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连接组蛋白H1.5在分化和致癌过程中是一个被低估的因素。

Linker histone H1.5 is an underestimated factor in differentiation and carcinogenesis.

作者信息

Behrends Marthe, Engmann Olivia

机构信息

Faculty of Medicine, Friedrich Schiller Universität, Jena, Thüringen 07747, Germany.

Institute for Human Genetics, Jena University Hospital, Am Klinikum 1, Thüringen 07747, Germany.

出版信息

Environ Epigenet. 2020 Oct 3;6(1):dvaa013. doi: 10.1093/eep/dvaa013. eCollection 2020.

DOI:10.1093/eep/dvaa013
PMID:33214908
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7660118/
Abstract

Human histone H1.5, in mice called H1b, belongs to the family of linker histones (H1), which are key players in chromatin organization. These proteins sit on top of nucleosomes, in part to stabilize them, and recruit core histone modifying enzymes. Through subtype-specific deposition patterns and numerous post-translational modifications, they fine-tune gene expression and chromatin architecture, and help to control cell fate and homeostasis. However, even though it is increasingly implicated in mammalian development, H1.5 has not received as much research attention as its relatives. Recent studies have focused on its prognostic value in cancer patients and its contribution to tumorigenesis through specific molecular mechanisms. However, many functions of H1.5 are still poorly understood. In this review, we will summarize what is currently known about H1.5 and its function in cell differentiation and carcinogenesis. We will suggest key experiments that are required to understand the molecular network, in which H1.5 is embedded. These experiments will advance our understanding of the epigenetic reprogramming occurring in developmental and carcinogenic processes.

摘要

人类组蛋白H1.5,在小鼠中称为H1b,属于连接组蛋白(H1)家族,是染色质组织的关键参与者。这些蛋白质位于核小体之上,部分作用是使其稳定,并募集核心组蛋白修饰酶。通过亚型特异性沉积模式和众多翻译后修饰,它们微调基因表达和染色质结构,并有助于控制细胞命运和体内平衡。然而,尽管H1.5越来越多地参与哺乳动物发育,但它并未像其亲属那样受到同样多的研究关注。最近的研究集中在其在癌症患者中的预后价值以及通过特定分子机制对肿瘤发生的贡献。然而,H1.5的许多功能仍知之甚少。在本综述中,我们将总结目前关于H1.5及其在细胞分化和致癌作用中的功能的了解。我们将提出了解H1.5所嵌入的分子网络所需的关键实验。这些实验将推进我们对发育和致癌过程中发生的表观遗传重编程的理解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4598/7660118/44a61212e833/dvaa013f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4598/7660118/8d0b1a3e0b16/dvaa013f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4598/7660118/44a61212e833/dvaa013f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4598/7660118/8d0b1a3e0b16/dvaa013f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4598/7660118/44a61212e833/dvaa013f2.jpg

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