CALCIUM INFLUX RECRUITS AN ADDITIONAL CLASS OF KINASES TO HYPERPHOSPHORYLATE-TAU

被引：9

作者：

SHEA, TB

KLINGER, EP

CRESSMAN, CM

机构：

[1] Center for Cellular Neurobiology and Neurodegeneration Research, Department of Biological Sciences, University of Massachusetts at Lowell One University Avenue, Lowell, MA

来源：

NEUROREPORT | 1995年 / 6卷 / 10期

关键词：

TAU; PHOSPHORYLATION; KINASES; ALZHEIMERS DISEASE; SIGNAL TRANSDUCTION; CALCIUM INFLUX; NEURODEGENERATION;

D O I：

10.1097/00001756-199507100-00019

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

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.

引用

页码：1437 / 1440

页数：4

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