# Kinase-dependent regulation of ciliary protein transport and its implications for therapy

**Authors:** Taro Chaya, Yuri Ayano, Takahisa Furukawa

PMC · DOI: 10.3389/fmolb.2025.1638737 · Frontiers in Molecular Biosciences · 2025-06-25

## TL;DR

This paper reviews how kinases regulate ciliary transport and their potential for treating ciliopathy-related diseases.

## Contribution

A comprehensive review of kinase roles in intraflagellar transport and their therapeutic implications for ciliopathies.

## Key findings

- Serine-threonine kinases regulate intraflagellar transport in primary cilia.
- Kinase activity influences ciliary function and is linked to ciliopathy development.
- Targeting these kinases may offer new therapies for ciliopathies and age-related obesity.

## Abstract

Primary cilia are evolutionarily conserved microtubule-based structures that extend from the surfaces of many different cell types and decode a wide range of extracellular chemical and physical stimuli. Ciliary defects cause human diseases, termed ciliopathies, which are characterized by a variety of symptoms, such as developmental and sensory abnormalities. The formation and function of primary cilia depend on intraflagellar transport (IFT), which is a bidirectional protein transport system coordinated by three multi-subunit protein complexes with kinesin and dynein motors along the ciliary axoneme. Accumulating evidence has demonstrated that several serine-threonine kinases play key roles in the regulation of IFT. Here, we review the current understanding of the roles of these kinases during the IFT process, as well as their regulatory mechanisms, physiological and pathophysiological significance, and potential to treat ciliopathies and age-related obesity.

## Linked entities

- **Proteins:** Khc (Kinesin heavy chain), Dhc64C (Dynein heavy chain 64C)
- **Diseases:** ciliopathies (MONDO:0005308)

## Full-text entities

- **Diseases:** Ciliary defects (MESH:D002925), ciliopathies (MESH:D000072661), developmental and sensory abnormalities (MESH:D012678), age- (MESH:D019588), obesity (MESH:D009765)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

_Full body text omitted from this summary view._ Fetch the complete paper as Markdown: https://tomesphere.com/paper/PMC12237634/full.md

## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12237634/full.md

## References

72 references — full list in the complete paper: https://tomesphere.com/paper/PMC12237634/full.md

---
Source: https://tomesphere.com/paper/PMC12237634