ArticleNature communications2024
Chk2 sustains PLK1 activity in mitosis to ensure proper chromosome segregation.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- A novel small molecule inhibitor targeting KHSRP methylation suppresses colon cancer progression.Acta pharmaceutica Sinica. B · 2026Article
- Loss of JAK1 Function Causes G2-M Cell-Cycle Defects Vulnerable to KIF18A Inhibition.Cancer research · 2026Article
- Centrosomal JAK2 Tyrosine Kinase Regulates Primary Cilia Length, Cell Proliferation, and Cilia Orientation During Cell Migration.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Identification of Immune&Driver Molecular Subtypes Optimizes Immunotherapy Strategies for Gastric Cancer.International journal of molecular sciences · 2026Article
- The mitotic ATR-Chk1 pathway promotes CDK1 activity for faithful chromosome segregation.Cell reports · 2025Article
- A minimal deterministic model reveals integration of spindle assembly and position checkpoints in mitosis.Scientific reports · 2025Article
- Targeted siRNA Delivery Using Cetuximab-Conjugated Starch for Epidermal Growth Factor Receptor-Driven Head and Neck Squamous Cell Carcinoma.Small science · 2025Article
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Abstract
Polo-like kinase 1 (PLK1) protects against genome instability by ensuring timely and accurate mitotic cell division, and its activity is tightly regulated throughout the cell cycle. Although the pathways that initially activate PLK1 in G2 are well-characterized, the factors that directly regulate mitotic PLK1 remain poorly understood. Here, we identify that human PLK1 activity is sustained by the DNA damage response kinase Checkpoint kinase 2 (Chk2) in mitosis. Chk2 directly phosphorylates PLK1 T210, a residue on its T-loop whose phosphorylation is essential for full PLK1 kinase activity. Loss of Chk2-dependent PLK1 activity causes increased mitotic errors, including chromosome misalignment, chromosome missegregation, and cytokinetic defects. Moreover, Chk2 deficiency increases sensitivity to PLK1 inhibitors, suggesting that Chk2 status may be an informative biomarker for PLK1 inhibitor efficacy. This work demonstrates that Chk2 sustains mitotic PLK1 activity and protects genome stability through discrete functions in interphase DNA damage repair and mitotic chromosome segregation.
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