Log in to save to my catalogue

Reversal of axonal growth defects in an extraocular fibrosis model by engineering the kinesin–microt...

Reversal of axonal growth defects in an extraocular fibrosis model by engineering the kinesin–microt...

https://devfeature-collection.sl.nsw.gov.au/record/TN_cdi_doaj_primary_oai_doaj_org_article_e1f2163676ed4f4f9ecb892722c22875

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

About this item

Full title

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

Publisher

London: Nature Publishing Group UK

Journal title

Nature communications, 2016-01, Vol.7 (1), p.10058-10058, Article 10058

Language

English

Formats

Publication information

Publisher

London: Nature Publishing Group UK

More information

Scope and Contents

Contents

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 re...

Alternative Titles

Full title

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

Identifiers

Primary Identifiers

Record Identifier

TN_cdi_doaj_primary_oai_doaj_org_article_e1f2163676ed4f4f9ecb892722c22875

Permalink

https://devfeature-collection.sl.nsw.gov.au/record/TN_cdi_doaj_primary_oai_doaj_org_article_e1f2163676ed4f4f9ecb892722c22875

Other Identifiers

ISSN

2041-1723

E-ISSN

2041-1723

DOI

10.1038/ncomms10058

How to access this item