AD-LIKE TAU-PHOSPHORYLATION IN HUMAN NEUROBLASTOMA-CELLS FOLLOWING PKC HYPERACTIVATION IS MEDIATED BY MAP KINASE

Citation
S. Pundreddy et Tb. Shea, AD-LIKE TAU-PHOSPHORYLATION IN HUMAN NEUROBLASTOMA-CELLS FOLLOWING PKC HYPERACTIVATION IS MEDIATED BY MAP KINASE, Neuroscience research communications, 21(3), 1997, pp. 173-177
Citations number
33
Categorie Soggetti
Neurosciences
ISSN journal
08936609
Volume
21
Issue
3
Year of publication
1997
Pages
173 - 177
Database
ISI
SICI code
0893-6609(1997)21:3<173:ATIHNF>2.0.ZU;2-X
Abstract
SH-SY-5Y human neuroblastoma cells were treated with the phorbol ester TPA and the MAP kinase kinase inhibitors PD98059. Microdensitometric analyses revealed that TPA treatment induced 60% and 46% increases in immunoreactivity towards monoclonal antibodies (AT8 and PHF-1, respect ively; p=0.0005) that recognize tau epitopes common to paired helical filaments. These increases were attenuated by the simultaneous treatme nt with PD98059. Steady-state AT-8 and PHF-1 immunoreactivity were not inhibited by PD98059. These analyses corroborate studies from other l aboratories that indicate that MAP kinase may not normally confer AD-l ike immunoreactivity to tau within intact cells, but demonstrate that hyperactivation of upstream kinase(s) may recruit otherwise benign kin ases to hyperphosphorylate tau. These findings further implicate the p otential involvement of hyperactivation of signal transduction pathway s in the early events that propagate PHF formation.