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: Itsushi Minoura, Hiroko Takazaki, Rie Ayukawa, Chihiro Saruta, You Hachikubo, Seiichi Uchimura, Tomonobu Hida, Hiroyuki Kamiguchi, Tomomi Shimogori, Etsuko Muto
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Lenguaje:EN
Publicado: Nature Portfolio 2016
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Acceso en línea:https://doaj.org/article/e1f2163676ed4f4f9ecb892722c22875
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spelling oai:doaj.org-article:e1f2163676ed4f4f9ecb892722c228752021-12-02T15:34:57ZReversal of axonal growth defects in an extraocular fibrosis model by engineering the kinesin–microtubule interface10.1038/ncomms100582041-1723https://doaj.org/article/e1f2163676ed4f4f9ecb892722c228752016-01-01T00:00:00Zhttps://doi.org/10.1038/ncomms10058https://doaj.org/toc/2041-1723How 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.Itsushi MinouraHiroko TakazakiRie AyukawaChihiro SarutaYou HachikuboSeiichi UchimuraTomonobu HidaHiroyuki KamiguchiTomomi ShimogoriEtsuko MutoNature PortfolioarticleScienceQENNature Communications, Vol 7, Iss 1, Pp 1-11 (2016)
institution DOAJ
collection DOAJ
language EN
topic Science
Q
spellingShingle Science
Q
Itsushi Minoura
Hiroko Takazaki
Rie Ayukawa
Chihiro Saruta
You Hachikubo
Seiichi Uchimura
Tomonobu Hida
Hiroyuki Kamiguchi
Tomomi Shimogori
Etsuko Muto
Reversal of axonal growth defects in an extraocular fibrosis model by engineering the kinesin–microtubule interface
description 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.
format article
author Itsushi Minoura
Hiroko Takazaki
Rie Ayukawa
Chihiro Saruta
You Hachikubo
Seiichi Uchimura
Tomonobu Hida
Hiroyuki Kamiguchi
Tomomi Shimogori
Etsuko Muto
author_facet Itsushi Minoura
Hiroko Takazaki
Rie Ayukawa
Chihiro Saruta
You Hachikubo
Seiichi Uchimura
Tomonobu Hida
Hiroyuki Kamiguchi
Tomomi Shimogori
Etsuko Muto
author_sort Itsushi Minoura
title Reversal of axonal growth defects in an extraocular fibrosis model by engineering the kinesin–microtubule interface
title_short Reversal of axonal growth defects in an extraocular fibrosis model by engineering the kinesin–microtubule interface
title_full Reversal of axonal growth defects in an extraocular fibrosis model by engineering the kinesin–microtubule interface
title_fullStr Reversal of axonal growth defects in an extraocular fibrosis model by engineering the kinesin–microtubule interface
title_full_unstemmed Reversal of axonal growth defects in an extraocular fibrosis model by engineering the kinesin–microtubule interface
title_sort reversal of axonal growth defects in an extraocular fibrosis model by engineering the kinesin–microtubule interface
publisher Nature Portfolio
publishDate 2016
url https://doaj.org/article/e1f2163676ed4f4f9ecb892722c22875
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