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- 저자 : Keping Wu (검색결과 2 건)
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Wu, Chao,Guo, Zhongjian,Chen, Keping,Shen, Hongxing Korean Society of Sericultural Science 2008 International Journal of Industrial Entomology Vol.16 No.2
Bombyx mori nucleopolyhedrovirus (BmNPV) orf47 gene was characterized for the first time. The coding sequence of Bm47 was amplified and subcloned into the prokaryotic expression vector pET-30a(+) in order to produce His-tagged fusion protein in the BL21 (DE3) cells. The His-Bm47 fusion protein was expressed efficiently after induction with IPTG. The purified fusion protein was used to immunize New Zealand white rabbits to prepare polyclonal antibody. As the genome of BmNPV is available in GenBank and the EST database of BmNPV is expanding, identification of novel genes of BmNPV was conceivable by data-mining techniques and bioinformatics tools. Structural bioinformatics approach to analyze the properties of Bm47 encodes protein.
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Zhihua Zheng,Jiasi Chen,Keping Wu,Yan Lei,Mingcheng Huang,Lokyu Cheng,Hui Guan,Jiawen Lin,Ming Zhong,Xiaohua Wang 대한내분비학회 2023 Endocrinology and metabolism Vol.38 No.2
Background: Ferroptosis, which is caused by an iron-dependent accumulation of lipid hydroperoxides, is a type of cell death linked todiabetic kidney disease (DKD). Previous research has shown that fatty acid binding protein 4 (FABP4) is involved in the regulation of ferroptosis in diabetic retinopathy. The present study was constructed to explore the role of FABP4 in the regulation of ferroptosis in DKD. Methods: We first detected the expression of FABP4 and proteins related to ferroptosis in renal biopsies of patients with DKD. Then, we used a FABP4 inhibitor and small interfering RNA to investigate the role of FABP4 in ferroptosis induced by high glucosein human renal proximal tubular epithelial (HG-HK2) cells. Results: In kidney biopsies of DKD patients, the expression of FABP4 was elevated, whereas carnitine palmitoyltransferase-1A (CPT1A), glutathione peroxidase 4, ferritin heavy chain, and ferritin light chain showed reduced expression. In HG-HK2 cells, the induction of ferroptosis was accompanied by an increase in FABP4. Inhibition of FABP4 in HG-HK2 cells changed the redox state, suppressing the production of reactive oxygen species, ferrous iron (Fe2+), and malondialdehyde, increasing superoxide dismutase, and reversing ferroptosis-associated mitochondrial damage. The inhibition of FABP4 also increased the expression of CPT1A, reversed lipiddeposition, and restored impaired fatty acid β-oxidation. In addition, the inhibition of CPT1A could induce ferroptosis in HK2 cells. Conclusion: Our results suggest that FABP4 mediates ferroptosis in HG-HK2 cells by inhibiting fatty acid β-oxidation.
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