Reversal of axonal growth defects in an extraocular fibrosis model by engineering the kinesin–microtubule interface
How mutations in β3-tubulin cause axonal growth defects in congenital fibrosis of the extraocular muscles type 3 remains elusive. Minoura et al. develop a model system using recombinant human tubulin that demonstrates a link between tubulin mutation, impaired kinesin motility and axonal growth defec...
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| Autores principales: | , , , , , , , , , |
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| Formato: | article |
| Lenguaje: | EN |
| Publicado: |
Nature Portfolio
2016
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| Materias: | |
| Acceso en línea: | https://doaj.org/article/e1f2163676ed4f4f9ecb892722c22875 |
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| Sumario: | How mutations in β3-tubulin cause axonal growth defects in congenital fibrosis of the extraocular muscles type 3 remains elusive. Minoura et al. develop a model system using recombinant human tubulin that demonstrates a link between tubulin mutation, impaired kinesin motility and axonal growth defects. |
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