P15(INK4B) IS A POTENTIAL EFFECTOR OF TGF-BETA-INDUCED CELL-CYCLE ARREST

被引：1920
|
作者：
HANNON, GJ [1 ]
BEACH, D [1 ]
机构：
[1] COLD SPRING HARBOR LAB,HOWARD HUGHES MED INST,COLD SPRING HARBOR,NY 11724
来源：
NATURE | 1994年 / 371卷 / 6494期
关键词：
D O I：
10.1038/371257a0
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：
TRANSFORMING growth factor-beta (TGF-beta) inhibits cell proliferation by inducing a G1-phase cell cycle arrest(1). Normal progression through G1 is promoted by the activity of the cyclin-dependent protein kinases CDK4 and CDK6 (ref. 2), which are inhibited by the protein p16(INK4). We have isolated a new member of the p16(INK4) family, p15(INK4B). p15 expression is induced similar to 30-fold in human keratinocytes by treatment with TGF-beta, suggesting that p15 may act as an effector of TGF-beta-mediated cell cycle arrest. The gene encoding p15 is located on chromosome 9 adjacent to the p16 gene at a frequent site of chromosomal abnormality in human tumours (9p21).
引用
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页码：257 / 261
页数：5
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