The DOI matches its Crossref record; 57 of the 71 references it cites were found in a registry or an index.
DNA damage induces phosphorylation of the amino terminus of p53
Open accessAbstract
Data are presented demonstrating that DNA damage leads to specific post-translational modifications of p53 protein. Using two-dimensional peptide mapping of in vivo radiolabeled p53 tryptic phosphopeptides, recombinant truncated p53 protein, and synthetic p53 tryptic peptides, a unique p53 phosphopeptide was identified after exposure of ML-1 cells to ionizing irradiation. This peptide represents the first 24 amino acids of p53 and contains three phosphorylated serine residues. A specific p53 phosphopeptide antibody identified serine-15 as one of the two serines in p53 that becomes phosphorylated following DNA damage induced by either ionizing irradiation (IR) or ultraviolet (UV) irradiation in multiple cell types. IR-induced phosphorylation of p53 does not affect the kinetics of p53 binding to or dissociating from DNA as assessed by electrophoretic mobility-shift assays. However, p53 phosphorylation induced by DNA damage correlates with enhanced transcription of downstream p53 target genes. Low levels of phosphoserine-15 p53 are detectable within 6 hr after IR in AT cells, whereas lymphoblasts from normal individuals exhibit this modification within 1 hr. In contrast, phosphorylation of p53 on serine-15 is similar in normal and AT cells after UV irradiation. Our results indicate that p53 is phosphorylated in response to DNA damage, that this de novo phosphorylation may be involved in the subsequent induction and activation of p53, and that although ATM affects the kinetics of p53 phosphorylation after IR, it is not absolutely required for phosphorylation of p53 on serine-15.
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“Doxorubicin treatment of early passage tumor cell lines revealed that five of five early generation mTerc Ink4a / Arf -/ -tumors maintained intact p53 response evidenced by p53 Ser-18 phosphorylation (37, 38) and associated induction of p21 CIP1 .”
From Ink4a / Arf tumor suppressor does not modulate the degenerative conditions or tumor spectrum of the telomerase-deficient mouse (2007) · cites this paper as [38]
Experimental — accuracy not yet measuredIn the citing paper
“Induction of double strand breaks in DNA by ionizing radiation or genotoxic chemotherapy leads to the rapid stabilization of p53 through phosphorylation of its N terminus (Shieh et al. 1997; Siliciano et al. 1997”
From p53 Deficiency Rescues the Adverse Effects of Telomere Loss and Cooperates with Telomere Dysfunction to Accelerate Carcinogenesis (1999) · cites this paper as Siliciano et al. 1997
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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
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
Participation of p53 protein in the cellular response to DNA damage.
Kastan, M. B., Onyekwere, O. C., Sidransky, D., Vogelstein, B., & Craig, R. W. (1991) · PubMed · Cited by 3,761
Self-citationRegulation 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×
“It has been demonstrated recently that the mechanism for this inhibition involves binding Mdm2 to p53 and targeting p53 for rapid degradation (Haupt et al. 1997; Kubbutat et al. 1997).”
BackgroundDérijard, B., Hibi, M., Wu, I.-H., Barrett, T., Su, B., Deng, T., Karin, M., & Davis, R. J. (1994) · Cell · doi:10.1016/0092-8674(94)90380-8 · Cited by 3,188
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Self-citationA Single Ataxia Telangiectasia Gene with a Product Similar to PI-3 Kinase
Savitsky, K., Bar-Shira, A., Gilad, S., Rotman, G., Ziv, Y., Vanagaite, L., Tagle, D. A., Smith, S., Uziel, T., Sfez, S., et al. (1995) · Science · doi:10.1126/science.7792600 · Cited by 2,785
Hartwell, L. H., & Kastan, M. B. (1994) · Science · doi:10.1126/science.7997877 · Cited by 2,539
Self-citationp53: puzzle and paradigm.Preprint
Ko, L. J., & Prives, C. L. (1996) · Genes & Development · doi:10.1101/gad.10.9.1054 · Cited by 2,346
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Regulation of the M-phase of cell cycle by CDK1, PP2A and CDC6
Dika, M. E. (2013) · doi:10.70675/55071395zf6b6z48d0zaae5z659fb6a2e630 · Cited by 1
The roles of FANCD2 in the maintenance of common fragile site stability
Fernandes, P. (2018) · theses.fr (ABES) · doi:10.70675/0d35c80ezf356z4cabza1edz594f25dbe717
Contribution à l'étude phytochimique et à la valorisation biologique du latex de Hura crepitans L.
Trinel, M. (2018) · theses.fr (ABES) · doi:10.70675/2c6d2e75zd74fz482az9392z0f6184f2d7c2
Rôle de la protéine ATM dans la régulation des gènes de latences du virus d’Epstein-Barr (EBV)
Tatfi, M. (2019) · theses.fr (ABES) · doi:10.70675/3b654584z65a5z4cbbzbbc2zde0a759cf1ab
Zhang, F., Liao, Y., Yang, P., & Guo, J. (2026) · Frontiers in Immunology · doi:10.3389/fimmu.2026.1850084
Therapeutic drugs in cancer and resistance.
Martin, A. P. (2009) · VCU Scholars Compass (Virginia Commonwealth University) · doi:10.25772/0158-v633
Dey, H. T. (2012) · Digital Archive @ GSU · doi:10.57709/3489823
Molekularer Mechanismus der Stickstoffmonoxid-vermittelten Akkumulation des Tumorsuppressors p53
Schneiderhan‐Marra, N. (2002)
Doctorate Program in Molecular Oncology and Endocrinology
Hoyos, J. M. (2006)
The interaction of CtIP with DNA damage response proteins
Abramowiçz, I. (2010) · University of Birmingham Institutional Research Archive (University of Birmingham)
Metadata
- Authors
- Siliciano, J. D., Canman, C. E., Taya, Y., Sakaguchi, K., Appella, E., & Kastan, M. B.
- Affiliations
- National Institutes of Health (US)
- Venue
- Genes & Development
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 1997-12-15
- Volume
- 11
- Issue
- 24
- Pages
- 3471-3481
- ISSN
- 0890-9369 (ISSN-L)
- 1549-5477
- PMC
- PMC316806
- OpenAlex
- W2149013144
- Cited by
- 818
- References
- 71
- Citations by year
- 2026: 4 · 2025: 3 · 2024: 5 · 2023: 7 · 2022: 10 · 2021: 10 · 2020: 12 · 2019: 14 · 2018: 12 · 2017: 18 · 2016: 22 · 2015: 17 · 2014: 24 · 2013: 21 · 2012: 27
- Type
- posted content
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Genes & Development (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- HighWire Press Open Archive (submittedVersion)
- Funders
- American Society of Hematology
- National Institutes of Health (ES05777)
- National Cancer Institute (CA71387, R01CA071387)
- National Institute of Environmental Health Sciences (R01ES005777, R37ES005777, ES05777)
- 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 › Protein Kinase Regulation and GTPase Signaling
- Keywords
- p53, DNA damage response, ionizing radiation, UV irradiation, post-translational modification, ATM kinase, lymphoblasts
- MeSH terms
- Ataxia Telangiectasia, Binding Sites, Cells, Cultured, DNA, DNA Damage, Electrophoresis, Humans, Lymphocytes, Nuclear Proteins, Peptide Fragments, Phosphorylation, Protein Processing, Post-Translational, Proto-Oncogene Proteins, Serine, Ultraviolet Rays, Signal Transduction, Tumor Suppressor Protein p53, Cyclins, Cyclin-Dependent Kinase Inhibitor p21, Proto-Oncogene Proteins c-mdm2
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