4篇
您的检索式：作者名="Du Xintong"
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| 1 | Pulsed electrodepo- sition of Pt particles on indium tin oxide substrates and their electrocatalytic properties for methanol oxidation 显示文摘 | Liu Jie Zhong Cheng Du Xintong | 2013 | Elec- trochim Acta2013，100，： | 1 |
| 2 | Whitefly adaptation to and manipulation of plant resistance显示文摘Insect herbivores resemble one of the most significant biotic stresses to plants in natural and agricultural ecosystems,due to their high diversity and abundance(Wu and Baldwin,2010).In the long-term coexistence between plants and insect herbivores,plants have evolved a diverse array of defense machineries to fend off attacks from insect herbivores. | Lilong Pan Hui Du Xintong Ye Xiaowei Wang | 2021 | Science China(Life Sciences)2021，64，4： | 0 |
| 3 | Long noncoding RNA GAS5 attenuates cigarette smoke-induced airway remodeling by regulating miR-217-5p/PTEN axis显示文摘Airway remodeling is a remarkable pathological characteristic of chronic obstructive pulmonary disease(COPD),and long noncoding RNAs have been demonstrated to participate in COPD development and pathogenesis.Here,we investigate the role of long noncoding RNA GAS5 in cigarette smoke(CS)-induced airway remodeling.GAS5 expression is significantly lower in lung tissues of CS-exposed mice than in tissues of control mice without exposure to CS.Forced GAS5 overexpression suppresses CS-induced airway inflammation and remodeling.GAS5 overexpression also inhibits CS extract-induced inflammatory-cytokine expression and fibroblast activation in vitro.Regarding the mechanism,GAS5 acts as a sponge of miR-217-5p,thereby increasing PTEN expression.MiR-217-5p overexpression and PTEN knockdown separately reverse the inhibitory effects of GAS5 overexpression on the inflammatory-cytokine expression and fibroblast activation.Collectively,these results suggest that GAS5 can suppress airway inflammation and fibroblast activation by regulating miR-217-5p/PTEN axis,which may help develop novel therapeutic strategies against COPD. | Yong Du Yi Ding Tianyun Shi Wei He Jingjing Feng Zhoufang Mei Xuru Chen Xintong Feng Xiaohua Zhang Zhijun Jie | 2022 | Acta Biochimica et Biophysica Sinica2022，54，7： | 0 |
| 4 | MALAT1-mediated EZH2 Recruitment to the GFER Promoter Region Curbs Normal Hepatocyte Proliferation in Acute Liver Injury显示文摘Background and Aims:The goal of this study was to investigate the mechanism by which the long noncoding RNA MALAT1 inhibited hepatocyte proliferation in acute liver injury(ALI).Methods:Lipopolysaccharide(LPS)was used to induce an ALI cellular model in HL7702 cells,in which lentivirus vectors containing MALAT1/EZH2/GFER overexpression or knockdown were introduced.A series of experiments were performed to determine their roles in liver injury,oxidative stress injury,and cell biological processes.The interaction of MALAT1 with EZH2 and enrichment of EZH2 and H3K27me3 in the GFER promoter region were identified.Rats were treated with MALAT1 knockdown or GFER overexpression before LPS induction to verify the results derived from the in vitro assay.Results:MALAT1 levels were elevated and GFER levels were reduced in ALI patients and the LPS-induced cell model.MALAT1 knockdown or GFER overexpression suppressed cell apoptosis and oxidative stress injury induced cell proliferation,and reduced ALI.Functionally,MALAT1 interacted directly with EZH2 and increased the enrichment of EZH2 and H3K27me3 in the GFER promoter region to reduce GFER expression.Moreover,MALAT1/EZH2/GFER was activated the AMPK/mTOR signaling pathway.Conclusion:Our study highlighted the inhibitory role of reduced MALAT1 in ALI through the modulation of EZH2-mediated GFER. | Li Chen Xintong Kang Xiujuan Meng Liang Huang Yiting Du Yilan Zeng Chunfeng Liao | 2023 | Journal of Clinical and Translational Hepatology2023，11，1： | 0 |
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