ReviewJournal of biomedicine & biotechnology2011
Functions of MDMX in the modulation of the p53-response.
Review in Journal of biomedicine & biotechnology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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.
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.
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Who cites it
28 citing papers in PubMed, 36 citations in OpenAlex.
- The Enigmatic Tumor Suppressor p53 Biomolecule: Its Role and Prognostic and Predictive Values in Cancer Therapy and Precision Medicine.Biomolecules · 2026Review
- Pharmacological targeting of SF3a1-MDM4 splicing vulnerability in ovarian cancer with rifaximin and antisense oligonucleotide.Journal of translational medicine · 2026Article
- Ubiquitination mediated by RING-type E3 ligases in the progression of digestive system tumors: mechanistic insights and potential therapeutic strategies.Frontiers in cell and developmental biology · 2026Review
- Decoding the molecular symphony: interactions between the mNAR cancer · 2024Review
- Cytotoxic Fractions fromMolecules (Basel, Switzerland) · 2021Article
- MDM4 alternative splicing and implication in MDM4 targeted cancer therapies.American journal of cancer research · 2021Review
- Traceless solid-phase synthesis and β-turn propensity of 1,3-thiazole-based peptidomimetics.RSC advances · 2020Article
- Pharmacogenomics and Pharmacogenetics in Osteosarcoma: Translational Studies and Clinical Impact.International journal of molecular sciences · 2020Review
- TP53 in bone and soft tissue sarcomas.Pharmacology & therapeutics · 2019Review
- Tumorigenesis promotes Mdm4-S overexpression.Oncotarget · 2017Article
- MDM4 actively restrains cytoplasmic mTORC1 by sensing nutrient availability.Molecular cancer · 2017Article
- Targeting MDM4 Splicing in Cancers.Genes · 2017Review
- The Zn-finger domain of MdmX suppresses cancer progression by promoting genome stability in p53-mutant cells.Oncogenesis · 2016Article
- Article
- MDMX (MDM4), a Promising Target for p53 Reactivation Therapy and Beyond.Cold Spring Harbor perspectives in medicine · 2016Review
- Antisense oligonucleotide-mediated MDM4 exon 6 skipping impairs tumor growth.The Journal of clinical investigation · 2016Article
- EZH2 inhibition re-sensitizes multidrug resistant B-cell lymphomas to etoposide mediated apoptosis.Oncoscience · 2016Article
- Mice engineered for an obligatory Mdm4 exon skipping express higher levels of the Mdm4-S isoform but exhibit increased p53 activity.Oncogene · 2015Article
- microRNAs and Alu elements in the p53-Mdm2-Mdm4 regulatory network.Journal of molecular cell biology · 2014Review
- Stress-induced alternative splice forms of MDM2 and MDMX modulate the p53-pathway in distinct ways.PloS one · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The MDM family proteins MDM2 and MDMX are two critical regulators of the p53 tumor suppressor protein. Expression of both proteins is necessary for allowing the embryonal development by keeping the activity of p53 in check. Upon stresses that need to activate p53 to perform its function as guardian of the genome, p53 has to be liberated from these two inhibitors. In this review, we will discuss the various mechanisms by which MDMX protein levels are downregulated upon various types of stress, including posttranslational modifications of the MDMX protein and the regulation of mdmx mRNA expression, including alternative splicing. In addition, the putative function(s) of the described MDMX splice variants, particularly in tumor development, will be discussed. Lastly, in contrast to common belief, we have recently shown the existence of a p53-MDMX feedback loop, which is important for dampening the p53-response at later phases after genotoxic stress.
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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 OpenQuestion graph.