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1
Regenerating muscle with arginine methylation.利用精氨酸甲基化再生肌肉。
Transcription. 2017 May 27;8(3):175-178. doi: 10.1080/21541264.2017.1291083. Epub 2017 Feb 17.
2
Protein arginine methylation regulates insulin signaling in L6 skeletal muscle cells.蛋白质精氨酸甲基化调节L6骨骼肌细胞中的胰岛素信号传导。
Biochem Biophys Res Commun. 2007 Dec 28;364(4):1015-21. doi: 10.1016/j.bbrc.2007.10.113. Epub 2007 Oct 29.
3
Arginine Methylation by PRMT1 Regulates Muscle Stem Cell Fate.PRMT1介导的精氨酸甲基化调控肌肉干细胞命运。
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Protein arginine methyltransferase biology in humans during acute and chronic skeletal muscle plasticity.在急性和慢性骨骼肌重塑过程中人类的蛋白质精氨酸甲基转移酶生物学。
J Appl Physiol (1985). 2019 Sep 1;127(3):867-880. doi: 10.1152/japplphysiol.00142.2019. Epub 2019 Aug 1.
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Arginine Methylation: The Coming of Age.精氨酸甲基化：崭露头角。
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Characterization of the Drosophila protein arginine methyltransferases DART1 and DART4.果蝇蛋白精氨酸甲基转移酶DART1和DART4的特性分析。
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Regulation of post-translational protein arginine methylation during HeLa cell cycle.HeLa细胞周期中蛋白质精氨酸甲基化修饰后的调控
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J Biol Chem. 2022 Sep;298(9):102290. doi: 10.1016/j.jbc.2022.102290. Epub 2022 Jul 20.

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Protein arginine methyltransferases PRMT1, PRMT4/CARM1 and PRMT5 have distinct functions in control of osteoblast differentiation.蛋白质精氨酸甲基转移酶PRMT1、PRMT4/CARM1和PRMT5在成骨细胞分化调控中具有不同功能。
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Protein arginine methyltransferase biology in humans during acute and chronic skeletal muscle plasticity.在急性和慢性骨骼肌重塑过程中人类的蛋白质精氨酸甲基转移酶生物学。
J Appl Physiol (1985). 2019 Sep 1;127(3):867-880. doi: 10.1152/japplphysiol.00142.2019. Epub 2019 Aug 1.
9
Asymmetric and Symmetric Protein Arginine Dimethylation: Concept and Postprandial Effects of High-Fat Protein Meals in Healthy Overweight Men.非对称和对称蛋白精氨酸二甲基化：健康超重男性高脂高蛋白膳食的概念和餐后效应。
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PRMT7 as a unique member of the protein arginine methyltransferase family: A review.PRMT7 作为蛋白质精氨酸甲基转移酶家族的独特成员：综述。
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本文引用的文献

1
Arginine Methylation: The Coming of Age.精氨酸甲基化：崭露头角。
Mol Cell. 2017 Jan 5;65(1):8-24. doi: 10.1016/j.molcel.2016.11.003.
2
Arginine Methylation by PRMT1 Regulates Muscle Stem Cell Fate.PRMT1介导的精氨酸甲基化调控肌肉干细胞命运。
Mol Cell Biol. 2017 Jan 19;37(3). doi: 10.1128/MCB.00457-16. Print 2017 Feb 1.
3
PRMT7 Preserves Satellite Cell Regenerative Capacity.蛋白质精氨酸甲基转移酶7维持卫星细胞的再生能力。
Cell Rep. 2016 Feb 16;14(6):1528-1539. doi: 10.1016/j.celrep.2016.01.022. Epub 2016 Feb 4.
4
Prmt5 is a regulator of muscle stem cell expansion in adult mice.Prmt5是成年小鼠肌肉干细胞增殖的调节因子。
Nat Commun. 2015 Jun 1;6:7140. doi: 10.1038/ncomms8140.
5
Carm1 regulates Pax7 transcriptional activity through MLL1/2 recruitment during asymmetric satellite stem cell divisions.Carm1 通过募集 MLL1/2 来调节 Pax7 的转录活性，从而在不对称卫星干细胞分裂过程中发挥作用。
Cell Stem Cell. 2012 Sep 7;11(3):333-45. doi: 10.1016/j.stem.2012.07.001. Epub 2012 Aug 2.
6
An absolute requirement for Pax7-positive satellite cells in acute injury-induced skeletal muscle regeneration.Pax7 阳性卫星细胞对于急性损伤诱导的骨骼肌再生是绝对必需的。
Development. 2011 Sep;138(17):3639-46. doi: 10.1242/dev.067595.
7
Polycomb EZH2 controls self-renewal and safeguards the transcriptional identity of skeletal muscle stem cells.多梳抑制酶 EZH2 控制着骨骼肌干细胞的自我更新和转录特性。
Genes Dev. 2011 Apr 15;25(8):789-94. doi: 10.1101/gad.2027911.
8
Eya protein phosphatase activity regulates Six1-Dach-Eya transcriptional effects in mammalian organogenesis.Eya蛋白磷酸酶活性在哺乳动物器官发生过程中调节Six1-Dach-Eya转录效应。
Nature. 2003 Nov 20;426(6964):247-54. doi: 10.1038/nature02083.
9
MyoD-induced expression of p21 inhibits cyclin-dependent kinase activity upon myocyte terminal differentiation.MyoD诱导的p21表达在肌细胞终末分化时抑制细胞周期蛋白依赖性激酶活性。
Mol Cell Biol. 1995 Jul;15(7):3823-9. doi: 10.1128/MCB.15.7.3823.

利用精氨酸甲基化再生肌肉。

Regenerating muscle with arginine methylation.

作者信息

Blanc Roméo S, Richard Stéphane

机构信息

a Terry Fox Molecular Oncology Group and the Bloomfield Center for Research on Aging, Lady Davis Institute for Medical Research, Sir Mortimer B. Davis Jewish General Hospital , Montréal , Québec , Canada.

b Departments of Oncology and Medicine , McGill University , Montréal , Québec , Canada.

出版信息

Transcription. 2017 May 27;8(3):175-178. doi: 10.1080/21541264.2017.1291083. Epub 2017 Feb 17.

DOI:10.1080/21541264.2017.1291083
PMID:28301308
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5501374/
Abstract

Protein arginine methyltransferase (PRMT) is a family of nine proteins catalyzing the methylation of arginine residues. They were recently shown to be essential for proper regeneration of skeletal muscles. However, the mechanisms triggering the methylation event, as well as how the methylated substrates regulate muscle stem cell function and fate decision remain to be determined. This point-of-view will discuss the recent findings on the specific role of PRMT1, CARM1/PRMT4, PRMT5, and PRMT7 in muscle stem cell fate guidance, and shed light on the future challenges which could help defining the therapeutic potential of PRMT inhibitors against muscular disorders and aging.

摘要

蛋白质精氨酸甲基转移酶（PRMT）是一个由九种蛋白质组成的家族，可催化精氨酸残基的甲基化。最近研究表明，它们对于骨骼肌的正常再生至关重要。然而，引发甲基化事件的机制，以及甲基化底物如何调节肌肉干细胞功能和命运决定仍有待确定。本观点将讨论PRMT1、CARM1/PRMT4、PRMT5和PRMT7在肌肉干细胞命运引导中的特定作用的最新发现，并阐明未来的挑战，这些挑战可能有助于确定PRMT抑制剂针对肌肉疾病和衰老的治疗潜力。