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RISS 인기검색어
- 검색키워드
- 저자 : You-Fei Qi (검색결과 3 건)
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Qi, You-Fei,Shu, Chang,Xiao, Zhan-Xiang,Luo, Ming-Yao,Fang, Kun,Guo, Yuan-Yuan,Zhang, Wen-Bo,Yue, Jie Korean Society for Molecular and Cellular Biology 2018 Molecules and cells Vol.41 No.3
Aortic dissection (AD) is a catastrophic disease with high mortality and morbidity, characterized with fragmentation of elastin and loss of smooth muscle cells. Although AD has been largely attributable to polymorphisms defect in the elastin-coding gene, tropoelastin (TE), other undermined factors also appear to play roles in AD onset. Here, we investigated the effects of post-transcriptional control of TE by microRNAs (miRNAs) on elastin levels in aortic smooth muscle cells (ASMC). We found that miR-144-3p is a miRNA that targets TE mRNA in both human and mouse. Bioinformatics analyses and dual luciferase reporter assay showed that miR-144-3p inhibited protein translation of TE, through binding to the 3'-UTR of the TE mRNA. Interestingly, higher miR-144-3p levels and lower TE were detected in the ASMC obtained from AD patients, compared to those from non-AD controls. In a mouse model for human AD, infusion of adeno-associated viruses (serotype 6) carrying antisense for miR-144-3p (asmiR-144-3p) under CAG promoter significantly reduced the incidence and severity of AD, seemingly through enhancement of TE levels in ASMC. Thus, our data suggest an essential role of miR-144-3p on the pathogenesis of AD.
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You-Fei Qi,Chang Shu,Zhan-Xiang Xiao,Ming-Yao Luo,Kun Fang,Yuan-Yuan Guo,Wen-Bo Zhang,Jie Yue 한국분자세포생물학회 2018 Molecules and cells Vol.41 No.3
Aortic dissection (AD) is a catastrophic disease with high mortality and morbidity, characterized with fragmentation of elastin and loss of smooth muscle cells. Although AD has been largely attributable to polymorphisms defect in the elastin-coding gene, tropoelastin (TE), other undermined factors also appear to play roles in AD onset. Here, we investigated the effects of post-transcriptional control of TE by microRNAs (miRNAs) on elastin levels in aortic smooth muscle cells (ASMC). We found that miR-144-3p is a miRNA that targets TE mRNA in both human and mouse. Bioinformatics analyses and dual luciferase reporter assay showed that miR-144-3p inhibited protein translation of TE, through binding to the 3-UTR of the TE mRNA. Interestingly, higher miR-144-3p levels and lower TE were detected in the ASMC obtained from AD patients, compared to those from non-AD controls. In a mouse model for human AD, infusion of adeno-associated viruses (serotype 6) carrying antisense for miR-144-3p (as-miR-144-3p) under CAG promoter significantly reduced the incidence and severity of AD, seemingly through enhancement of TE levels in ASMC. Thus, our data suggest an essential role of miR-144-3p on the pathogenesis of AD.
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Ying-Hua Liang,Ping-Zhan Si,Ting-Ting Qi,Xin-You Wang,Fei-Yang Wang,Qiong Wu,Hong-Liang Ge,Jihoon Park,Chul-Jin Choi 한국자기학회 2024 Journal of Magnetics Vol.29 No.1
Both Mn₄C (=Mn₃MnC) and Mn₃GaC have been studied previously. However, the reports on Mn<SUB>3+x</SUB>Ga<SUB>1-x</SUB>C (0 ≤ x ≤ 1) with intermediate compositions are very rare. In this work, the structure and magnetic properties of Mn<SUB>3+x</SUB>Ga<SUB>1-x</SUB>C prepared by using solid state reaction were studied systematically. High purity anti-perovskitetype Mn<SUB>3+x</SUB>Ga<SUB>1-x</SUB>C were obtained in the composition range of 0 ≤ x ≤ 0.5, above which Mn₂₃C₆ precipitates and the fraction of Mn₂₃C₆ in the samples increases with increasing x. The structural stability, lattice parameters, and room temperature saturation magnetization of ferromagnetic Mn<SUB>3+x</SUB>Ga<SUB>1-x</SUB>C (0 ≤ x ≤ 1) decreases with increasing x. The Curie temperature of Mn<SUB>3+x</SUB>Ga<SUB>1-x</SUB>C (0 ≤ x ≤ 1) increases with increasing x. Most Mn<SUB>3+x</SUB>Ga<SUB>1-x</SUB>C with varied x exhibit near-zero coercivity and zero remanent magnetization. This work indicates that the temperature coefficient of magnetization of Mn<SUB>3+x</SUB>Ga<SUB>1-x</SUB>C may be tuned by tuning the fraction of the Ga atoms.
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