ArticleOncogene2017
p53 binds the mdmx mRNA and controls its translation.
Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 26 citations in OpenAlex.
- Foxg1 and companions: Not only transcription factors.Neural regeneration research · 2026Article
- RNA Binding Properties of SOX Family Members.Cells · 2024Article
- The p53 endoplasmic reticulum stress-response pathway evolved in humans but not in mice via PERK-regulated p53 mRNA structures.Cell death and differentiation · 2023Article
- Biological roles of the RNA mExperimental & molecular medicine · 2022Review
- DNA and RNA Binding Proteins: From Motifs to Roles in Cancer.International journal of molecular sciences · 2022Review
- The Mettl3 epitranscriptomic writer amplifies p53 stress responses.Molecular cell · 2022Article
- The Therapeutic Potential of the Restoration of the p53 Protein Family Members in theInternational journal of molecular sciences · 2022Review
- Preferential translation of p53 target genes.RNA biology · 2022Article
- Review
- MDM4 alternative splicing and implication in MDM4 targeted cancer therapies.American journal of cancer research · 2021Review
- c-Myc inactivation of p53 through the pan-cancer lncRNA MILIP drives cancer pathogenesis.Nature communications · 2020Article
- Review
- Review
- Shaping the regulation of the p53 mRNA tumour suppressor: the co-evolution of genetic signatures.BMC cancer · 2019Review
- A single synonymous mutation determines the phosphorylation and stability of the nascent protein.Journal of molecular cell biology · 2019Article
- The long and the short of it: the MDM4 tail so far.Journal of molecular cell biology · 2019Review
- 40 Years of Research Put p53 in Translation.Cancers · 2018Review
- p53-mediated suppression of BiP triggers BIK-induced apoptosis during prolonged endoplasmic reticulum stress.Cell death and differentiation · 2017Article
- Transcription factors SOHLH1 and SOHLH2 coordinate oocyte differentiation without affecting meiosis I.The Journal of clinical investigation · 2017Article
Corrections and comments
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Authors and funding
10 authors at 6 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MDMX and MDM2 are two nonredundant essential regulators of p53 tumor suppressor activity. MDM2 controls p53 expression levels, whereas MDMX is predominantly a negative regulator of p53 trans-activity. The feedback loops between MDM2 and p53 are well studied and involve both negative and positive regulation on transcriptional, translational and post-translational levels but little is known on the regulatory pathways between p53 and MDMX. Here we show that overexpression of p53 suppresses mdmx mRNA translation in vitro and in cell-based assays. The core domain of p53 binds the 5' untranslated region (UTR) of the mdmx mRNA in a zinc-dependent manner that together with a trans-suppression domain located in p53 N-terminus controls MDMX synthesis. This interaction can be visualized in the nuclear and cytoplasmic compartment. Fusion of the mdmx 5'UTR to the ovalbumin open reading frame leads to suppression of ovalbumin synthesis. Interestingly, the transcription inactive p53 mutant R273H has a different RNA-binding profile compared with the wild-type p53 and differentiates the synthesis of MDMX isoforms. This study describes p53 as a trans-suppressor of the mdmx mRNA and adds a further level to the intricate feedback system that exist between p53 and its key regulatory factors and emphasizes the important role of mRNA translation control in regulating protein expression in the p53 pathway.
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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.