The DOI matches its Crossref record; 94 of the 95 references it cites were found in a registry or an index.
MDMX: from bench to bedside
Open accessAbstract
The tumor suppressor protein p53 is negatively regulated by Mdm2, a ubiquitin ligase protein that targets p53 for degradation. Mdmx (also known as Mdm4) is a relative of Mdm2 that was identified on the basis of its ability to physically interact with p53. An increasing body of evidence, including recent genetic studies, suggests that Mdmx also acts as a key negative regulator of p53. Aberrant expression of MDMX could thus contribute to tumor formation. Indeed, MDMX amplification and/or overexpression occurs in several diverse tumors. Strikingly, recent work identifies MDMX as a specific chemotherapeutic target for treatment of retinoblastoma. Specific MDMX antagonists should therefore be developed as a tool to ensure activation of `dormant' p53 activity in tumors that retain wild-type p53.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“The oncogene Mdmx is overexpressed in many human malignancies, and together with Mdm2, negatively regulates the p53 tumor suppressor.”
From Mdmx promotes genomic instability independent of p53 and Mdm2 (2015) · cites this paper as [25]
In the citing paper
“While Mdmx negatively regulates p53, it does so through inhibiting p53 transcriptional activity rather than promoting p53 degradation through ubiquitination, as is the case for Mdm2.24,25”
From Mdmx promotes genomic instability independent of p53 and Mdm2 (2015) · cites this paper as [25]
In the citing paper
“While it is clear Mdmx regulates p53,25,43”
From Mdmx promotes genomic instability independent of p53 and Mdm2 (2015) · cites this paper as [25]
In the citing paper
“it is known that Mdmx can regulate p53 independent of Mdm2.25,43”
From Mdmx promotes genomic instability independent of p53 and Mdm2 (2015) · cites this paper as [25]
In the citing paper
“Genetic analyses demonstrate that the major cellular target (at least in development) for both Mdm2 and Mdmx is p53 [49].”
From The p53 orchestra: Mdm2 and Mdmx set the tone (2010) · cites this paper as [49]
In the citing paper
“In vitro and in vivo studies show that damage-induced modifications of Mdm2 and Mdmx lead to their destabilization and degradation, reducing their ability to antagonize p53 [49,50].”
From The p53 orchestra: Mdm2 and Mdmx set the tone (2010) · cites this paper as [49]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
WAF1, a potential mediator of p53 tumor suppression
El-Deiry, W. S., Tokino, T., Velculescu, V. E., Levy, D. B., Parsons, R., Trent, J. M., Lin, D., Mercer, W. E., Kinzler, K. W., & Vogelstein, B. (1993) · Cell · doi:10.1016/0092-8674(93)90500-p · Cited by 8,321
In Vivo Activation of the p53 Pathway by Small-Molecule Antagonists of MDM2
Vassilev, L. T., Vu, B. T., Graves, B., Carvajal, D., Podlaski, F., Filipovic, Z., Kong, N., Kammlott, U., Lukacs, C., Klein, C., et al. (2004) · Science · doi:10.1126/science.1092472 · Cited by 4,661
Mdm2 promotes the rapid degradation of p53
Haupt, Y., Maya, R., Kazaz, A., & Oren, M. (1997) · Nature · doi:10.1038/387296a0 · Cited by 4,506
Regulation of p53 stability by Mdm2
Kubbutat, M. H. G., Jones, S. N., & Vousden, K. H. (1997) · Nature · doi:10.1038/387299a0 · Cited by 3,312 · cited 1×
“Mdm2 is a RING-finger-containing protein that acts as an E3 ligase, which is essential for ubiquitylation and subsequent degradation of p53 (Haupt et al., 1997; Kubbutat et al., 1997).”
BackgroundLive or let die: the cell's response to p53
Vousden, K. H., & Lü, X. (2002) · Nature reviews. Cancer · doi:10.1038/nrc864 · Cited by 3,231
Momand, J., Zambetti, G. P., Olson, D. C., George, D., & Levine, A. J. (1992) · Cell · doi:10.1016/0092-8674(92)90644-r · Cited by 3,113
Amplification of a gene encoding a p53-associated protein in human sarcomas
Oliner, J. D., Kinzler, K. W., Meltzer, P. S., George, D. L., & Vogelstein, B. (1992) · Nature · doi:10.1038/358080a0 · Cited by 1,949
The p53-mdm-2 autoregulatory feedback loop.
