ArticleMolecular cancer research : MCR2016
p53 Activity Dominates That of p73 upon Mdm4 Loss in Development and Tumorigenesis.
Article in Molecular cancer research : MCR, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed, 6 citations in OpenAlex.
- Structural diversity of p63 and p73 isoforms.Cell death and differentiation · 2022Review
- The long and the short of it: the MDM4 tail so far.Journal of molecular cell biology · 2019Review
- Article
- Anatomy of Mdm2 and Mdm4 in evolution.Journal of molecular cell biology · 2017Review
- p53 pathway is involved in cell competition during mouse embryogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Zinc and zinc-containing biomolecules in childhood brain tumors.Journal of molecular medicine (Berlin, Germany) · 2016Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 2 countries.
Funding
Abstract
unlabelledMdm4 negatively regulates the p53 tumor suppressor. Mdm4 loss in mice leads to an embryonic lethal phenotype that is p53-dependent. Biochemical studies indicate that Mdm4 also binds p73, a member of the p53 family, with higher affinity than p53. In this study, the significance of the Mdm4 and p73 interaction in vivo during embryogenesis and tumorigenesis was examined. The data revealed that p73 loss did not rescue either the early Mdm4-deficient embryonic lethality or the runted phenotype of Mdm4(Δ2/Δ2) p53(+/-) embryos. Furthermore, studies in the developing central nervous system wherein both genes have prominent roles indicated that loss of p73 also did not rescue the Mdm4-null brain phenotype as did p53 loss. This p53 dependency occurred despite evidence for p73-specific transcriptional activity. In tumor studies, the combination of Mdm4 overexpression and p73 loss did not alter survival of mice or the tumor spectrum as compared with Mdm4 overexpression alone. In summary, these data demonstrate that the Mdm4-p73 axis cannot override the dominant role of p53 in development and tumorigenesis. IMPLICATIONS: Genetic characterization of the Mdm4 and p73 interaction during development and tumorigenesis suggests new insight into the role of p53 family members, which may influence treatment options for patients.
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Registered trials
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