Neuron-specific phosphorylation of Alzheimer's β-amyloid precursor protein by cyclin-dependent kinase 5

被引：207
作者：
Iijima, K
Ando, K
Takeda, S
Satoh, Y
Seki, T
Itohara, S
Greengard, P
Kirino, Y
Nairn, AC
Suzuki, T
机构：
[1] Univ Tokyo, Sch Pharmaceut Sci, Lab Neurobiophys, Bunkyo Ku, Tokyo 1130033, Japan
[2] Biooriented Technol Res Advancement Inst, Tokyo, Japan
[3] Juntendo Univ, Sch Med, Dept Anat, Tokyo 113, Japan
[4] Rockefeller Univ, Mol & Cellular Neurosci Lab, New York, NY 10021 USA
来源：
JOURNAL OF NEUROCHEMISTRY | 2000年 / 75卷 / 03期
关键词：
Alzheimer's beta-amyloid precursor protein; Alzheimer's disease; cyclin-dependent kinase 5; protein phosphorylation;
D O I：
10.1046/j.1471-4159.2000.0751085.x
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：
The mature form of Alzheimer's P-amyloid precursor protein (APP) is phosphorylated specifically at Thr(668) in neurons. In mature neurons, phosphorylated APP is detected in neurites, with dephosphorylated APP being found mostly in the cell body. In vitro, active cyclin-dependent kinase 5 (Cdk5) phosphorylated the cytoplasmic domain of APP at Thr(668). Treatment of mature neurons with an antisense oligonucleotide to Cdk5 suppressed Cdk5 expression and significantly diminished the level of phosphorylated APP, The expression of APP was unaffected in antisense-treated neurons. These results indicate that in neurons APP is phosphorylated by Cdk5, and that this may play a role in its localization.
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收藏
页码：1085 / 1091
页数：7
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