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Enhanced Phosphorylation of p53 by ATM in Response to DNA Damage
Abstract
The ATM protein, encoded by the gene responsible for the human genetic disorder ataxia telangiectasia (A-T), regulates several cellular responses to DNA breaks. ATM shares a phosphoinositide 3-kinase–related domain with several proteins, some of them protein kinases. A wortmannin-sensitive protein kinase activity was associated with endogenous or recombinant ATM and was abolished by structural ATM mutations. In vitro substrates included the translation repressor PHAS-I and the p53 protein. ATM phosphorylated p53 in vitro on a single residue, serine-15, which is phosphorylated in vivo in response to DNA damage. This activity was markedly enhanced within minutes after treatment of cells with a radiomimetic drug; the total amount of ATM remained unchanged. Various damage-induced responses may be activated by enhancement of the protein kinase activity of ATM.
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In the citing paper
“ATM phosphorylates p53 on serine 15, enhancing its transcriptional activity (Banin et al, 1998).”
From ATM and Chk2-dependent phosphorylation of MDMX contribute to p53 activation after DNA damage (2005) · cites this paper as Banin et al, 1998
In the citing paper
“ATM also activates Chk2, which in turn phosphorylates p53 on serine 20 and inhibits MDM2 binding (Shieh et al, 1997;Banin et al, 1998;Chehab et al, 2000;Shieh et al, 2000).”
From ATM and Chk2-dependent phosphorylation of MDMX contribute to p53 activation after DNA damage (2005) · cites this paper as Banin et al, 1998
In the citing paper
“Several landmark studies showed that DNA double strand breaks induce phosphorylation of p53 S15 by DNA-PK and ATM (Mayo et al, 1997;Shieh et al, 1997;Banin et al, 1998;Prives and Hall, 1999).”
From ATM activates p53 by regulating MDM2 oligomerization and E3 processivity (2009) · cites this paper as Banin et al, 1998
In the citing paper
“ATM also activates Chk2, which in turn phosphorylates p53 on S20, which is a part of the MDM2-binding site (Shieh et al, 1997(Shieh et al, , 2000;;Banin et al, 1998;Chehab et al, 2000).”
From ATM activates p53 by regulating MDM2 oligomerization and E3 processivity (2009) · cites this paper as Banin et al, 1998
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Metadata
- Authors
- Banin, S., Moyal, L., Shieh, S.-Y., Taya, Y., Anderson, C. W., Chessa, L., Smorodinsky, N. I., Prives, C., Reiss, Y., Shiloh, Y., & Ziv, Y.
- Affiliations
- Tel Aviv University (IL)
- Corresponding author
- Shiloh, Y.
- Venue
- Science
- Published
- 1998-09-11
- Volume
- 281
- Issue
- 5383
- Pages
- 1674-1677
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- OpenAlex
- W4212962560
- Cited by
- 1,797
- References
- 29
- Citations by year
- 2026: 26 · 2025: 27 · 2024: 24 · 2023: 31 · 2022: 41 · 2021: 47 · 2020: 47 · 2019: 44 · 2018: 44 · 2017: 51 · 2016: 43 · 2015: 49 · 2014: 62 · 2013: 65 · 2012: 57
- FWCI
- 43.26
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Science (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of Neurological Disorders and Stroke (R01NS031763, NS 31763)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Keywords
- ATM kinase, p53 phosphorylation, DNA damage response, ataxia telangiectasia, protein kinase activity, radiomimetic drugs
- MeSH terms
- Wortmannin, Androstadienes, Ataxia Telangiectasia, Carrier Proteins, Cell Line, DNA Damage, DNA-Binding Proteins, Enzyme Inhibitors, Humans, Mutation, Zinostatin, Phosphoproteins, Phosphorylation, Protein Kinases, Proteins, Recombinant Proteins, Tumor Cells, Cultured, Tumor Suppressor Protein p53, Protein Serine-Threonine Kinases, Cell Cycle Proteins, Phosphatidylinositol 3-Kinases, Tumor Suppressor Proteins, Protein Kinase Inhibitors, Adaptor Proteins, Signal Transducing, Ataxia Telangiectasia Mutated Proteins
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