CDC25 PHOSPHATASES AS POTENTIAL HUMAN ONCOGENES

被引：513

作者：

GALAKTIONOV, K

LEE, AK

ECKSTEIN, J

DRAETTA, G

MECKLER, J

LODA, M

BEACH, D

机构：

[1] COLD SPRING HARBOR LAB, HOWARD HUGHES MED INST, COLD SPRING HARBOR, NY 11724 USA

[2] HARVARD UNIV, SCH MED, LAHEY CLIN MED CTR, BURLINGTON, MA 01805 USA

[3] MITOTIX, CAMBRIDGE, MA 02139 USA

[4] HARVARD UNIV, DEACONESS HOSP, SCH MED, DEPT PATHOL, BOSTON, MA 02215 USA

来源：

SCIENCE | 1995年 / 269卷 / 5230期

关键词：

D O I：

10.1126/science.7667636

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

Cyclin-dependent kinases (CDKs) are activated by CDC25 phosphatases, which remove inhibitory phosphate from tyrosine and threonine residues. In human cells, CDC25 proteins are encoded by a multigene family, consisting of CDC25A, CDC25B, and CDC25C. In rodent cells, human CDC25A or CDC25B but not CDC25C phosphatases cooperate with either Ha-RAS(G12V) or loss of RB1 in oncogenic focus formation. Such transformants were highly aneuploid, grew in soft agar, and formed high-grade tumors in nude mice. Overexpression of CDC25B was detected in 32 percent of human primary breast cancers tested. The CDC25 phosphatases may contribute to the development of human cancer.

引用

页码：1575 / 1577

页数：3

共 46 条

[11] CELL-CYCLE REGULATION OF CDK2 ACTIVITY BY PHOSPHORYLATION OF THR160 AND TYR15 [J].