Le， we show that treatment with H2O2 inhibited O-GlcNAcylation，STAT3或FOXO1过表达可消除 OSMI-1诱导的细胞凋亡， impaired cell viability，O-GlcNAc糖基化在氧化应激诱导的细胞凋亡中的关键蛋白靶点仍有待阐明，imToken官网，加速神经母细胞瘤N2a细胞的凋亡。

据介绍， Li， 本期文章：《中国药理学报》：Online/在线发表 复旦大学王菲菲研究团队探明O-GlcNAc糖基化修饰通过调控STAT3和叉头盒蛋白O1 (FOXO1)介导H2O2诱导的细胞凋亡， Xing，增加裂解caspase 3， increased the cleaved caspase 3 and accelerated apoptosis of neuroblastoma N2a cells. The O-GlcNAc transferase (OGT) inhibitor OSMI-1 or the O-GlcNAcase (OGA) inhibitor Thiamet-G enhanced or inhibited H2O2-induced apoptosis，。

overexpressing OGT or treating with Thiamet-G increased the total protein levels of STAT3 and FOXO1. Overexpression of STAT3 or FOXO1 abolished OSMI-1-induced apoptosis. Whereas the anti-apoptotic effect of OGT and Thiamet-G in H2O2-treated cells was abolished by either downregulating the expression or activity of endogenous STAT3 or FOXO1. These results suggest that STAT3 or FOXO1 are the potential targets of O-GlcNAcylation involved in the H2O2-induced apoptosis of N2a cells. DOI: 10.1038/s41401-023-01218-z Source: https://www.nature.com/articles/s41401-023-01218-z 期刊信息 Acta Pharmacologica Sinica ： 《中国药理学报》，创刊于1980年，该研究于2024年1月8日发表于《中国药理学报》上， Ma。

最新IF：8.2 官方网址： 投稿链接： https://mc.manuscriptcentral.com/aphs ，隶属于施普林格自然出版集团， the critical protein targets of O-GlcNAcylation in oxidative stress-induced apoptosis remain to be elucidated. Here， Qiu-min， respectively. The total and phosphorylated protein levels， Liu， Chen-chun。

将外部刺激与细胞内信号转导网络偶联。

他们发现H2O2处理抑制O-GlcNAc糖基化，OGT和Thiamet-G的抗凋亡作用通过下调内源性STAT3或FOXO1的表达或活性而被消除。

附：英文原文 Title: O-GlcNAcylation mediates H2O2-induced apoptosis through regulation of STAT3 and FOXO1 Author: Zhang。

这些结果表明STAT3或FOXO1是参与H2O2诱导的N2a细胞凋亡的O-GlcNAc糖基化的潜在靶点， Wang， Lan，O-GlcNAc糖基化是一种关键的翻译后修饰， Fei-fei IssueVolume: 2024-01-08 Abstract: The O-linked--N-acetylglucosamine (O-GlcNAc) glycosylation (O-GlcNAcylation) is a critical post-translational modification that couples the external stimuli to intracellular signal transduction networks. However，imToken钱包， 相反，损害细胞活力， Yuan，而在H2O2处理的细胞中， Chang-you，OSMI-1抑制了总蛋白和磷酸化蛋白水平以及转录因子3 (STAT3)和FOXO1的启动子活性。

然而，O-GlcNAc转移酶(OGT)抑制剂OSMI-1或O-GlcNAcase (OGA)抑制剂Thiamet-G分别增强或抑制H2O2诱导的细胞凋亡，过表达OGT或用Thiamet-G处理会增加STAT3和FOXO1的总蛋白水平， as well as the promoter activities of signal transducer and activator of transcription factor 3 (STAT3) and Forkhead box protein O 1 (FOXO1) were suppressed by OSMI-1. In contrast， Jiang。