E2F和组蛋白去乙酰化酶在角质形成细胞周期停滞期间介导转化生长因子β对cdc25A的抑制作用。
E2F and histone deacetylase mediate transforming growth factor beta repression of cdc25A during keratinocyte cell cycle arrest.
作者信息
Iavarone A, Massagué J
机构信息
Cell Biology Program and Howard Hughes Medical Institute, Memorial Sloan-Kettering Cancer Center, New York, New York, USA.
出版信息
Mol Cell Biol. 1999 Jan;19(1):916-22. doi: 10.1128/MCB.19.1.916.
Abstract
cdc25A is a tyrosine phosphatase that activates G1 cyclin-dependent kinases (Cdk's). In human keratinocytes, cdc25A expression is down-regulated after the initial drop in Cdk activity caused by cell exposure to the antimitogenic cytokine transforming growth factor beta (TGF-beta) or removal of serum factors. Here we show that the TGF-beta-inhibitory-response element in the cdc25A promoter maps to an E2F site at nucleotides -62 to -55 from the transcription start site. This site is not required for basal transcription in keratinocytes. We provide evidence that the cell cycle arrest program activated by TGF-beta in human keratinocytes includes the generation of E2F4-p130 complexes that in association with histone deacetylase HDAC1 inhibit the activity of the cdc25A promoter from this repressor E2F site. This mechanism is part of a program that places keratinocytes in the quiescent state following the initial drop in Cdk activity caused by cell exposure to TGF-beta.
摘要
细胞周期蛋白依赖性激酶25A（cdc25A）是一种酪氨酸磷酸酶，可激活G1期细胞周期蛋白依赖性激酶（Cdk）。在人角质形成细胞中，细胞暴露于抗有丝分裂细胞因子转化生长因子β（TGF-β）或去除血清因子导致Cdk活性最初下降后，cdc25A的表达会下调。在此我们表明，cdc25A启动子中的TGF-β抑制反应元件定位于转录起始位点上游核苷酸-62至-55处的一个E2F位点。该位点对于角质形成细胞中的基础转录并非必需。我们提供的证据表明，TGF-β在人角质形成细胞中激活的细胞周期停滞程序包括生成E2F4-p130复合物，该复合物与组蛋白脱乙酰酶HDAC1结合，从这个阻遏性E2F位点抑制cdc25A启动子的活性。这种机制是一个程序的一部分，该程序使角质形成细胞在细胞暴露于TGF-β导致Cdk活性最初下降后进入静止状态。
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