INHIBITION OF RAS-INDUCED PROLIFERATION AND CELLULAR-TRANSFORMATION BY P16(INK4)

被引：413

作者：

SERRANO, M

GOMEZLAHOZ, E

DEPINHO, RA

BEACH, D

BARSAGI, D

机构：

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

[2] ALBERT EINSTEIN COLL MED, DEPT IMMUNOL & MICROBIOL, NEW YORK, NY 10461 USA

[3] ALBERT EINSTEIN COLL MED, DEPT MED, NEW YORK, NY 10461 USA

来源：

SCIENCE | 1995年 / 267卷 / 5195期

关键词：

D O I：

10.1126/science.7809631

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：

The cyclin-dependent kinase 4 (CDK4) regulates progression through the G(1) phase of the cell cycle. The activity of CDK4 is controlled by the opposing effects of the D-type cyclin, an activating subunit, and p16(INK4), inhibitory subunit. Ectopic expression of p16(INK4) blocked entry into S phase of the cell cycle induced by oncogenic Ha-Ras, and this block was relieved by coexpression of a catalytically inactive CDK4 mutant. Expression of p16(INK4) suppressed cellular transformation of primary rat embryo fibroblasts by oncogenic Ha-Ras and Myc, but not by Ha-Ras and E1a. Together, these observations provide direct evidence that p16(INK4) inhibit cell growth.

引用

页码：249 / 252

页数：4

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