ArticleCancer cell2009
Increased radioresistance and accelerated B cell lymphomas in mice with Mdmx mutations that prevent modifications by DNA-damage-activated kinases.
Article in Cancer cell, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
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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
60 citing papers in PubMed, 75 citations in OpenAlex.
- The Enigmatic Tumor Suppressor p53 Biomolecule: Its Role and Prognostic and Predictive Values in Cancer Therapy and Precision Medicine.Biomolecules · 2026Review
- Dual-stress-responsive-pathways prevent HCC initiation via p53 suppression of MTHFD1L-RNA mResearch square · 2026Article
- MDMX reprograms glycolysis of hepatocellular carcinoma via 14-3-3γ/FOXO1.Cell death discovery · 2025Article
- Small-molecule MMRi36 induces apoptosis in p53-mutant lymphomas by targeting MDM2/MDM4/XIAP for degradation.Frontiers in oncology · 2024Article
- FDG PET/CT parameters and correlations with tumor-absorbed doses in a phase 1 trial ofEuropean journal of nuclear medicine and molecular imaging · 2021Article
- Role of Dietary Antioxidants in p53-Mediated Cancer Chemoprevention and Tumor Suppression.Oxidative medicine and cellular longevity · 2021Review
- RBM10, a New Regulator of p53.Cells · 2020Review
- The long and the short of it: the MDM4 tail so far.Journal of molecular cell biology · 2019Review
- SRSF1 modulates PTPMT1 alternative splicing to regulate lung cancer cell radioresistance.EBioMedicine · 2018Article
- Review
- Peli1 Modulates the Subcellular Localization and Activity of Mdmx.Cancer research · 2018Article
- MDMX acidic domain inhibits p53 DNA binding in vivo and regulates tumorigenesis.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Article
- Monitoring p53 by MDM2 and MDMX is required for endocrine pancreas development and function in a spatio-temporal manner.Developmental biology · 2017Article
- Negative auto-regulators trap p53 in their web.Journal of molecular cell biology · 2017Review
- Mouse modelling of the MDM2/MDMX-p53 signalling axis.Journal of molecular cell biology · 2017Review
- Intra molecular interactions in the regulation of p53 pathway.Translational cancer research · 2016Article
- Regulation of the Mdm2-p53 signaling axis in the DNA damage response and tumorigenesis.Translational cancer research · 2016Article
- Mdm2 Phosphorylation Regulates Its Stability and Has Contrasting Effects on Oncogene and Radiation-Induced Tumorigenesis.Cell reports · 2016Article
- The importance of p53 pathway genetics in inherited and somatic cancer genomes.Nature reviews. Cancer · 2016Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Mdmx is a critical negative regulator of the p53 pathway that is stoichiometrically limiting in some tissues. Posttranslational modification and degradation of Mdmx after DNA damage have been proposed to be essential for p53 activation. We tested this model in vivo, where critical stoichiometric relationships are preserved. We generated an Mdmx mutant mouse in which three conserved serines (S341, S367, S402) targeted by DNA-damage-activated kinases were replaced by alanines to investigate whether modifications of these residues are important for Mdmx degradation and p53 activation. The mutant mice were remarkably resistant to radiation, and very susceptible to Myc-induced lymphomagenesis. These data demonstrate that Mdmx downregulation is crucial for effective p53-mediated radiation responses and tumor suppression in vivo.
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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.