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

被引：1945

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 [理学]; 0710 [生物学]; 09 [农学];

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

页码：257 / 261

页数：5

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