Nucleophosmin/B23 is a target of CDK2/Cyclin E in centrosome duplication

被引：562

作者：

Okuda, M

Horn, HF

Tarapore, P

Tokuyama, Y

Smulian, AG

Chan, PK

Knudsen, ES

Hofmann, IA

Snyder, JD

Bove, KE

Fukasawa, K ^{[1
]}

机构：

[1] Univ Cincinnati, Coll Med, Dept Cell Biol Neurobiol & Anat, Cincinnati, OH 45267 USA

[2] Univ Cincinnati, Coll Med, Div Infect Dis, Cincinnati, OH 45267 USA

[3] Baylor Coll Med, Dept Pharmacol, Houston, TX 77030 USA

[4] Childrens Hosp Res Fdn, Cincinnati, OH 45229 USA

来源：

CELL | 2000年 / 103卷 / 01期

关键词：

D O I：

10.1016/S0092-8674(00)00093-3

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：

In animal cells, duplication of centrosomes and DNA is coordinated. Since CDK2/cyclin E triggers initiation of both events, activation of CDK2/cyclin E is thought to link these two events. We identified nucleophosmin (NPM/B23) as a substrate of CDK2/cyclin E in centrosome duplication. NPM/B23 associates specifically with unduplicated centrosomes, and NPM/B23 dissociates from centrosomes by CDK2/cyclin E-mediated phosphorylation. An anti-NPM/B23 antibody, which blocks this phosphorylation, suppresses the initiation of centrosome duplication in vivo. Moreover, expression of a nonphosphorylatable mutant NPM/ B23 in cells effectively blocks centrosome duplication. Thus, NPM/B23 is a target of CDK2/cyclin E in the initiation of centrosome duplication.

引用

页码：127 / 140

页数：14

共 39 条

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