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–microtubule interface
About this item
Full title
Author / Creator
Publisher
London: Nature Publishing Group UK
Journal title
Language
English
Formats
Publication information
Publisher
London: Nature Publishing Group UK
Subjects
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
Authors, Artists and Contributors
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