Abstract:
:Alternative splicing of tau exon 10 generates tau isoforms with three or four microtubule-binding repeats, named 3R- or 4R-tau. Normal adult human brain expresses equal levels of them. Imbalance of 3R-tau and 4R-tau associates with several tauopathies. Splicing factor 9G8 suppresses tau exon 10 inclusion and its function is regulated by phosphorylation. Here, we found that cyclic AMP-dependent protein kinase (PKA) phosphorylated 9G8. The catalytic subunits α and β of PKA interacted with 9G8, and activation of PKA enhanced the interaction. Up-regulation of PKA activity prevented 9G8 from inhibition of tau exon 10 inclusion. These findings provide novel insights into the regulation of tau exon 10 splicing and further our understanding of neurodegeneration associated with dysregulation of tau exon 10 splicing.
journal_name
FEBS Lettjournal_title
FEBS lettersauthors
Gu J,Shi J,Wu S,Jin N,Qian W,Zhou J,Iqbal IG,Iqbal K,Gong CX,Liu Fdoi
10.1016/j.febslet.2012.05.046subject
Has Abstractpub_date
2012-07-30 00:00:00pages
2239-44issue
16eissn
0014-5793issn
1873-3468pii
S0014-5793(12)00432-2journal_volume
586pub_type
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