Abstract:
:Mutations in the tau gene cause frontotemporal dementia and parkinsonism linked to chromosome-17 (FTDP-17). Functionally, about half of the known mutations increase the alternative mRNA splicing of exon 10 of the tau gene, resulting in the overproduction of tau isoforms with four microtubule-binding repeats. The other mutations reduce the ability of tau to interact with microtubules, with some mutations also increasing the propensity of tau to assemble into filaments. Here we have examined the functional effects of the recently described tau gene mutations deltaN296 and N296H. Both mutations reduced the ability of tau to promote microtubule assembly, without having a significant effect on tau filament formation. By exon trapping, they increased the splicing of exon 10. DeltaN296 and N296H thus define a class of tau mutations with effects at both the RNA and the protein level.
journal_name
J Neurochemjournal_title
Journal of neurochemistryauthors
Yoshida H,Crowther RA,Goedert Mdoi
10.1046/j.0022-3042.2001.00729.xkeywords:
subject
Has Abstractpub_date
2002-02-01 00:00:00pages
548-51issue
3eissn
0022-3042issn
1471-4159journal_volume
80pub_type
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