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造血:深入了解 BET 蛋白。

Hematopoiesis: a BETter understanding.

机构信息

Sanford Burnham Prebys Medical Discovery Institute, La Jolla, CA, USA.

出版信息

EMBO Rep. 2023 Oct 9;24(10):e57927. doi: 10.15252/embr.202357927. Epub 2023 Aug 31.

Abstract

Epigenetic modifications are known to be crucial for hematopoietic stem cell (HSC) differentiation, with the BET family member BRD4 playing a vital role in this as an epigenetic reader. In this issue of EMBO reports, Yang et al (2023) demonstrate that the absence of BRD4 leads to senescence in HSCs and hematopoietic progenitor cells (HPCs), affecting the expression of crucial genes involved in myeloid and erythroid development. These data suggest that BRD4 has a protective role in preserving histone tails, thereby sustaining normal HSC/HPC functions.

摘要

表观遗传修饰对于造血干细胞(HSC)分化至关重要,BET 家族成员 BRD4 作为一种表观遗传读取器在这方面起着至关重要的作用。在本期《EMBO 报告》中,Yang 等人(2023 年)表明 BRD4 的缺失会导致 HSCs 和造血祖细胞(HPCs)衰老,影响涉及髓系和红细胞发育的关键基因的表达。这些数据表明,BRD4 具有保护组蛋白尾巴的作用,从而维持正常的 HSC/HPC 功能。

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本文引用的文献

1
Loss of BRD4 induces cell senescence in HSC/HPCs by deregulating histone H3 clipping.
EMBO Rep. 2023 Oct 9;24(10):e57032. doi: 10.15252/embr.202357032. Epub 2023 Aug 31.
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Signal Transduct Target Ther. 2023 Feb 17;8(1):71. doi: 10.1038/s41392-023-01342-6.
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