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Article

Reversal of axonal growth defects in an extraocular fibrosis model by engineering the kinesin-microtubule interface.

Nature communications - 18 Jan 2016

Minoura Itsushi, Takazaki Hiroko, Ayukawa Rie, Saruta Chihiro, Hachikubo You, Uchimura Seiichi, Hida Tomonobu, Kamiguchi Hiroyuki, Shimogori Tomomi, Muto Etsuko

Abstract excerpt

Mutations in human β3-tubulin (TUBB3) cause an ocular motility disorder termed congenital fibrosis of the extraocular muscles type 3 (CFEOM3). In CFEOM3, the oculomotor nervous system develops abnormally due to impaired axon guidance and maintenance; however, the underlying mechanism linking TUBB3 mutations to axonal growth defects remains unclear. Here, we investigate microtubule (MT)-based motility in vitro...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Source

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Identifiers

PMID: 26775887
DOI: 10.1038/ncomms10058
PMCID: PMC4735607

Genes

TUBB3

Variants

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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Reversal of axonal growth defects in an extraocular fibrosis model by engineering the kinesin-microtubule interface.PMID 26775887Read ↗

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Evidence of an asymmetrical endophenotype in congenital fibrosis of extraocular muscles type 3 resulting from TUBB3 mutations.Semantic proximity Read ↗

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