ArticleCells2025
Molecular Insights into Outer Dynein Arm Defects in Primary Ciliary Dyskinesia: Involvement of ZMYND10 and GRP78.
Article in Cells, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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.
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Who cites it
4 citing papers in PubMed.
- Primary Cilia as Integrative Hubs of Metabolic Signaling in Type 2 Diabetes: Inter-Organ Evidence From Central, Peripheral, and Pancreatic Islet Tissues.Journal of cellular physiology · 2026Review
- Article
- A conserved minimal core and modular extensions make the fungal flagellum.Scientific reports · 2026Article
- A homozygous splice-site variant inFrontiers in medicine · 2026Article
Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPrimary ciliary dyskinesia (PCD) is a rare genetic disorder characterized by recurrent sinopulmonary infections due to motile cilia defects. The disease is genetically heterogeneous, with abnormalities in structural ciliary proteins. Zinc finger MYND-type containing 10 (ZMYND10) is essential for the assembly of outer dynein arms (ODA), with chaperones like Glucose-regulated protein 78 (GRP78) facilitating protein folding. This study investigates ZMYND10 and Dynein axonemal heavy chain 5
methodsEight individuals aged 14-22 with clinical PCD symptoms and confirmed
resultsThe corrected total cell fluorescence (CTCF) levels of
conclusionsThe altered expression of DNAH5, ZMYND10, and GRP78, along with metabolic shifts, points to a complex link between ciliary dysfunction and cellular stress in PCD. Further studies are needed to clarify the underlying mechanisms.
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Registered trials
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