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Stem cell epigenetics最新文献

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Pub Date : 2020-01-01 DOI: 10.1016/b978-0-12-814085-7.10000-5
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引用次数: 0
Copyright 版权
Pub Date : 2020-01-01 DOI: 10.1016/b978-0-12-814085-7.09993-1
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引用次数: 0
Contributors 贡献者
Pub Date : 2020-01-01 DOI: 10.1016/b978-0-12-814085-7.09990-6
S. Aranda, O. A. Arcidiacono, Jérôme Artus, E. Bártová, S. Battle, D. Bavli, A. Biran, M. R. Branco, R. Bressan, N. Caporale, L. Di Croce, Camille Dion, Inma Gonzalez, R. D. Hawkins, Chen Kozulin, J. Krejčí, Soňa Legartová, Harry G. Leitch, Alejandro López-Tobón, J. E. Mermoud, E. Meshorer, P. Navarro, Nick D. L. Owens, A. Platania, S. Pollard, R. Poot, Oren Ram, Sharon Schlesinger, T. Sexton, L. Stixová, G. Testa, Sebastiano Trattaro
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引用次数: 0
Bacterial Short Chain Fatty Acids Push All The Buttons Needed To Reactivate Latent Viruses. 细菌短链脂肪酸推动所有需要重新激活潜伏病毒的按钮。
Pub Date : 2015-01-01 DOI: 10.14800/sce.532
Fengchun Ye, Jonathan Karn

The genomes of herpesviruses and HIV become silent during latency through multiple chromatin silencing mechanisms including: histone deacetylation, repressive histone methylation, and DNA methylation. Reactivation of the latent virus requires removal of the chromatin silencing marks and their replacement by activating modifications such as histone acetylation and activating histone methylation. In a complementary mechanism, RNA Polymerase II (RNAP II) elongation is regulated by the positive transcription elongation factor b (P-TEFb)-dependent phosphorylation of Ser2 residues on its C-terminal domain. In resting T-cells latently infected by HIV, expression of P-TEFb is restricted. We found that a group of short chain fatty acids (SCFAs) produced by oral bacteria not only promote histone acetylation but also change the histone methylation dynamics by decreasing repressive histone methylation while increasing activating histone methylation. SCFAs also block DNA methylation and activate P-TEFb to enable elongation of stalled RNA polymerase II. Thus these molecules do not simply act as histone deacetylase (HDAC) inhibitors as previously claimed. Instead, they impact multiple complementary epigenetic regulatory mechanisms to promote highly efficient reactivation of latent viruses.

疱疹病毒和HIV的基因组通过多种染色质沉默机制在潜伏期沉默,包括:组蛋白去乙酰化、抑制性组蛋白甲基化和DNA甲基化。潜伏病毒的再激活需要去除染色质沉默标记,并通过激活组蛋白乙酰化和组蛋白甲基化等修饰来替代它们。在一个互补的机制中,RNA聚合酶II (RNAP II)的延伸受正转录延伸因子b (P-TEFb)依赖于其c端结构域Ser2残基磷酸化的调控。在潜伏感染HIV的静止t细胞中,P-TEFb的表达受到限制。我们发现口腔细菌产生的一组短链脂肪酸(SCFAs)不仅促进组蛋白乙酰化,而且通过降低抑制性组蛋白甲基化而增加激活性组蛋白甲基化来改变组蛋白甲基化动力学。SCFAs还阻断DNA甲基化,激活P-TEFb,使停滞的RNA聚合酶II延长。因此,这些分子并不像先前声称的那样,仅仅作为组蛋白去乙酰化酶(HDAC)抑制剂。相反,它们影响多种互补的表观遗传调控机制,以促进潜伏病毒的高效再激活。
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引用次数: 17
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Stem cell epigenetics
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