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198 results on '"Xu, Fanfan"'

11. FOSL1-mediated LINC01566 negatively regulates CD4+ T-cell activation in myasthenia gravis.

Author

Li, Lifang, Li, Danyang, Jin, Jingnan, Xu, Fanfan, He, Ni, Ren, Yingjie, Wang, Xiaokun, Tian, Liting, Chen, Biying, Li, Xiaoju, Chen, Zihong, Zhang, Lanxin, Qiao, Lukuan, Wang, Lihua, and Wang, Jianjian

Subjects
GENE expression, FLUORESCENCE in situ hybridization, MYASTHENIA gravis, LINCRNA, TRANSCRIPTION factors
Abstract

Background: Myasthenia gravis (MG) is an autoimmune disease characterized by pathogenic antibodies that target structures of the neuromuscular junction. The evidence suggests that the regulation of long noncoding RNAs (lncRNAs) that is mediated by transcription factors (TFs) plays a key role in the pathophysiology of MG. Nevertheless, the detailed molecular mechanisms of lncRNAs in MG remain largely undetermined. Methods: Using microarray analysis, we analyzed the lncRNA levels in MG. By bioinformatics analysis, LINC01566 was found to potentially play an important role in MG. First, qRT‒PCR was performed to verify the LINC1566 expressions in MG patients. Then, fluorescence in situ hybridization was conducted to determine the localization of LINC01566 in CD4 + T cells. Finally, the impact of LINC01566 knockdown or overexpression on CD4 + T-cell function was also analyzed using flow cytometry and CCK-8 assay. A dual-luciferase reporter assay was used to validate the binding of the TF FOSL1 to the LINC01566 promoter. Results: Based on the lncRNA microarray and differential expression analyses, we identified 563 differentially expressed (DE) lncRNAs, 450 DE mRNAs and 19 DE TFs in MG. We then constructed a lncRNA-TF-mRNA network. Through network analysis, we found that LINC01566 may play a crucial role in MG by regulating T-cell-related pathways. Further experiments indicated that LINC01566 is expressed at low levels in MG patients. Functionally, LINC01566 is primarily distributed in the nucleus and can facilitate CD4 + T-cell apoptosis and inhibit cell proliferation. Mechanistically, we hypothesized that LINC01566 may negatively regulate the expressions of DUSP3, CCR2, FADD, SIRPB1, LGALS3 and SIRPB1, which are involved in the T-cell activation pathway, to further influence the cellular proliferation and apoptosis in MG. Moreover, we found that the effect of LINC01566 on CD4 + T cells in MG was mediated by the TF FOSL1, and in vitro experiments indicated that FOSL1 can bind to the promoter region of LINC01566. Conclusions: In summary, our research revealed the protective roles of LINC01566 in clinical samples and cellular experiments, illustrating the potential roles and mechanism by which FOSL1/LINC01566 negatively regulates CD4 + T-cell activation in MG. [ABSTRACT FROM AUTHOR]

Published
2024
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12. MSGD: a manually curated database of genomic, transcriptomic, proteomic and drug information for multiple sclerosis

Author

Wu, Tao, primary, Hou, Yaopan, additional, Xin, Guanghao, additional, Niu, Jingyan, additional, Peng, Shanshan, additional, Xu, Fanfan, additional, Li, Ying, additional, Chen, Yuling, additional, Yu, Yifangfei, additional, Zhang, Huixue, additional, Kong, Xiaotong, additional, Cao, Yuze, additional, Ning, Shangwei, additional, Wang, Lihua, additional, and Hao, Junwei, additional

Published
2024
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35. Revealing and Optimizing the Dialectical Relationship Between NOR and OER: Cation Vacancy Engineering Enables RuO2 With Unanticipated High Electrochemical Nitrogen Oxidation Performance.

Author

Xu, Fanfan, Liu, Xia, Zhang, Linlin, Guo, Mingxia, Li, Mingzhu, Ding, Xin, and Zhang, Lixue

Subjects
*OXYGEN evolution reactions, *SULFURIC acid, *CATIONS, *NITROGEN, *BOND ratings
Abstract

The electrochemical N2 oxidation reaction (NOR) using water and atmospheric N2 represents a sustainable approach to nitric acid production; while, the parasitic oxygen evolution reaction (OER) usually results in poor conversion selectivity of N2 oxidation. Although the side‐reaction can be partially suppressed by using OER‐inactive catalysts or substrates, the optimized performance is usually obtained at the cost of low yield. Revealing the internal relationship between NOR and OER, providing an effective pathway to optimize the dialectical relationship between OER and NOR is desirable and of socio‐economic significance. Herein, RuO2, the well‐known OER electrocatalyst, is defectively engineered to enhance the cooperation rather than competition between NOR and OER; a Faradaic efficiency (FE) of 6.70% at 1.36 V and a maximum yield of 767.92 µg h−1 mgcat−1 at 1.44 V are obtained on D‐RuO2 in acid electrolyte, superior to all the previously reported works. Experiments and DFT calculations suggest that the OER intermediates play a crucial role and the real rate‐determining step during nitrogen oxidation is the transition from *O to *OOH involved in the formation of *NN(OH). The outstanding NOR activity is ascribed to the enhanced stabilization of *OH and the promotion of OO bond breakage in the rate determining step of *NN(OH) formation. [ABSTRACT FROM AUTHOR]

Published
2023
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47. Association of internal exposure to polycyclic aromatic hydrocarbons with inflammation and oxidative stress in prediabetic and healthy individuals

Author

Zhang, Hanxiyue, primary, Han, Yiqun, additional, Qiu, Xinghua, additional, Wang, Yanwen, additional, Li, Weiju, additional, Liu, Jinming, additional, Chen, Xi, additional, Li, Ran, additional, Xu, Fanfan, additional, Chen, Wu, additional, Yang, Qiaoyun, additional, Fang, Yanhua, additional, Fan, Yunfei, additional, Wang, Junxia, additional, Zhang, Hongyin, additional, and Zhu, Tong, additional

Published
2020
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