ArticleCommunications biology2026
β-tubulin phosphorylation by Chk1 is required for normal spindle formation during cell division.
Article in Communications biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
1 citing paper in PubMed.
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
The mitotic spindle is a microtubule-based apparatus that is responsible for accurate segregation of chromosomes into two daughter cells. In this study, we show that the DNA damage kinase Chk1 is required for optimal density and efficient nucleation of spindle microtubules during unperturbed mitosis in vertebrate cells. Chk1 phosphorylates β-tubulin at the identified conserved site threonine-285 (T285) in vitro, and at mitotic centrosomes in prometaphase and metaphase. Impaired β-tubulin-T285 phosphorylation correlates with improper spindles, delayed anaphase onset, erroneous chromosome alignment and segregation, unequal daughter cell-size and reduced cell proliferation. The ATR-interacting protein ATRIP promotes localization of ATR kinase and the mediator protein TopBP1 to mitotic centrosomes; furthermore, interaction of ATRIP with ATR and TopBP1 is required for Chk1 activation and β-tubulin-T285 phosphorylation. These results identify a signaling pathway that promotes spindle maturation and function in human cells, through Chk1-mediated β-tubulin-T285 phosphorylation.
Indexed as
Identifiers
What OpenQuestion holds
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.