Crossref journal-article
Wiley
FEBS Letters (311)
Abstract

Tau is a neuronal microtubule‐associated protein whose function is modulated by phosphorylation. GSK‐3β is a tau kinase. GSK‐3β is part of the wingless signalling pathway and stimulation by wingless is predicted to down‐regulate GSK‐3β activity. In Drosophila imaginal disc cells, overexpression of dishevelled, a component of the wingless pathway, mimics the wingless signal. We have therefore studied the effect that overexpression of the murine dishevelled‐1 protein has on GSK‐3β‐mediated phosphorylation of tau in transfected CHO cells. We find that co‐transfection with dishevelled‐1 is inhibitory to GSK‐3β‐mediated tau phosphorylation. Tau is hyperphosphorylated in Alzheimer's disease and the possible relevance of these findings to Alzheimer's disease pathogenesis are discussed.

Bibliography

Wagner, U., Brownlees, J., Irving, N. G., Lucas, F. R., Salinas, P. C., & Miller, C. C. J. (1997). Overexpression of the mouse dishevelled‐1 protein inhibits GSK‐3β‐mediated phosphorylation of tau in transfected mammalian cells. FEBS Letters, 411(2–3), 369–372. Portico.

Dates
Type When
Created 23 years, 1 month ago (July 25, 2002, 1:54 p.m.)
Deposited 1 year, 11 months ago (Sept. 17, 2023, 3:34 a.m.)
Indexed 1 year, 2 months ago (June 18, 2024, 5:04 a.m.)
Issued 28 years, 1 month ago (July 14, 1997)
Published 28 years, 1 month ago (July 14, 1997)
Published Online 24 years, 8 months ago (Dec. 14, 2000)
Published Print 28 years, 1 month ago (July 14, 1997)
Funders 0

None

@article{Wagner_1997, title={Overexpression of the mouse dishevelled‐1 protein inhibits GSK‐3β‐mediated phosphorylation of tau in transfected mammalian cells}, volume={411}, ISSN={1873-3468}, url={http://dx.doi.org/10.1016/s0014-5793(97)00733-3}, DOI={10.1016/s0014-5793(97)00733-3}, number={2–3}, journal={FEBS Letters}, publisher={Wiley}, author={Wagner, Uta and Brownlees, Janet and Irving, Nicholas G and Lucas, Fiona R and Salinas, Patricia C and Miller, Christopher C.J}, year={1997}, month=jul, pages={369–372} }