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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發表在:Nat Commun
Main Authors: Minoura, Itsushi, Takazaki, Hiroko, Ayukawa, Rie, Saruta, Chihiro, Hachikubo, You, Uchimura, Seiichi, Hida, Tomonobu, Kamiguchi, Hiroyuki, Shimogori, Tomomi, Muto, Etsuko
格式: Artigo
語言:Inglês
出版: Nature Publishing Group 2016
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在線閱讀: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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