The DOI matches its Crossref record; 46 of the 48 references it cites were found in a registry or an index.
ATM Phosphorylation of Mdm2 Ser394 Regulates the Amplitude and Duration of the DNA Damage Response in Mice
Open accessAbstract
DNA damage induced by ionizing radiation activates the ATM kinase, which subsequently stabilizes and activates the p53 tumor suppressor protein. Although phosphorylation of p53 by ATM was found previously to modulate p53 levels and transcriptional activities in vivo, it does not appear to be a major regulator of p53 stability. We have utilized mice bearing altered Mdm2 alleles to demonstrate that ATM phosphorylation of Mdm2 serine 394 is required for robust p53 stabilization and activation after DNA damage. In addition, we demonstrate that dephosphorylation of Mdm2 Ser394 regulates attenuation of the p53-mediated response to DNA damage. Therefore, the phosphorylation status of Mdm2 Ser394 governs p53 protein levels and functions in cells undergoing DNA damage.
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
“By contrast, the mutation of Ser394 to alanine (Ser394Ala) in mouse MDM2 in vivo removes an ATM phosphorylation site, engenders radioresistance and increases the rate of spontaneous tumorigenesis to that observed in Trp53-hemizygous animals47.”
From MDM2, MDMX and p53 in oncogenesis and cancer therapy (2013) · cites this paper as [47]
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
p53 Mutations in Human Cancers
Hollstein, M., Sidransky, D., Vogelstein, B., & Harris, C. C. (1991) · Science · doi:10.1126/science.1905840 · Cited by 8,018
Lane, D. P. (1992) · Nature · doi:10.1038/358015a0 · Cited by 5,138
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
Mice deficient for p53 are developmentally normal but susceptible to spontaneous tumours
Donehower, L. A., Harvey, M., Slagle, B. L., McArthur, M. J., Montgomery, C. A., Butel, J. S., & Bradley, A. (1992) · Nature · doi:10.1038/356215a0 · Cited by 4,649
Live 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
DNA damage-induced phosphorylation of p53 alleviates inhibition by MDM2
Shieh, S.-Y., Ikeda, M., Taya, Y., & Prives, C. (1997) · Cell · doi:10.1016/s0092-8674(00)80416-x · Cited by 2,100
Tumor spectrum analysis in p53-mutant mice
Jacks, T., Remington, L., Williams, B. O., Schmitt, E. M., Halachmi, S., Bronson, R. T., & Weinberg, R. A. (1994) · Current Biology · doi:10.1016/s0960-9822(00)00002-6 · Cited by 2,051
Oncoprotein MDM2 is a ubiquitin ligase E3 for tumor suppressor p53
Honda, R., Tanaka, H., & Yasuda, H. (1997) · FEBS Letters · doi:10.1016/s0014-5793(97)01480-4 · Cited by 1,951
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
Flagged first, then by citations
2 of the 48 references couldn’t be matched to a known paper.
Cited by
Sorted by citations
Items 101–103 of 103
Ohbayashi, I., Hsu, T.-Y., Faustine, J., Chiang, P.-C., Miyashita, T., Yonekura, T., Iwamoto, A., Furutani, M., & Sugiyama, M. (2026) · Plant and Cell Physiology · doi:10.1093/pcp/pcag096
MDM2/X mediates reduced apoptosis in the plateau zokor: a mechanism of high-altitude adaptation
Zhang, M., Li, Y., Lin, H., Yu, T., Xia, F., Chatoo, M., Li, K., Yu, H., Nevo, E., Du, J., et al. (2026) · Journal of Zhejiang University SCIENCE B · doi:10.1631/jzus.b2500281
Metadata
- Authors
- Gannon, H. S., Woda, B. A., & Jones, S. N.
- Affiliations
- University of Massachusetts Chan Medical School (US)
- Corresponding author
- Jones, Stephen N.
- ORCID
- Gannon, Hugh S.
- Venue
- Cancer Cell
- Publisher
- Elsevier BV
- Published
- 2012-05
- Volume
- 21
- Issue
- 5
- Pages
- 668-679
- ISSN
- 1535-6108 (ISSN-L)
- PMC
- PMC3360886
- OpenAlex
- W2117932700
- Cited by
- 105
- References
- 48
- Citations by year
- 2026: 7 · 2025: 1 · 2024: 5 · 2023: 3 · 2022: 4 · 2021: 9 · 2020: 7 · 2019: 9 · 2018: 10 · 2017: 5 · 2016: 13 · 2015: 4 · 2014: 11 · 2013: 10 · 2012: 6
- FWCI
- 4.90
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (vor, 442 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Cancer Cell (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- The Journal of the American Medical Association (JAMA) Network (American Medical Association) (submittedVersion)
- Funders
- National Institute of Diabetes and Digestive and Kidney Diseases (CA077735)
- National Cancer Institute
- Topics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Heat shock proteins research
- Keywords
- ATM kinase, MDM2, p53 stabilization, DNA damage response, ionizing radiation, p53 activation
- MeSH terms
- Animals, DNA Damage, DNA-Binding Proteins, Enzyme Activation, Intestine, Small, Mice, Inbred C57BL, Phosphorylation, Radiation Tolerance, Serine, Spleen, Thymus Gland, Time Factors, Tumor Suppressor Protein p53, Apoptosis, Protein Serine-Threonine Kinases, Cell Cycle Proteins, Mutation, Missense, Tumor Suppressor Proteins, Mice, Proto-Oncogene Proteins c-mdm2, Protein Stability, Mice, 129 Strain, Ataxia Telangiectasia Mutated 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
