The alternative splicing of tau exon 10 and its regulatory proteins CLK2 and TRA2-BETA1 changes in sporadic Alzheimer's disease.

@article{Glatz2006TheAS,
  title={The alternative splicing of tau exon 10 and its regulatory proteins CLK2 and TRA2-BETA1 changes in sporadic Alzheimer's disease.},
  author={Daniela C Glatz and Dan Rujescu and Yesheng Tang and Frank J Berendt and Annette M Hartmann and Frank Faltraco and Carlyn K. Rosenberg and Christine Hulette and Kurt Jellinger and Harald Hampel and Peter Franz Riederer and Hans-J M{\"o}ller and Athena Andreadis and Kerstin Henkel and Stefan Stamm},
  journal={Journal of neurochemistry},
  year={2006},
  volume={96 3},
  pages={635-44}
}
Pathological inclusions containing fibrillar aggregates of hyperphosphorylated tau protein are a characteristic feature in tauopathies, which include Alzheimer's disease (AD). Tau is a microtubule-associated protein whose transcript undergoes alternative splicing in the brain. Exon 10 encodes one of four microtubule-binding repeats. Exon 10 inclusion gives rise to tau protein isoforms containing four microtubule-binding repeats (4R) whereas exclusion leads to isoforms containing only three… CONTINUE READING
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