H3K56Ac有别于其他位点的乙酰化修饰，这是一个位于核小体内部的球形区修饰，它的发现是表观遗传领域的一个小高潮。 围绕H3K56Ac修饰，众多科学家致力于揭示该修饰的功能，寻找该修饰相关的因子，并解析其结构解释其发挥作用的分子基础。 在进入正题前，先说说发现Rtt109的趣闻。 适逢其会，我博后期间加入Mayo Clinic 张志国教授的实验室，参与H3K56Ac在染色质的复制中作用，同时了解了催化该修饰的酶的发现过程。

2025年1月2日 · Here, we show that histone H3K56 acetylation (H3K56ac), a mark on newly-synthesized H3, facilitates the remodeling of disorganized nucleosomes in nascent chromatin, and its removal at the...

大量研究表明，H3 组蛋白 (H3K56ac) 56 位赖氨酸乙酰化在各种 DNA 事务中发挥着重要作用，包括对 DNA 损伤的反应及其与人类癌症的关联。 生物物理学研究表明，H3K56ac 通过促进 DNA 末端的自发和瞬时展开运动来增加 DNA 的可及性。 然而，这种乙酰化标记如何调节核小体结构和动力学，以促进修复因子和其他蛋白质接近受损 DNA，目前仍知之甚少。 在这里，我们利用大约 5-6 微秒的原子分子动力学模拟来描绘 H3K56 乙酰化对核小体结构和动力学的影响，并阐明当大 …

2019年9月26日 · Histone H3-K56 acetylation (H3K56Ac) enhances these turnover events and promotes nucleosome assembly during S phase. Here we sequence nascent transcripts to investigate the impact of H3K56Ac on...

2009年3月8日 · Acetylation within the globular core domain of histone H3 on lysine 56 (H3K56) has been shown to have a critical role in packaging DNA into chromatin during DNA replication and repair in budding...

2022年4月22日 · Importantly, genome-wide analyses demonstrated the general roles of H3K56 deacetylation and H2A.Z deposition in aberrant spreading of heterochromatin. Together, our results illustrate a previously unappreciated regulatory process that mediates aberrant heterochromatin spreading.

2009年3月8日 · 最近表明，赖氨酸 56 (h3k56) 上的组蛋白 h3 球状核心域内的乙酰化在 dna 复制和修复后将 dna 包装成染色质方面具有关键作用。

2012年4月13日 · We now report the presence of H3K56 monomethylation (H3K56me1) in mammalian cells and find that the histone lysine methytransferase G9a/KMT1C is required for H3K56me1 both in vivo and in vitro. We also find that disruption of …

2021年11月1日 · H3K56ac induces the nearby DNA to bulge away from the H3 histone and it distorts the H3 αN helix. H3K56ac causes more DNA exposure when it is damaged by a benzo [a]pyrene-derived lesion than when unmodified. H3K56ac amplifies the structural and dynamic distortions imposed by the DNA lesion.

2022年5月1日 · H3K56 acetylation is essential for conferring DNA accessibility during NER. Recruitment of NER factor Rad16 post UV is H3K56 acetylation dependent. H3K56 acetylation promotes UV-induced hyperacetylation of H3K9 and H3K14. H3K56 acetylation is thus a critical modification that regulate early NER events.