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您的检索式：作者名="Xingmiao Zhao"
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| 1 | C19orf66 Inhibits Japanese Encephalitis Virus Replication by Targeting-1 PRF and the NS3 Protein显示文摘The Japanese encephalitis serogroup of the neurogenic Flavivirus has a specific feature that expresses a non-structural protein NS1'produced through a programmed-1 ribosomal frameshifting(-1 PRF).Herein,C19orf66,a novel member of interferon-stimulated gene(ISG)products,exhibited significant activity of antagonizing Japanese encephalitis virus(JEV)infection.Overexpression of C19orf66 in 293T cells significantly inhibited JEV replication,while knock-down of endogenous C19orf66 in HeLa cells and A549 cells significantly increased virus replication.Notably,C19orf66 had an inhibitory effect on frameshift production of JEV NS1'.The inhibition was more significant when C19orf66 and JEV NS1-NS2A were co-expressed in the 293T cells.Both C19orf66-209 and C19orf66-Zinc^(mut) did not significantly change the NS1'to NS1 ratio and had weaker antiviral effects than C19orf66.Similarly,C19orf66-209 and C19orf66-Zinc^(mut) had no significant effect on the expression of the JEV NS3 protein,whose expression was down-regulated by C19orf66 via the lysosome-dependent pathway.These findings suggest that C19orf66 may possess at least two different mechanisms of antagonizing JEV infection.This study identified C19orf66 as a novel interferon-stimulated gene product that can inhibit JEV replication by targeting-1 PRF and the NS3 protein.The study provides baseline information for the future development of broad-spectrum antiviral agents against JEV. | Du Yu Yundi Zhao Junhui Pan Xingmiao Yang Zhenjie Liang Shengda Xie Ruibing Cao | 2021 | Virologica Sinica2021，36，6： | 0 |
| 2 | 用于精确调控单层二氧化钛介孔涂层的限域界面胶束组装法显示文摘文章简介课题组首次采用限域界面胶束组装法,在不同材料表面精准地涂覆了一层锐钛矿TiO_2,为有序介孔晶体材料的涂覆打开了一扇新的大门。这些介孔来自于胶束的自组装,而不是纳米晶体的堆积,这种简便、可重复的方法依赖于甘油在组装过程中的限域效应和溶剂选择。整体组装过程有着精确的可控性和极大的通用性,甚至可以调控TiO_2涂层的厚度、介孔孔径等参数。 | Kun Lan Yuan Xia Ruicong Wang Zaiwang Zhao Wei Zhang Xingmiao Zhang Ahmed Elzatahry 赵东元 | 2020 | 科学新闻2020，，2： | 0 |
| 3 | CPAL, as a New Mediator of Cardiomyocyte Metabolic Alterations and Pyroptosis, Regulates Myocardial Infarction Injury in Mice显示文摘Myocardial infarction (MI), the most serious of the ischemic heart diseases, is accompanied by myocardial metabolic disorders and the loss of cardiomyocytes. Increasing evidence has shown that long noncoding RNAs (lncRNAs) are involved in various pathological conditions such as cancer and cardiovascular diseases (CVDs), and are emerging as a novel biomarker for these disorders. This study aims to investigate the regulatory role and mechanisms of lncRNAs in myocardial remodeling in the setting of MI. We find that post-infarcted hearts exhibit a reduction of adenosine triphosphate (ATP) and an alteration of the glucose and lipid metabolism genes cluster of differentiation 36 (CD36), hexokinase 1 (HK1), and clucose transporter 4 (GLUT4), accompanied by cardiomyocyte pyroptosis. We then identify a previously unknown conserved lncRNA, AK009126 (cardiomyocyte pyroptosis-associated lncRNA, CPAL), which is remarkably upregulated in the myocardial border zone of MI mice. Importantly, the adeno-associated virus 9 (AAV9)-mediated silencing of endogenous CPAL by its short hairpin RNA (shRNA) partially abrogates myocardial metabolic alterations and cardiomyocyte pyroptosis during MI in mice. Mechanistically, CPAL is shown to bind directly to nuclear factor kappa B (NFκB) and to act as an activator of NFκB to induce NFκB phosphorylation in cardiomyocytes. We also find that CPAL upregulates caspase-1 expression at the transcriptional level and consequently promotes the release of interleukin (IL)-18 and IL-1β from cardiomyocytes. Collectively, our findings reveal the conserved lncRNA CPAL as a new regulator of cardiac metabolic abnormalities and cardiomyocyte pyroptosis in the setting of MI and suggest CPAL as a new therapeutic target to protect cardiomyocytes against ischemic injury in infarcted hearts. | Jiamin Li Hongru Xue Ning Xu Liling Gong Ming Li Sijia Li Di Huang Qingwei Zhang Pengyu Li Qingsui Li Hang Yu Yining Liu Yadong Xue Haixin Chen Jiali Liu Wanyu Zhang Mingbin Liu Siyu Chang Xianzhi Lang Xingmiao Zhao Weijie Du Benzhi Cai Ning Wang Baofeng Yang | 2023 | Engineering2023，，1： | 0 |
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