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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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Self-citationSakaguchi, K., Saito, S., Higashimoto, Y., Roy, S., Anderson, C. W., & Appella, E. (2000) · Journal of Biological Chemistry · doi:10.1074/jbc.275.13.9278 · Cited by 293
Self-citationMahajan, K. N., Nick McElhinny, S. A., Mitchell, B. S., & Ramsden, D. A. (2002) · Molecular and Cellular Biology · doi:10.1128/mcb.22.14.5194-5202.2002 · Cited by 293
Buschmann, T., Potapova, O., Bar‐Shira, A., Ivanov, V. N., Fuchs, S. Y., Henderson, S. C., Fried, V. A., Minamoto, T., Alarcon-Vargas, D., Pincus, M. R., et al. (2001) · Molecular and Cellular Biology · doi:10.1128/mcb.21.8.2743-2754.2001 · Cited by 292
Effect of Extracellular Signal-regulated Kinase on p53 Accumulation in Response to Cisplatin
Persons, D. L., Yazlovitskaya, E. M., & Pelling, J. C. (2000) · Journal of Biological Chemistry · doi:10.1074/jbc.m004267200 · Cited by 293
A Stapled p53 Helix Overcomes HDMX-Mediated Suppression of p53
Bernal, F., Wade, M. R., Godes, M., Davis, T. N., Whitehead, D. G., Kung, A. L., Wahl, G. M., & Walensky, L. D. (2010) · Cancer Cell · doi:10.1016/j.ccr.2010.10.024 · Cited by 288
The convergence of radiation and immunogenic cell death signaling pathways
Golden, E. B., Pellicciotta, I., Demaria, S., Barcellos‐Hoff, M. H., & Formenti, S. C. (2012) · Frontiers in Oncology · doi:10.3389/fonc.2012.00088 · Cited by 289
Control of the G2/M Transition
Stark, G. R., & Taylor, W. R. (2006) · Molecular Biotechnology · doi:10.1385/mb:32:3:227 · Cited by 282
Hubackova, S., Krejcikova, K., Bartek, J., & Hodny, Z. (2012) · Aging · doi:10.18632/aging.100520 · Cited by 272
ATM: A mediator of multiple responses to genotoxic stress
Rotman, G., & Shiloh, Y. (1999) · Oncogene · doi:10.1038/sj.onc.1203124 · Cited by 273
Maclean, K. H., Dorsey, F. C., Cleveland, J. L., & Kastan, M. B. (2007) · Journal of Clinical Investigation · doi:10.1172/jci33700 · Cited by 281
Self-citationBuschmann, T., Fuchs, S. Y., Lee, C.-G., Pan, Z., & Ronai, Z. A. (2000) · Cell · doi:10.1016/s0092-8674(00)80887-9 · Cited by 267
RetractedSánchez‐Prieto, R., Rojas, J. M., Taya, Y., & Gutkind, J. S. (2000) · PubMed · Cited by 264
Self-citationp300/CBP/p53 interaction and regulation of the p53 response
Grossman, S. R. (2001) · European Journal of Biochemistry · doi:10.1046/j.1432-1327.2001.02226.x · Cited by 275
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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