ArticleMolecular and cellular biology2010
Widespread overexpression of epitope-tagged Mdm4 does not accelerate tumor formation in vivo.
Article in Molecular and cellular biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
26 citing papers in PubMed, 35 citations in OpenAlex.
- MDM4 at the Crossroads: Beyond p53 and MDM2.Cancers · 2026Review
- Review
- Mechanisms of TP53 Pathway Inactivation in Embryonic and Somatic Cells-Relevance for Understanding (Germ Cell) Tumorigenesis.International journal of molecular sciences · 2021Review
- Case Report:Frontiers in endocrinology · 2021Article
- Aberrant expression and regulatory network of splicing factor-SRSF3 in tumors.Journal of Cancer · 2020Review
- Regulation of the p53 Family Proteins by the Ubiquitin Proteasomal Pathway.International journal of molecular sciences · 2019Review
- The long and the short of it: the MDM4 tail so far.Journal of molecular cell biology · 2019Review
- Context-dependent roles of MDMX (MDM4) and MDM2 in breast cancer proliferation and circulating tumor cells.Breast cancer research : BCR · 2019Article
- Targeting MDM4 Splicing in Cancers.Genes · 2017Review
- Molecular Mechanisms of p53 Deregulation in Cancer: An Overview in Multiple Myeloma.International journal of molecular sciences · 2016Review
- Attenuating the p53 Pathway in Human Cancers: Many Means to the Same End.Cold Spring Harbor perspectives in medicine · 2016Review
- MDMX (MDM4), a Promising Target for p53 Reactivation Therapy and Beyond.Cold Spring Harbor perspectives in medicine · 2016Review
- The Roles of MDM2 and MDMX in Cancer.Annual review of pathology · 2016Review
- Antisense oligonucleotide-mediated MDM4 exon 6 skipping impairs tumor growth.The Journal of clinical investigation · 2016Article
- Article
- The Mdm network and its regulation of p53 activities: a rheostat of cancer risk.Human mutation · 2014Review
- Mouse models of Mdm2 and Mdm4 and their clinical implications.Chinese journal of cancer · 2013Review
- MDM2, MDMX and p53 in oncogenesis and cancer therapy.Nature reviews. Cancer · 2013Review
- Functional analysis and consequences of Mdm2 E3 ligase inhibition in human tumor cells.Oncogene · 2012Article
- MDM4 is a key therapeutic target in cutaneous melanoma.Nature medicine · 2012Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Mdm2 and Mdm4 are critical negative regulators of p53. A large body of evidence indicates that elevated expression of either Mdm2 or Mdm4 may favor tumor formation by inhibiting p53 tumor suppression function. To explore this possibility in vivo, we generated conditional Mdm2 and Mdm4 transgenic mice. We show that although both transgenes are designed to be expressed ubiquitously and at comparable levels, only the Mdm4 transgenic protein is produced at high levels in vivo. In contrast, exogenous Mdm2 is constitutively degraded in a proteasome-dependent manner, indicating that cells are equipped with efficient mechanisms that prevent Mdm2 accumulation in vivo. Mice that are homozygous for the Mdm4 transgene die during embryogenesis owing to severe vascular maturation defects. Importantly, this lethality is not rescued on a p53-null background, indicating that high levels of Mdm4 impact on a pathway(s) other than p53 that controls vascular and embryonic development. Mice expressing a single copy of the Mdm4 transgene are viable and, surprisingly, are not prone to spontaneous, radiation-induced or Eμ-myc-induced tumor formation. The findings have clear implications for cancer etiology as well as for cancer therapy.
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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.