ArticleGenes & development2026
CDK1 and CEP97 cooperatively control centriole length to orchestrate ciliogenesis and developmental patterning.
Article in Genes & development, 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
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
Abstract
Architecture is critical for organelle function. The lengths of centrioles, key components of centrosomes, are tightly regulated. We adapted centrosome purification approaches to measure centrosomal protein phosphorylation. Centrosome-specific phosphoproteomics with and without cyclin-dependent kinase 1 (CDK1) activity revealed that CDK1 phosphorylates many centriolar proteins involved in centriole length control, including Centrobin. CDK1 regulated centriole length synergistically with CEP97-CCP110, a local centriolar complex. CEP97 restricted Centrobin localization to centrioles, whereas CDK1-dependent phosphorylation suppressed Centrobin's ability to promote centriole elongation. Thus, CDK1 and CEP97-CCP110 both restrict centriole elongation by inhibiting the function of Centrobin, a centriole elongation factor, but via different mechanisms. Overelongated centrioles failed to support ciliogenesis in human cells and in mouse embryos. Removing CEP97 during mouse development caused centriole overelongation, impaired ciliogenesis and attenuated Hedgehog (HH) signaling, disrupting mouse heart development. We conclude that CEP97-CCP110 and CDK1 cooperatively restrict Centrobin function to control centriole length, critical for mammalian development.
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.