Cited by 544DNA Repair MechanismsPI3K/AKT/mTOR signaling in cancerProtein Kinase Regulation and GTPase Signaling

Initiating Cellular Stress Responses

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Bakkenist, Christopher J, Kastan, Michael B·2004·Cell

Abstract

The phosphoinositide 3-kinase related kinases (PIKKs) mediate responses to diverse stresses, including DNA double-strand breaks (DSBs), abnormal replication fork progression, the recognition of premature termination codons in mRNAs, and inadequate nutrient availability. Rigorous control of these kinases limits cellular damage and promotes cell viability in the presence of stress. Control mechanisms include the localization of PIKKs into multiprotein complexes at the sites of damage and mediation of protein-protein contacts such that substrates are allowed access to the PIKK catalytic domains.

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Crossref · 10.1016/j.cell.2004.06.023

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Authors
Bakkenist, C. J., & Kastan, M. B.
Affiliations
St. Jude Children's Research Hospital (US)
Corresponding author
Kastan, Michael B
Venue
Cell
Publisher
Elsevier BV
Published
2004-07
Volume
118
Issue
1
Pages
9-17
ISSN
0092-8674 (ISSN-L)
OpenAlex
W2010895845
Cited by
544
References
55
Citations by year
2026: 1 · 2025: 3 · 2024: 8 · 2023: 8 · 2022: 4 · 2021: 6 · 2020: 5 · 2019: 7 · 2018: 14 · 2017: 19 · 2016: 17 · 2015: 18 · 2014: 17 · 2013: 23 · 2012: 21
FWCI
5.66
Type
journal article
Language
en
Open access
Locations
  • Cell (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
Keywords
PIKKs, cellular stress response, DNA double-strand breaks, replication fork stalling, nutrient deprivation, protein-protein interaction, protein complexes, kinase localization, DNA damage response
MeSH terms
Animals, Cell Survival, DNA Damage, DNA Replication, DNA-Binding Proteins, Enzyme Activation, Humans, Models, Biological, Stress, Physiological, Substrate Specificity, Protein Structure, Tertiary, Phosphatidylinositol 3-Kinases, Catalytic Domain

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