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Article

Molecular basis underlying the ciliary defects caused by IFT52 variations found in skeletal ciliopathies.

Molecular biology of the cell - 1 Aug 2022

Ishida Yamato, Tasaki Koshi, Katoh Yohei, Nakayama Kazuhisa

Abstract excerpt

Bidirectional protein trafficking within cilia is mediated by the intraflagellar transport (IFT) machinery, which contains the IFT-A and IFT-B complexes powered by the kinesin-2 and dynein-2 motors. Mutations in genes encoding subunits of the IFT-A and dynein-2 complexes cause skeletal ciliopathies. Some subunits of the IFT-B complex, including IFT52, IFT80, and IFT172, are also mutated in skeletal ciliopathies....

Topics

Adaptor Proteins, Signal Transducing
Cilia
Ciliopathies
Cytoskeletal Proteins
Dyneins
Flagella
Humans
Mutation
Protein Transport

Source

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Identifiers

PMID: 35704471
DOI: 10.1091/mbc.E22-05-0188
PMCID: PMC9582644

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 29 Aug 2026. Prepared record publication-35704471-2026-08-29.1. Manifest publication-graph-cohort-2026-08-29.1.

Source receipt: PubMed via Helena Literature Corpus, retrieved 29 Aug 2026.

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Molecular basis underlying the ciliary defects caused by IFT52 variations found in skeletal ciliopathies.PMID 35704471Read ↗

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