P15(INK4B) IS A POTENTIAL EFFECTOR OF TGF-BETA-INDUCED CELL-CYCLE ARREST
P15(INK4B) IS A POTENTIAL EFFECTOR OF TGF-BETA-INDUCED CELL-CYCLE ARREST
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DOI：
10.1038/371257a0
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发表时间：
1994-09-15
期刊：
影响因子：
64.8
通讯作者：
BEACH, D
中科院分区：
文献类型：
--
作者：
HANNON, GJ;BEACH, D
转化生长因子- β (tgf - β)通过诱导g1期细胞周期阻滞来抑制细胞增殖(1)。细胞周期蛋白依赖性蛋白激酶CDK4和CDK6的活性促进了G1的正常进展（参考文献2），它们被蛋白p16（INK4）抑制。我们分离出p16（INK4）家族的新成员p15（INK4B）。在人角质形成细胞中，tgf - β可诱导p15的表达达到30倍，这表明p15可能是tgf - β介导的细胞周期阻滞的效应因子。编码p15的基因位于人类肿瘤中染色体异常的常见位点9号染色体上，毗邻p16基因（9p21）。
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).