ReviewSystems and synthetic biology2014
When genome integrity and cell cycle decisions collide: roles of polo kinases in cellular adaptation to DNA damage.
Review in Systems and synthetic biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 25 citations in OpenAlex.
- Yeast centrosomes act as organizing centers to promote Polo kinase-mediated adaptation to persistent DNA damage.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- The Polo kinase Cdc5 is regulated at multiple levels in the adaptation response to telomere dysfunction.Genetics · 2023Article
- DNA damage checkpoint execution and the rules of its disengagement.Frontiers in cell and developmental biology · 2022Review
- Adaptation to DNA Damage, an Asymptotic Approach for a Cooperative Non-local System.Acta applicandae mathematicae · 2022Article
- Adaptation to DNA damage as a bet-hedging mechanism in a fluctuating environment.Royal Society open science · 2021Article
- Mitotic entry upon Topo II catalytic inhibition is controlled by Chk1 and Plk1.The FEBS journal · 2020Article
- A guiding torch at the poles: the multiple roles of spindle microtubule-organizing centers during cell division.Cell cycle (Georgetown, Tex.) · 2020Review
- Review
- MCPH1 is essential for cellular adaptation to the GFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Adaptation in replicative senescence: a risky business.Current genetics · 2019Review
- Adaptation to DNA damage checkpoint in senescent telomerase-negative cells promotes genome instability.Genes & development · 2018Article
- Article
- Checkpoint adaptation: Keeping Cdc5 in the T-loop.Cell cycle (Georgetown, Tex.) · 2016Article
- Reduced kinase activity of polo kinase Cdc5 affects chromosome stability and DNA damage response in S. cerevisiae.Cell cycle (Georgetown, Tex.) · 2016Article
- Slx4 and Rtt107 control checkpoint signalling and DNA resection at double-strand breaks.Nucleic acids research · 2016Article
- Mitotic entry in the presence of DNA damage is a widespread property of aneuploidy in yeast.Molecular biology of the cell · 2015Article
- The danger model approach to the pathogenesis of the rheumatic diseases.Journal of immunology research · 2015Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The drive to proliferate and the need to maintain genome integrity are two of the most powerful forces acting on biological systems. When these forces enter in conflict, such as in the case of cells experiencing DNA damage, feedback mechanisms are activated to ensure that cellular proliferation is stopped and no further damage is introduced while cells repair their chromosomal lesions. In this circumstance, the DNA damage response dominates over the biological drive to proliferate, and may even result in programmed cell death if the damage cannot be repaired efficiently. Interestingly, the drive to proliferate can under specific conditions overcome the DNA damage response and lead to a reactivation of the proliferative program in checkpoint-arrested cells. This phenomenon is known as adaptation to DNA damage and is observed in all eukaryotic species where the process has been studied, including normal and cancer cells in humans. Polo-like kinases (PLKs) are critical regulators of the adaptation response to DNA damage and they play key roles at the interface of cell cycle and checkpoint-related decisions in cells. Here, we review recent progress in defining the specific roles of PLKs in the adaptation process and how this conserved family of eukaryotic kinases can integrate the fundamental need to preserve genomic integrity with effective cellular proliferation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.