ReviewJournal of cell communication and signaling2025
CEP162: A critical regulator of ciliary transition zone assembly and its implications in ciliopathies.
Review in Journal of cell communication and signaling, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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.
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
3 citing papers in PubMed.
- Dynamic centrosomes: functional diversity and remodeling across cell types.Acta pharmacologica Sinica · 2026Review
- Article
- The primary cilium-autophagy axis in vascular homeostasis and cardiovascular disease: mechanistic crosstalk and evidence boundaries.Frontiers in cardiovascular medicine · 2026Review
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
No grant is acknowledged in the PubMed record.
Abstract
CEP162, a 162-kDa centrosome protein, is a crucial centrosomal adapter, mediating cell differentiation and polarization. CEP162 maintains mitosis by dynamically stabilizing microtubules. CEP162 promotes the transition zone (TZ) assembly in the basal body through interaction with CEP131, CEP290, and axoneme microtubules as well as the distal centriole. TZ ensures the normal distribution of soluble proteins between the cytoplasm and cilia. It also facilitates retinal development and sperm flagellar motility. However, fluctuations in TZ permeability caused by abnormal expression of CEP162, including truncated mutations and naturally occurring mutations, lead to cilia abnormality and dysfunction in ciliogenesis through the regulation of intraflagellar transport, resulting in retinal degeneration and infertility. LncRNAs can induce SNP events in the CEP162 transcript by altering alternative splicing. Naturally occurring mutations are closely linked to retinal ciliopathy and diabetic retinopathy. This review summarizes the latest research progress to better understand the biology and pathophysiology of CEP162 and the clinical manifestations caused by CEP162 variants.
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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.