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蛋白质精氨酸甲基转移酶1(PRMT1)在对选择性抑制和DNA损伤作出反应的胞质小体中积累。

PRMT1 arginine methyltransferase accumulates in cytoplasmic bodies that respond to selective inhibition and DNA damage.

作者信息

Suchánková J, Legartová S, Sehnalová P, Kozubek S, Valente S, Labella D, Mai A, Eckerich C, Fackelmayer F O, Sorokin D V, Bartova E

机构信息

Academy of Sciences of the Czech Republic.

出版信息

Eur J Histochem. 2014 May 2;58(2):2389. doi: 10.4081/ejh.2014.2389.

Abstract

Protein arginine methyltransferases (PRMTs) are responsible for symmetric and asymmetric methylation of arginine residues of nuclear and cytoplasmic proteins. In the nucleus, PRMTs belong to important chromatin modifying enzymes of immense functional significance that affect gene expression, splicing and DNA repair. By time-lapse microscopy we have studied the sub-cellular localization and kinetics of PRMT1 after inhibition of PRMT1 and after irradiation. Both transiently expressed and endogenous PRMT1 accumulated in cytoplasmic bodies that were located in the proximity of the cell nucleus. The shape and number of these bodies were stable in untreated cells. However, when cell nuclei were microirradiated by UV-A, the mobility of PRMT1 cytoplasmic bodies increased, size was reduced, and disappeared within approximately 20 min. The same response occurred after γ-irradiation of the whole cell population, but with delayed kinetics. Treatment with PRMT1 inhibitors induced disintegration of these PRMT1 cytoplasmic bodies and prevented formation of 53BP1 nuclear bodies (NBs) that play a role during DNA damage repair. The formation of 53BP1 NBs was not influenced by PRMT1 overexpression. Taken together, we show that PRMT1 concentrates in cytoplasmic bodies, which respond to DNA injury in the cell nucleus, and to treatment with various PRMT1 inhibitors.

摘要

蛋白质精氨酸甲基转移酶(PRMTs)负责核蛋白和胞质蛋白中精氨酸残基的对称和不对称甲基化。在细胞核中,PRMTs属于具有重要功能意义的重要染色质修饰酶,可影响基因表达、剪接和DNA修复。通过延时显微镜观察,我们研究了PRMT1在受到抑制以及照射后的亚细胞定位和动力学。瞬时表达的和内源性的PRMT1均聚集在位于细胞核附近的胞质小体中。在未处理的细胞中,这些小体的形状和数量是稳定的。然而,当细胞核受到UV-A微照射时,PRMT1胞质小体的移动性增加,尺寸减小,并在大约20分钟内消失。对整个细胞群体进行γ照射后也出现了相同的反应,但动力学延迟。用PRMT1抑制剂处理会导致这些PRMT1胞质小体解体,并阻止在DNA损伤修复过程中发挥作用的53BP1核小体(NBs)的形成。53BP1 NBs的形成不受PRMT1过表达的影响。综上所述,我们表明PRMT1集中在胞质小体中,这些胞质小体对细胞核中的DNA损伤以及各种PRMT1抑制剂的处理有反应。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8db6/4083328/d710d41b5d55/ejh-2014-2-2389-g001.jpg

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