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Reversal of axonal growth defects in an extraocular fibrosis model by engineering the kinesin–microtubule interface
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 m...
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| Pubblicato in: | Nat Commun |
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| Autori principali: | , , , , , , , , , |
| Natura: | Artigo |
| Lingua: | Inglês |
| Pubblicazione: |
Nature Publishing Group
2016
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| Soggetti: | |
| Accesso online: | https://ncbi.nlm.nih.gov/pmc/articles/PMC4735607/ https://ncbi.nlm.nih.gov/pubmed/26775887 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1038/ncomms10058 |
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