ArticleCell cycle (Georgetown, Tex.)2019
Dephosphorylation of Plk1 occurs through PP2A-B55/ENSA/Greatwall pathway during mitotic DNA damage recovery.
Article in Cell cycle (Georgetown, Tex.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- TUFT1 regulates cancer progression by suppressing centrosome amplification and mitotic spindle multipolarity.Cell death & disease · 2025Article
- Dissecting the cell cycle regulation, DNA damage sensitivity and lifespan effects of caffeine in fission yeast.Microbial cell (Graz, Austria) · 2025Article
- Checkpoint kinase 2 controls insulin secretion and glucose homeostasis.Nature chemical biology · 2024Article
- Identification of PP2A-B55 targets uncovers regulation of emerin during nuclear envelope reassembly inOpen biology · 2023Article
- Kinetochore phosphatases suppress autonomous Polo-like kinase 1 activity to control the mitotic checkpoint.The Journal of cell biology · 2020Article
- PP2A and tumor radiotherapy.Hereditas · 2020Review
- Review
- Polo-like kinase 1 (Plk1) is a positive regulator of DNA replication in theCell cycle (Georgetown, Tex.) · 2020Article
- Cell Cycle and DNA Repair Regulation in the Damage Response: Protein Phosphatases Take Over the Reins.International journal of molecular sciences · 2020Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recovery from DNA damage is critical for cell survival. However, serious damage cannot be repaired, leading to cell death for prevention of abnormal cell growth. Previously, we demonstrated that 4N-DNA accumulates via the initiation of an abnormal interphase without cytokinesis and that re-replication occurs during a prolonged recovery period in the presence of severe DNA damage in mitotic cells. Mitotic phosphorylated Plk1 is typically degraded during mitotic exit. However, Plk1 has unusually found to be dephosphorylated in mitotic slippage without cytokinesis during recovery from mitotic DNA damage. Here, we investigated how Plk1 dephosphorylation is established during recovery from mitotic DNA damage. Mitotic DNA damage activated ATM and Chk1/2 and repressed Cdk1 and Greatwall protein kinase, followed by PP2A activation through the dissociation of ENSA and PP2A-B55. Interaction between Plk1 and PP2A-B55α or PP2A-B55δ was strongly induced during recovery from mitotic DNA damage. Moreover, the depletion of PP2A-B55α and/or PP2A-B55δ by siRNA transfection led to the recovery of Plk1 phosphorylation and progression of the cell cycle into the G
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