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E2F and histone deacetylase mediate transforming growth factor beta repression of cdc25A during keratinocyte cell cycle arrest.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。
Mol Cell Biol. 1999 Jan;19(1):916-22. doi: 10.1128/MCB.19.1.916.
2
Serum-induced expression of the cdc25A gene by relief of E2F-mediated repression.通过解除E2F介导的抑制作用，血清诱导细胞周期蛋白依赖性激酶25A（cdc25A）基因的表达。
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E2F4-RB and E2F4-p107 complexes suppress gene expression by transforming growth factor beta through E2F binding sites.E2F4-RB和E2F4-p107复合物通过E2F结合位点转化生长因子β来抑制基因表达。
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E2F-Rb complexes assemble and inhibit cdc25A transcription in cervical carcinoma cells following repression of human papillomavirus oncogene expression.在人乳头瘤病毒癌基因表达受抑制后，E2F-Rb复合物在宫颈癌细胞中组装并抑制细胞周期蛋白依赖性激酶25A（cdc25A）转录。
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Human papillomavirus type 16 E7 maintains elevated levels of the cdc25A tyrosine phosphatase during deregulation of cell cycle arrest.在细胞周期阻滞失调期间，人乳头瘤病毒16型E7蛋白使细胞周期蛋白依赖性激酶25A（cdc25A）酪氨酸磷酸酶水平持续升高。
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本文引用的文献

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The regulation of E2F by pRB-family proteins.pRB 家族蛋白对 E2F 的调控。
Genes Dev. 1998 Aug 1;12(15):2245-62. doi: 10.1101/gad.12.15.2245.
2
TGF-beta1 actions on FRTL-5 cells provide a model for the physiological regulation of thyroid growth.转化生长因子β1（TGF-β1）对FRTL-5细胞的作用为甲状腺生长的生理调节提供了一个模型。
Oncogene. 1998 Mar;16(11):1455-65. doi: 10.1038/sj.onc.1201662.
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Rb interacts with histone deacetylase to repress transcription.Rb与组蛋白去乙酰化酶相互作用以抑制转录。
Cell. 1998 Feb 20;92(4):463-73. doi: 10.1016/s0092-8674(00)80940-x.
4
Retinoblastoma protein represses transcription by recruiting a histone deacetylase.视网膜母细胞瘤蛋白通过招募组蛋白去乙酰化酶来抑制转录。
Nature. 1998 Feb 5;391(6667):601-5. doi: 10.1038/35410.
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Retinoblastoma protein recruits histone deacetylase to repress transcription.视网膜母细胞瘤蛋白招募组蛋白去乙酰化酶以抑制转录。
Nature. 1998 Feb 5;391(6667):597-601. doi: 10.1038/35404.
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E2F activity is regulated by cell cycle-dependent changes in subcellular localization.E2F活性受亚细胞定位的细胞周期依赖性变化调控。
Mol Cell Biol. 1997 Dec;17(12):7268-82. doi: 10.1128/MCB.17.12.7268.
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Characterization of an E2F-p130 complex formed during growth arrest.生长停滞期间形成的E2F-p130复合物的特性分析。
Oncogene. 1997 Aug 7;15(6):657-68. doi: 10.1038/sj.onc.1201224.
8
pRB and p107/p130 are required for the regulated expression of different sets of E2F responsive genes.pRB以及p107/p130对于不同组E2F反应基因的调控表达是必需的。
Genes Dev. 1997 Jun 1;11(11):1447-63. doi: 10.1101/gad.11.11.1447.
9
Repression of the CDK activator Cdc25A and cell-cycle arrest by cytokine TGF-beta in cells lacking the CDK inhibitor p15.在缺乏细胞周期蛋白依赖性激酶（CDK）抑制剂p15的细胞中，细胞因子转化生长因子-β（TGF-β）对CDK激活剂Cdc25A的抑制作用及细胞周期阻滞。
Nature. 1997 May 22;387(6631):417-22. doi: 10.1038/387417a0.
10
Histone deacetylases associated with the mSin3 corepressor mediate mad transcriptional repression.与mSin3共抑制因子相关的组蛋白去乙酰化酶介导了mad转录抑制。
Cell. 1997 May 2;89(3):349-56. doi: 10.1016/s0092-8674(00)80215-9.

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.

DOI:10.1128/MCB.19.1.916
PMID:9858615
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC83949/
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。