Cited by 1,046DNA Repair MechanismsCancer-related Molecular PathwaysProtein Kinase Regulation and GTPase Signaling

A role for ATR in the DNA damage-induced phosphorylation of p53

Open access
Tibbetts, R. S., Brumbaugh, K. M., Williams, J. M., Sarkaria, J. N., Cliby, W. A., Shieh, S.-Y., Taya, Y., Prives, C. +1 more·1999·Genes & Development

Abstract

Phosphorylation at Ser-15 may be a critical event in the up-regulation and functional activation of p53 during cellular stress. In this report we provide evidence that the ATM-Rad3-related protein ATR regulates phosphorylation of Ser-15 in DNA-damaged cells. Overexpression of catalytically inactive ATR (ATRki) in human fibroblasts inhibited Ser-15 phosphorylation in response to gamma-irradiation and UV light. In gamma-irradiated cells, ATRki expression selectively interfered with late-phase Ser-15 phosphorylation, whereas ATRki blocked UV-induced Ser-15 phosphorylation in a time-independent manner. ATR phosphorylated p53 at Ser-15 and Ser-37 in vitro, suggesting that p53 is a target for phosphorylation by ATR in DNA-damaged cells.

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.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1101/gad.13.2.152

Cites

35 of 35 references verified0 citation errors · 0 not checkable

Statistics

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.

A few free checks a day · papers already verified open instantly · results are public

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 human cells, ATM is activated by double-strand breaks such as those caused by ionizing radiation, while ATR is activated by RPA-coated ssDNA and mainly triggers checkpoint activation after UV irradiation or replication stress.

    “In fact, ATM (Ataxia Telangiectasia Mutated) is activated by double-strand breaks (DSBs) caused, for example, by ionizing radiation (IR), while ATR (ATM and Rad3-Related) is activated by ssDNA coated with the RPA heterotrimeric complex and mainly triggers checkpoint activation after UV irradiation or replication-stress.”

    From Mind the gap: keeping UV lesions in check (2011) · cites this paper as [38]

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Authors
Tibbetts, R. S., Brumbaugh, K. M., Williams, J. M., Sarkaria, J. N., Cliby, W. A., Shieh, S.-Y., Taya, Y., Prives, C., & Abraham, R. T.
Affiliations
  • Duke University (US)
  • Mayo Clinic (US)
Venue
Genes & Development
Published
1999-01-15
Volume
13
Issue
2
Pages
152-157
ISSN
0890-9369 (ISSN-L)
OpenAlex
W2155640249
Cited by
1,046
References
35
Citations by year
2026: 12 · 2025: 10 · 2024: 19 · 2023: 20 · 2022: 21 · 2021: 30 · 2020: 21 · 2019: 16 · 2018: 25 · 2017: 30 · 2016: 23 · 2015: 37 · 2014: 39 · 2013: 37 · 2012: 34
Type
posted content
Language
en
Open access
Locations
  • Genes & Development (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (CA58316)
  • National Cancer Institute (R37CA058316, CA76193, U01CA052995, CA-52995, R01CA076193, U19CA052995, T32CA009441, R01CA058316, CA 58316)
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
ATR kinase, p53, DNA damage response, gamma irradiation, UV-induced DNA damage, p53 activation
MeSH terms
DNA Damage, DNA-Binding Proteins, Doxycycline, Fibroblasts, Gamma Rays, Humans, Mutation, Phosphorylation, Precipitin Tests, Proteins, Recombinant Fusion Proteins, Serine, Time Factors, Transfection, Tumor Cells, Cultured, Ultraviolet Rays, Tumor Suppressor Protein p53, Protein Serine-Threonine Kinases, Cell Cycle Proteins, K562 Cells, Tumor Suppressor Proteins, 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