Calcium influx recruits an additional class of kinases to hyperphosphorylate tau

SH-SY-5Y human neuroblastoma cells were treated with combinations of the kinase inhibitors HA-1004, W-7 and H-7 and calcium ionophore A23187. Microdensitometric analyses revealed that, in the absence of ionophore-mediated calcium influx, PHF-1 levels were reduced by approximately half in cultures tr...

Full description

Saved in:
Bibliographic Details
Published inNeuroreport Vol. 6; no. 10; p. 1437
Main Authors Shea, T B, Klinger, E P, Cressman, C M
Format Journal Article
LanguageEnglish
Published England 10.07.1995
Subjects
Antibodies, Monoclonal - pharmacology
Brain Neoplasms - enzymology
Calcimycin - pharmacology
Calcium - metabolism
Densitometry
Humans
Immunohistochemistry
Ionophores - pharmacology
Neuroblastoma - enzymology
Phosphorylation
Protein Kinase Inhibitors
Protein Kinases - metabolism
tau Proteins - metabolism
Tumor Cells, Cultured
Online AccessGet more information

Cover

More Information
Summary:SH-SY-5Y human neuroblastoma cells were treated with combinations of the kinase inhibitors HA-1004, W-7 and H-7 and calcium ionophore A23187. Microdensitometric analyses revealed that, in the absence of ionophore-mediated calcium influx, PHF-1 levels were reduced by approximately half in cultures treated with HA-1004 or W-7, but were not reduced by H-7. By contrast, the doubling in PHF-1 immunoreactivity that resulted following ionophore treatment was prevented by all three inhibitors. These analyses demonstrate the recruitment of an additional kinase or kinases in tau phosphorylation following calcium influx, and underscore the possibility that de novo hyperactivation of calcium-dependent kinases may be involved in the early events that propagate PHF formation.
ISSN:0959-4965
DOI:10.1097/00001756-199507100-00019