ReviewBiology2026
New Roles of Chk1 in Spindle Formation and Genome Integrity.
Review in Biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
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Authors and funding
3 authors.
Funding
Abstract
During mitosis sister chromatids are accurately segregated into two daughter cells through a microtubule-based structure known as the mitotic spindle. Errors in mitotic spindle formation have been associated with human diseases and tumorigenesis. Chk1 has well established roles in DNA damage response and replication checkpoints. Recently, new roles have emerged in the onset of mitosis, chromosome segregation and cytokinesis. In this review, we recapitulate the known roles of Chk1 in cell division and highlight new roles of Chk1 in mitotic spindle assembly and its contribution to genome stability. Specifically, it was recently reported that, during the first stages of mitosis, ATRIP and its interacting partners, ATR and TopBP1, are recruited to centrosomes, where they activate Chk1. Then, Chk1 phosphorylates β-tubulin at Threonine 285 (T285), promoting microtubule nucleation and mitotic spindle formation. β-tubulin phosphorylation by Chk1 is required for proper mitotic progression, cytokinesis with equal-sized daughter cells and cell proliferation. This novel ATR-Chk1 signaling pathway reinforces the crosstalk between the cell cycle regulation and DNA damage response.
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Registered trials
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