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干扰素β-1b诱导G蛋白信号负调节因子RGS1的表达。

Interferonβ-1b Induces the Expression of RGS1 a Negative Regulator of G-Protein Signaling.

作者信息

Tran Tiffany, Paz Pedro, Velichko Sharlene, Cifrese Jill, Belur Praveen, Yamaguchi Ken D, Ku Karin, Mirshahpanah Parham, Reder Anthony T, Croze Ed

机构信息

Bayer HealthCare, Applied Research, Richmond, CA 94804, USA.

出版信息

Int J Cell Biol. 2010;2010:529376. doi: 10.1155/2010/529376. Epub 2011 Jan 17.

DOI:10.1155/2010/529376
PMID:21274427
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3026965/
Abstract

We present evidence of a link between interferonβ-1b (IFN-β) and G-protein signaling by demonstrating that IFN-β can induce the expression of the negative regulator of G-protein signaling 1 (RGS1). RGS1 reduces G-protein activation and immune cell migration by interacting with heterotrimeric G-proteins and enhancing their intrinsic GTPase activity. In this study, IFN-β treatment resulted in the induction of RGS1 in peripheral blood mononuclear cells (PBMCs), monocytes, T cells, and B cells. Induction of RGS1 by IFN-β was concentration dependent and observed at both the RNA and protein level. Other members of the RGS family were not induced by IFN-β, and induction of RGS1 required the activation of the IFN receptor. In addition, RGS1 induction was observed in PBMCs obtained from IFN-β-treated multiple sclerosis patients suggesting a possible, as yet unexplored, involvement of G-protein regulation in disease treatment. The upregulation of RGS1 by IFN-β has not been previously reported.

摘要

我们通过证明干扰素β-1b（IFN-β）可诱导G蛋白信号负调节因子1（RGS1）的表达，提供了IFN-β与G蛋白信号传导之间存在联系的证据。RGS1通过与异源三聚体G蛋白相互作用并增强其内在GTP酶活性，来降低G蛋白活化和免疫细胞迁移。在本研究中，IFN-β处理导致外周血单核细胞（PBMC）、单核细胞、T细胞和B细胞中RGS1的诱导。IFN-β对RGS1的诱导呈浓度依赖性，且在RNA和蛋白质水平均有观察到。RGS家族的其他成员未被IFN-β诱导，RGS1的诱导需要IFN受体的激活。此外，在从接受IFN-β治疗的多发性硬化症患者获得的PBMC中观察到RGS1的诱导，这表明G蛋白调节在疾病治疗中可能存在尚未探索的参与情况。IFN-β对RGS1的上调作用此前尚未见报道。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3879/3026965/ba2f9b9e0976/IJCB2010-529376.008.jpg
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本文引用的文献

1
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CNS Drugs. 2011 Jan;25(1):67-88. doi: 10.2165/11206430-000000000-00000.
2
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Genes Immun. 2010 Jul;11(5):397-405. doi: 10.1038/gene.2010.28. Epub 2010 Jun 17.
3
Integration of genetic risk factors into a clinical algorithm for multiple sclerosis susceptibility: a weighted genetic risk score.
一种 基因变异可预测 HBeAg 阳性慢性乙型肝炎患者聚乙二醇干扰素-α治疗应答。
J Clin Microbiol. 2024 Feb 14;62(2):e0139623. doi: 10.1128/jcm.01396-23. Epub 2024 Jan 23.
4
Gene expression analyses reveal differences in children's response to malaria according to their age.基因表达分析揭示了儿童对疟疾的反应因年龄而异。
bioRxiv. 2023 Oct 26:2023.10.24.563751. doi: 10.1101/2023.10.24.563751.
5
Stress-induced differential gene expression in cardiac tissue.应激诱导的心脏组织差异基因表达。
Sci Rep. 2021 Apr 28;11(1):9129. doi: 10.1038/s41598-021-88267-8.
6
The Effects of Juice Consumption on the mRNA Expression Profile in Peripheral Blood Mononuclear Cells in Subjects at Cardiovascular Risk.果汁摄入对心血管疾病风险人群外周血单个核细胞 mRNA 表达谱的影响。
Nutrients. 2020 May 20;12(5):1484. doi: 10.3390/nu12051484.
7
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J Clin Med. 2020 Feb 26;9(3):625. doi: 10.3390/jcm9030625.
8
Replication study of GWAS risk loci in Greek multiple sclerosis patients.GWAS 风险基因座在希腊多发性硬化症患者中的复制研究。
Neurol Sci. 2019 Feb;40(2):253-260. doi: 10.1007/s10072-018-3617-6. Epub 2018 Oct 26.
9
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Biochem Pharmacol. 2016 Aug 15;114:40-52. doi: 10.1016/j.bcp.2016.04.005. Epub 2016 Apr 9.
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AAPS J. 2016 May;18(3):545-9. doi: 10.1208/s12248-016-9883-4. Epub 2016 Feb 22.
将遗传风险因素整合到多发性硬化易感性临床算法中：加权遗传风险评分
Lancet Neurol. 2009 Dec;8(12):1111-9. doi: 10.1016/S1474-4422(09)70275-3. Epub 2009 Oct 29.
4
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BioDrugs. 2009;23(2):111-24. doi: 10.2165/00063030-200923020-00004.
5
Monocyte dependent regulation of autoimmune inflammation.单核细胞对自身免疫性炎症的依赖性调节。
Curr Mol Med. 2009 Feb;9(1):23-9. doi: 10.2174/156652409787314499.
6
New concepts on the pathogenesis of autoimmune diseases: a role for immune homeostasis, immunoregulation, and immunosenescence.自身免疫性疾病发病机制的新概念：免疫稳态、免疫调节和免疫衰老的作用。
Crit Rev Immunol. 2008;28(5):363-76. doi: 10.1615/critrevimmunol.v28.i5.10.
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J Neurol Sci. 2008 Nov 15;274(1-2):48-53. doi: 10.1016/j.jns.2008.06.029. Epub 2008 Aug 5.
10
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