Cited by 601DNA Repair MechanismsCancer-related Molecular PathwaysProtein Kinase Regulation and GTPase Signaling

ATM and ATR: networking cellular responses to DNA damage

Shiloh, Yosef·2001·Current Opinion in Genetics & Development

Abstract

Maintenance of genome stability depends on the appropriate response to DNA damage. This response is based on complex networks of signaling pathways that activate numerous processes and lead ultimately to damage repair and cellular survival - or apoptosis. The protein kinases ATM and ATR are master controllers of some of these networks, acting either in concert or separately to orchestrate the responses to specific types of DNA damage or stalled replication. Understanding their mode of action is essential to our understanding of how cells cope with genotoxic stress.

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Crossref · 10.1016/s0959-437x(00)00159-3

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Authors
Shiloh, Y.
Affiliations
Tel Aviv University (IL)
Corresponding author
Shiloh, Yosef
Venue
Current Opinion in Genetics & Development
Publisher
Elsevier BV
Published
2001-02
Volume
11
Issue
1
Pages
71-77
ISSN
0959-437X (ISSN-L)
OpenAlex
W2080409413
Cited by
601
References
72
Citations by year
2026: 5 · 2025: 6 · 2024: 8 · 2023: 13 · 2022: 6 · 2021: 16 · 2020: 15 · 2019: 8 · 2018: 10 · 2017: 14 · 2016: 14 · 2015: 14 · 2014: 21 · 2013: 22 · 2012: 21
FWCI
4.66
Type
journal article
Language
en
Open access
closed
Locations
  • Current Opinion in Genetics & Development (publishedVersion)
  • PubMed (publishedVersion)
Funders
Tel Aviv University
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, ATR kinase, DNA damage response, genome stability, DNA repair, signaling pathways, apoptosis, genotoxic stress, checkpoint kinase
MeSH terms
DNA Damage, DNA Repair, DNA-Binding Proteins, Endodeoxyribonucleases, Exodeoxyribonucleases, Fungal Proteins, Humans, Recombination, Genetic, Apoptosis, Protein Serine-Threonine Kinases, Cell Cycle Proteins, BRCA1 Protein, Tumor Suppressor Proteins, Saccharomyces cerevisiae Proteins, Ataxia Telangiectasia Mutated Proteins

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