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本文引用的文献

1
HPV16-E6 associated hTERT promoter acetylation is E6AP dependent, increased in later passage cells and enhanced by loss of p300.人乳头瘤病毒16型E6（HPV16-E6）相关的端粒酶逆转录酶（hTERT）启动子乙酰化依赖于E6相关蛋白（E6AP），在传代后期细胞中增加，并因p300缺失而增强。
Int J Cancer. 2006 Oct 15;119(8):1878-85. doi: 10.1002/ijc.22064.
2
p53-Dependent transcriptional repression of c-myc is required for G1 cell cycle arrest.G1期细胞周期阻滞需要p53依赖的c-myc转录抑制。
Mol Cell Biol. 2005 Sep;25(17):7423-31. doi: 10.1128/MCB.25.17.7423-7431.2005.
3
Hormones and growth factors regulate telomerase activity in ageing and cancer.激素和生长因子在衰老和癌症过程中调节端粒酶活性。
Mol Cell Endocrinol. 2005 Aug 30;240(1-2):11-22. doi: 10.1016/j.mce.2005.05.009.
4
mSin3A corepressor regulates diverse transcriptional networks governing normal and neoplastic growth and survival.mSin3A共抑制因子调控着多种转录网络，这些网络控制着正常及肿瘤性生长与存活。
Genes Dev. 2005 Jul 1;19(13):1581-95. doi: 10.1101/gad.1286905.
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Genomic maps and comparative analysis of histone modifications in human and mouse.人类和小鼠的基因组图谱及组蛋白修饰的比较分析
Cell. 2005 Jan 28;120(2):169-81. doi: 10.1016/j.cell.2005.01.001.
6
The E6AP ubiquitin ligase is required for transactivation of the hTERT promoter by the human papillomavirus E6 oncoprotein.人乳头瘤病毒E6癌蛋白对hTERT启动子进行反式激活需要E6AP泛素连接酶。
J Biol Chem. 2005 Mar 18;280(11):10807-16. doi: 10.1074/jbc.M410343200. Epub 2005 Jan 17.
7
Chd1 chromodomain links histone H3 methylation with SAGA- and SLIK-dependent acetylation.Chd1染色质结构域将组蛋白H3甲基化与SAGA和SLIK依赖性乙酰化联系起来。
Nature. 2005 Jan 27;433(7024):434-8. doi: 10.1038/nature03242. Epub 2005 Jan 12.
8
Identification of a novel telomerase repressor that interacts with the human papillomavirus type-16 E6/E6-AP complex.一种与16型人乳头瘤病毒E6/E6-AP复合物相互作用的新型端粒酶抑制因子的鉴定。
Genes Dev. 2004 Sep 15;18(18):2269-82. doi: 10.1101/gad.1214704.
9
Upregulation of the Catalytic Telomerase Subunit by the Transcription Factor ER81 and Oncogenic HER2/Neu, Ras, or Raf.转录因子ER81与致癌性HER2/Neu、Ras或Raf对端粒酶催化亚基的上调作用。
Mol Cell Biol. 2004 Jan;24(1):25-35. doi: 10.1128/MCB.24.1.25-35.2004.
10
Regulation of telomerase reverse transcriptase gene activity by upstream stimulatory factor.上游刺激因子对端粒酶逆转录酶基因活性的调控
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NFX1与mSin3A/组蛋白去乙酰化酶相互作用，以抑制角质形成细胞中hTERT的转录。

NFX1 interacts with mSin3A/histone deacetylase to repress hTERT transcription in keratinocytes.

作者信息

Xu Mei, Luo Weifeng, Elzi David J, Grandori Carla, Galloway Denise A

机构信息

Division of Human Biology, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109, USA.

出版信息

Mol Cell Biol. 2008 Aug;28(15):4819-28. doi: 10.1128/MCB.01969-07. Epub 2008 May 27.

DOI:10.1128/MCB.01969-07
PMID:18505829
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2493374/
Abstract

Transcription of the catalytic subunit of telomerase (hTERT) in keratinocytes can be induced by human papillomavirus type 16 (HPV16) E6/E6AP ubiquitin ligase through degradation of the repressor, NFX1-91. Here, we demonstrate that NFX1-91 interacts with the corepressor complex mSin3A/histone deacetylase (HDAC) at the hTERT promoter. By degrading NFX1-91, E6/E6AP changes the chromatin structure at the hTERT promoter as indicated by enhanced acetylation of histones H3 and H4 as well as dimethylation of H3K4. Knockdown of NFX1-91 by short hairpin RNA (shRNA) mimics the effect of E6 and leads to acetylation of histones H3 and H4. Conversely, knockdown of E6AP by shRNA suppresses histone acetylation at the hTERT promoter. These data demonstrate that targeted degradation of NFX1-91 by E6/E6AP dissociates the mSin3A/HDAC complex from the hTERT promoter and induces hTERT transcription.

摘要

人乳头瘤病毒16型（HPV16）E6/E6相关蛋白（E6AP）泛素连接酶可通过降解阻遏物NFX1-91来诱导角质形成细胞中端粒酶催化亚基（hTERT）的转录。在此，我们证明NFX1-91在hTERT启动子处与共阻遏复合物mSin3A/组蛋白去乙酰化酶（HDAC）相互作用。通过降解NFX1-91，E6/E6AP改变了hTERT启动子处的染色质结构，这表现为组蛋白H3和H4乙酰化增强以及H3K4二甲基化。用短发夹RNA（shRNA）敲低NFX1-91模拟了E6的作用，并导致组蛋白H3和H4乙酰化。相反，用shRNA敲低E6AP可抑制hTERT启动子处的组蛋白乙酰化。这些数据表明，E6/E6AP对NFX1-91的靶向降解使mSin3A/HDAC复合物从hTERT启动子上解离，并诱导hTERT转录。