ArticleNature communications2025
PBK/TOPK mediates Ikaros, Aiolos and CTCF displacement from mitotic chromosomes and alters chromatin accessibility at selected C2H2-zinc finger protein binding sites.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Elevated Plasma T-LAK cell-originated protein kinase Owned the Potential for Predicting Favorable Outcomes in Acute Ischemic Stroke Patients.Cellular and molecular neurobiology · 2026Article
- Advances in T-Lymphokine-activated Killer Cell-originated Protein Kinase Research in Cancer Over the Past Thirty Years.Journal of cancer prevention · 2026Review
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Authors and funding
14 authors.
Funding
Abstract
PBK/TOPK is a mitotic kinase implicated in haematological and non-haematological cancers. Here we show that the key haemopoietic regulators Ikaros and Aiolos require PBK-mediated phosphorylation to dissociate from chromosomes in mitosis. Eviction of Ikaros is rapidly reversed by addition of the PBK-inhibitor OTS514, revealing dynamic regulation by kinase and phosphatase activities. To identify more PBK targets, we analysed loss of mitotic phosphorylation events in Pbk
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