Implications for Checkpoint Inhibitor Immunotherapy.Cells · 2024Review
- MDM2/MDMX inhibition by Sulanemadlin synergizes with anti-Programmed Death 1 immunotherapy in wild-type p53 tumors.iScience · 2024Article
- Evaluation of P53 immunostaining in patients with cutaneous melanoma.Biomedical reports · 2024Article
- Molecular Design of Cyclic Peptides with Cell Membrane Permeability and Development of MDMX-p53 Inhibitor.ACS medicinal chemistry letters · 2023Article
- Advances in the Anti-Tumor Activity of Biflavonoids inInternational journal of molecular sciences · 2023Review
- p53 and Myofibroblast Apoptosis in Organ Fibrosis.International journal of molecular sciences · 2023Review
- EBNA1 Upregulates P53-Inhibiting Genes in Burkitt's Lymphoma Cell Line.Reports of biochemistry & molecular biology · 2023Article
30 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
p53, a critical tumor suppressor, is activated by various cellular stresses to prevent and repair damages that can lead to tumor development. In response to these stresses, p53 activation can cause very serious cellular effects including permanent cell cycle arrest and cell death. p53 must therefore be very tightly regulated to avoid unnecessary pathological effects. The homologs MDM2 and MDMX have been shown to be the major, essential negative regulators of p53. In normal cells, MDM2 and MDMX suppress p53 activity, but in the event of cellular stress, they themselves must be inhibited so that p53 may respond to the stress. MDM2 and MDMX are known to bind together, and play multifaceted, non-redundant roles in modulating p53 protein activity. Recently, evidence has emerged showing that MDM2 and MDMX most effectively inhibit p53 as a complex, and possibly play non-redundant roles because they must function as one to control p53. In this review, we give an overview of MDM2 and MDMX and discuss a few ways in which they are modified so that p53 may be activated. Lastly, we discuss the non-redundant roles of MDM2 and MDMX and how it is important to investigate the effect on the complex as a whole when investigating either protein.
Identifiers
23002429PMC3448287W1925535727What 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.