DNA damage checkpoints: from initiation to recovery or adaptation.
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Summary
A plethora of mechanistic studies have provided exciting insights into the biology and pathology of checkpoint initiation and signal propagation, and have revealed the various ways in which the response can be terminated: through recovery, adaptation or cancer-prone subversion
- Type
- review
- Published
- 2007-04-01
- Cited by
- 832
- References
- 65
- OpenAlex
- https://openalex.org/W1988280121
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:32126252
Keywords
Biology, DNA damage, G2-M DNA damage checkpoint, Context (archaeology), DNA repair
References
- Cell-cycle checkpoints and cancer
- Degradation of Cdc25A by β-TrCP during S phase and in response to DNA damage
- The pathological response to DNA damage does not contribute to p53-mediated tumour suppression
- Rad17 phosphorylation is required for claspin recruitment and Chk1 activation in response to replication stress.
- Regulation of G2/M events by Cdc25A through phosphorylation‐dependent modulation of its stability
- Mdc1 couples DNA double‐strand break recognition by Nbs1 with its H2AX‐dependent chromatin retention
- Claspin, a novel protein required for the activation of Chk1 during a DNA replication checkpoint response in Xenopus egg extracts.
- Checking on DNA damage in S phase
- Distinct spatiotemporal dynamics of mammalian checkpoint regulators induced by DNA damage
- Recruitment of ATR to sites of ionising radiation-induced DNA damage requires ATM and components of the MRN protein complex
- Initiating cellular stress responses.
- Adaptation to the ionizing radiation-induced G2 checkpoint occurs in human cells and depends on checkpoint kinase 1 and Polo-like kinase 1 kinases.
- gammaH2AX and MDC1: anchoring the DNA-damage-response machinery to broken chromosomes.
- Destruction of Claspin by SCFbetaTrCP restrains Chk1 activation and facilitates recovery from genotoxic stress.
- ATM Activation in Normal Human Tissues and Testicular Cancer
- DNA damage activates ATM through intermolecular autophosphorylation and dimer dissociation
- Chromatin relaxation in response to DNA double-strand breaks is modulated by a novel ATM- and KAP-1 dependent pathway
- Retinoblastoma pathway defects show differential ability to activate the constitutive DNA damage response in human tumorigenesis.
- MDC1 directly binds phosphorylated histone H2AX to regulate cellular responses to DNA double-strand breaks.
- Autophosphorylation at serine 1987 is dispensable for murine Atm activation in vivo
Cited by
- The repair and signaling responses to DNA double-strand breaks.
- Checkpoint recovery after DNA damage: a rolling stop for CDKs
- Accumulation of DNA Damage and Cell Death after Fractionated Irradiation
- Cytokinetically quiescent (G0/G1) human multiple myeloma cells are susceptible to simultaneous inhibition of Chk1 and MEK1/2.
- Validation of Polo-like kinase 1 as a therapeutic target in pancreatic cancer cells
- Working hard for recovery: mitotic kinases in the DNA damage checkpoint
- The transcription factor FOXM1 (Forkhead box M1): proliferation-specific expression, transcription factor function, target genes, mouse models, and normal biological roles.
- FBXW7 and USP7 regulate CCDC6 turnover during the cell cycle and affect cancer drugs susceptibility in NSCLC
- Trial Watch: Targeting ATM–CHK2 and ATR–CHK1 pathways for anticancer therapy
- Molecular mechanisms underlying human papillomavirus E6 and E7 oncoprotein-induced cell transformation.
- Xanthatin triggers Chk1‐mediated DNA damage response and destabilizes Cdc25C via lysosomal degradation in lung cancer cells
- FOXM1 (Forkhead box M1) in tumorigenesis: overexpression in human cancer, implication in tumorigenesis, oncogenic functions, tumor-suppressive properties, and target of anticancer therapy.
- Histone modifications across the cell cycle in undifferentiated and differentiating mouse embryonic stem cells
- BRIT1/MCPH1 MEDIATES THE DNA DAMAGE RESPONSE BY INDUCING P53 STABILITY AND PROMOTING ATR SIGNALING
- A focus on foci: How spatio-temporal regulation of the DNA damage response is crucial for DDR activation and cell fate
- The multiple checkpoint functions of CHK1 and CHK2 in maintenance of genome stability.
- Methods to study cancer therapeutic drugs that target cell cycle checkpoints.
- The Regulation of Cellular Stress Resistance and DNA Repair in a Long-Lived Mutant Mouse.
- Physiological aspects of UV-excitation of DNA.
- DNA-Reparatur und Alterung
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- Ensuring the Stability of the Genome: DNA Damage Checkpoints
- Hypersensitivity to DNA damage in antephase as a safeguard for genome stability