ArticleProceedings of the National Academy of Sciences of the United States of America2025
EFCAB10 anchors AK8 to the radial spoke for proper ciliary motility.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed.
- AK8 deficiency causes primary ciliary dyskinesia by disrupting energy homeostasis in the airways.American journal of respiratory and critical care medicine · 2026Article
- Proteomic composition and mutual assembly of the C2a projection in vertebrate motile cilia.eLife · 2026Article
- Filippi syndrome-associated CKAP2L modulates microtubule dynamics essential for mitosis and ciliary length regulation.Journal of molecular cell biology · 2026Article
- RGS22 is a metazoa-specific radial spoke component required for coordinated ciliary beating.Nature communications · 2026Article
- JHY enables the transition from switchable to fixed ciliary waveforms in metazoan evolution.EMBO reports · 2026Article
- The primary cilium as a compartmentalized signaling hub in tissue immunity and homeostasis.Frontiers in cell and developmental biology · 2026Review
Corrections and comments
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Authors and funding
14 authors.
Funding
Abstract
Radial spokes in motile cilia and flagella regulate rhythmic ciliary motility, which is essential for rapid cell movement and extracellular fluid flow. In humans, defective radial spokes can cause a genetic disorder known as primary ciliary dyskinesia (PCD), resulting in respiratory defects and infertility. Despite their critical role in ciliary motility, the molecular composition and related physiological functions remain to be elucidated. Here, we identify EF-hand calcium-binding domain protein 10 (EFCAB10) and adenylate kinase (AK8) as radial spoke proteins and describe their roles in mouse motile cilia. Using
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Registered trials
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