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- W2051233811 abstract "Mutations in the tau gene are pathogenic causing autosomal dominant frontotemporal dementia with Parkinsonism-chromosome 17 type (FTDP-17). Some mutations intau exon 10 (E10) and immediately adjacent sequences cause disease by altering E10 splicing. To determine the mechanism of normal E10 splicing regulation and how FTDP-17 mutations alter splicing, mutational analysis of E10 was performed. The results show that E10 contains a complex array of both enhancer and inhibitorcis-acting elements that modulate usage of a weak 5′ splice site. The 5′ end of E10 contains a previously unrecognized multipartite exon splicing enhancer (ESE) composed of an SC35-like binding sequence, a purine-rich sequence, and an AC-rich element. Downstream of this ESE is a purine-rich exon splicing inhibitor. Intronic sequences immediately downstream of E10 also are inhibitory. The results support an alternative model in which I10 inhibitory sequences appear to function as a linear sequence. The cis-elements described are not redundant, and all appear required for normal E10 splicing. Results with double mutations demonstrate that the ESE and the intronic inhibitory element collaborate to regulate splicing. Thus splicing oftau E10 is regulated by a complex set ofcis-acting elements that span nearly the entire exon and also include intronic sequences." @default.
- W2051233811 created "2016-06-24" @default.
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- W2051233811 date "2000-06-01" @default.
- W2051233811 modified "2023-10-01" @default.
- W2051233811 title "Determinants of 4-Repeat Tau Expression" @default.
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- W2051233811 doi "https://doi.org/10.1074/jbc.m909470199" @default.
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