ALZHEIMERS-DISEASE ABNORMALLY PHOSPHORYLATED-TAU IS DEPHOSPHORYLATED BY PROTEIN PHOSPHATASE-2B (CALCINEURIN)

被引：0
|
作者：
GONG, CX [1 ]
SINGH, TJ [1 ]
GRUNDKEIQBAL, I [1 ]
IQBAL, K [1 ]
机构：
[1] NEW YORK STATE INST BASIC RES DEV DISABIL,STATEN ISL,NY 10314
来源：
JOURNAL OF NEUROCHEMISTRY | 1994年 / 62卷 / 02期
关键词：
PROTEIN PHOSPHATASE-2B; TAU PROTEIN; DEPHOSPHORYLATION; PHOSPHORYLATION SITES; NEUROFIBRILLARY DEGENERATION; ALZHEIMERS DISEASE;
D O I：
暂无
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
Abnormally hyperphosphorylated tau is the major protein subunit of paired helical filaments in Alzheimer brains. We have examined its site-specific dephosphorylation by different protein phosphatases. Dephosphorylation of tau was monitored by its interaction with several phosphorylation-dependent antibodies. Alzheimer tau was dephosphorylated by brain protein phosphatase-2B at the abnormally phosphorylated sites Ser(46), Ser(199), Ser(202), Ser(235), Ser(396), and Ser(404)m and its relative mobility on sodium dodecyl sulfate-polyacrylamide gel electrophoresis shifted to that of normal tau. Protein phosphatases-1 and -2A could dephosphorylate only some of the above six phosphorylation sites. These results indicate that protein phosphatase-2B might be involved in hyperphosphorylation of tau in Alzheimer's disease.
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页码：803 / 806
页数：4
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