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Splicing factor SF3B3,a NS5-binding protein,restricts ZIKV infection by targeting GCH1
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作者 Tanxiu Chen Hao Yang +13 位作者 Penghui Liu Moliduer Hamiti Xintian Zhang Yi Xu Wenqi Quan Yong Zhang Wenhai Yu Li Jiao Tingfu Du Juemin Xi Bin Yin Wei Zhou Shuaiyao Lu Xiaozhong Peng 《Virologica Sinica》 SCIE CAS CSCD 2023年第2期222-232,共11页
Zika virus(ZIKV),a positive-sense single-stranded RNA virus,causes congenital ZIKV syndrome in children and Guillain-Barre Syndrome(GBS)in adults.ZIKV expresses nonstructural protein 5(NS5),a large protein that is ess... Zika virus(ZIKV),a positive-sense single-stranded RNA virus,causes congenital ZIKV syndrome in children and Guillain-Barre Syndrome(GBS)in adults.ZIKV expresses nonstructural protein 5(NS5),a large protein that is essential for viral replication.ZIKV NS5 confers the ability to evade interferon(IFN)signalling;however,the exact mechanism remains unclear.In this study,we employed affinity pull-down and liquid chromatography-tandem mass spectrometry(LC-MS/MS)analyses and found that splicing factor 3b subunit 3(SF3B3)is associated with the NS5-Flag pull-down complex through interaction with NS5.Functional assays showed that SF3B3 overexpression inhibited ZIKV replication by promoting IFN-stimulated gene(ISG)expression whereas silencing of SF3B3 inhibited expression of ISGs to promote ZIKV replication.GTP cyclohydrolase I(GCH1)is the first and ratelimiting enzyme in tetrahydrobiopterin(BH4)biosynthesis.NS5 upregulates the expression of GCH1 during ZIKV infection.And GCH1 marginally promoted ZIKV replication via the IFN pathway.Additionally,GCH1 expression is related to the regulation of SF3B3.Overexpression of the SF3B3 protein effectively reduced GCH1 protein levels,whereas SF3B3 knockdown increased its levels.These findings indicated that ZIKV NS5 binding protein SF3B3 contributed to the host immune response against ZIKV replication by modulating the expression of GCH1. 展开更多
关键词 Nonstructural protein 5(NS5) Splicing factor 3b subunit 3(sf3b3) GTP cyclohydrolase I(GCH1) IFN-stimulated gene(ISGs) IFN signalling Pathway
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Multi-omics approaches identify SF3B3 and SIRT3 as candidate autophagic regulators and druggable targets in invasive breast carcinoma 被引量:5
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作者 Shouyue Zhang Jin Zhang +5 位作者 Yang An Xiaoxi Zeng Ziyi Qin Yuqian Zhao Heng Xu Bo Liu 《Acta Pharmaceutica Sinica B》 SCIE CAS CSCD 2021年第5期1227-1245,共19页
Autophagy is a critical cellular homeostatic mechanism,and its dysfunction is linked to invasive breast carcinoma(BRCA).Recently,several omics methods have been applied to explore autophagic regulators in BRCA;however... Autophagy is a critical cellular homeostatic mechanism,and its dysfunction is linked to invasive breast carcinoma(BRCA).Recently,several omics methods have been applied to explore autophagic regulators in BRCA;however,more reliable and robust approaches for identifying crucial regulators and druggable targets remain to be discovered.Thus,we report here the results of multi-omics approaches to identify potential autophagic regulators in BRCA,including gene expression(EXP),DNA methylation(MET)and copy number alterations(CNAs)from The Cancer Genome Atlas(TCGA).Newly identified candidate genes,such as SF3 B3,TRAPPC10,SIRT3,MTERFD1,and FBXO5,were confirmed to be involved in the positive or negative regulation of autophagy in BRCA.SF3 B3 was identified firstly as a negative autophagic regulator,and siRNA/shRNA-SF3 B3 were shown to induce autophagyassociated cell death in in vitro and in vivo breast cancer models.Moreover,a novel small-molecule activator of SIRT3,1-methylbenzylamino amiodarone,was discovered to induce autophagy in vitro and in vivo.Together,these results provide multi-omics approaches to identify some key candidate autophagic regulators,such as the negative regulator SF3 B3 and positive regulator SIRT3 in BRCA,and highlight SF3 B3 and SIRT3 as new druggable targets that could be used to fill the gap between autophagy and cancer drug development. 展开更多
关键词 Invasive breast carcinoma Multi-omics approach SIRT3 sf3b3 Autophagic regulator ANTI-PROLIFERATION Migration Druggable target
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剪接因子——SF3b 被引量:3
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作者 袁丽华 罗小洋 张吉翔 《生命的化学》 CAS CSCD 北大核心 2009年第5期746-749,共4页
真核生物前体mRNA的蛋白编码区(即外显子)被间隔序列(即内含子)分隔开,需切除内含子才能形成成熟的mRNA。内含子的精确切除是由剪接体催化的。剪接体由五种snRNP(U1、U2、U4/U6和U5)和许多非snRNP蛋白质组成。由SAP49、SAP130、SAP145、... 真核生物前体mRNA的蛋白编码区(即外显子)被间隔序列(即内含子)分隔开,需切除内含子才能形成成熟的mRNA。内含子的精确切除是由剪接体催化的。剪接体由五种snRNP(U1、U2、U4/U6和U5)和许多非snRNP蛋白质组成。由SAP49、SAP130、SAP145、SAP155、SAP14b、SAP10和SAP14a七种蛋白质组成的SF3b作为U2snRNP和U11/U12di-snRNP的组成部分参与整个剪接过程。SF3b在剪接前体的组装和识别内含子的分支点中起重要作用。本文主要介绍了剪接体的组装、SF3b的结构及SF3b成分的作用。 展开更多
关键词 剪接体 RNA剪接 剪接因子3b(SF3b)
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