Wu, X., Bayle, J. H., Olson, D., & Levine, A. J. (1993) · Genes & Development · doi:10.1101/gad.7.7a.1126 · Cited by 1,801
The RB and p53 pathways in cancer
Sherr, C. J., & McCormick, F. (2002) · Cancer Cell · doi:10.1016/s1535-6108(02)00102-2 · Cited by 1,690
Rescue of early embryonic lethality in mdm2-deficient mice by deletion of p53
de Oca Luna, R. M., Wagner, D. S., & Lozano, G. (1995) · Nature · doi:10.1038/378203a0 · Cited by 1,420 · cited 1×
“Mdm2-deficient mice die very early in development prior to implantation, whereas mice lacking both p53 and Mdm2 are viable and indistinguishable from mice lacking only p53 (Montes de Oca Luna et al., 1995; Jones et al., 1995).”
Background
Flagged first, then by citations
1 of the 95 references couldn’t be matched to a known paper.
Cited by
Sorted by citations
Blinded by the Light: The Growing Complexity of p53
Vousden, K. H., & Prives, C. (2009) · Cell · doi:10.1016/j.cell.2009.04.037 · Cited by 3,163
Mutant p53: one name, many proteinsPreprint
Freed-Pastor, W. A., & Prives, C. L. (2012) · Genes & Development · doi:10.1101/gad.190678.112 · Cited by 1,290
Linking the p53 tumour suppressor pathway to somatic cell reprogramming
Kawamura, T., Suzuki, J., Wang, Y. V., Menendez, S., Morera, L. B., Raya, A., Wahl, G. M., & Belmonte, J. C. I. (2009) · Nature · doi:10.1038/nature08311 · Cited by 1,115
Chang, Y. S., Graves, B. J., Guerlavais, V., Tovar, C., Packman, K. E., To, K.-H., Olson, K. A., Kesavan, K. P., Gangurde, P., Mukherjee, A., et al. (2013) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1303002110 · Cited by 681
p53 post-translational modification: deregulated in tumorigenesis
Dai, C., & Gu, W. J. (2010) · Trends in Molecular Medicine · doi:10.1016/j.molmed.2010.09.002 · Cited by 545
Metadata
- Authors
- Marine, J.-C. W., Dyer, M. A., & Jochemsen, A. G.
- Affiliations
- Vlaams Instituut voor Biotechnologie (BE)
- St. Jude Children's Research Hospital (US)
- Leiden University Medical Center (NL)
- Corresponding author
- Marine, Jean-Christophe W.
- Venue
- Journal of Cell Science
- Publisher
- The Company of Biologists
- Published
- 2007-02-01
- Volume
- 120
- Issue
- 3
- Pages
- 371-378
- ISSN
- 0021-9533 (ISSN-L)
- 1477-9137
- OpenAlex
- W2141224144
- Cited by
- 228
- References
- 95
- Citations by year
- 2026: 2 · 2025: 1 · 2024: 5 · 2023: 3 · 2022: 3 · 2021: 8 · 2020: 10 · 2019: 2 · 2018: 8 · 2017: 6 · 2016: 12 · 2015: 10 · 2014: 18 · 2013: 14 · 2012: 21
- FWCI
- 2.78
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Cell Science (publishedVersion)
- PubMed (publishedVersion)
- Ghent University Academic Bibliography (Ghent University) (submittedVersion, other-oa)
- Topics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ubiquitin and proteasome pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Heat shock proteins research
- Keywords
- MDMX, MDM2, p53, tumor suppressor regulation, ubiquitin ligase, retinoblastoma, chemotherapeutic target, wild-type p53
- MeSH terms
- Animals, Humans, Models, Biological, Neoplasms, Nuclear Proteins, Proto-Oncogene Proteins, Gene Expression Regulation, Neoplastic, Tumor Suppressor Protein p53, Cell Cycle Proteins
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
