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- 저자 : Bi‑Wen Xie (검색결과 5 건)
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The complete mitochondrial genome of a threatened loach (Sinibotia reevesae) and its phylogeny
Yuan‑Chao Zou,Bi‑Wen Xie,Chuan‑Jie Qin,Yong‑Ming Wang,Deng‑Yue Yuan,Rui Li,Zheng‑Yong Wen 한국유전학회 2017 Genes & Genomics Vol.39 No.7
In present study, the complete mitochondrial genome of Sinibotia reevesae was first sequenced using the next-generation sequencing technology and annotated using bioinformatic tools. The circular mitochondrial genome was 16,572 bp in length, and contained 13 proteincoding genes, 2 ribosomal RNA genes, 22 transfer RNA genes, and 1 displacement loop locus. It presents a typical gene organization and order for completely sequenced cypriniformes mitogenomes. The control region could be divided into three parts included the extended termination associated sequence domain, the central conserved domain and the conserved sequence block. Interestingly, two stemloop domains were found in control region and OL region, respectively. Furthermore, phylogenetic analyses using concatenated amino acid and nucleotide sequences of the 13 protein-coding genes with two different methods (Maximum likelihood and Bayesian analysis) both highly supported the close relationship of S. reevesae and Sinibotia superciliaris, which was in line with the previous classifications based on morphological and molecular studies. These data provide useful information for a better understanding of the mitogenomic diversities and evolution in fish as well as novel genetic markers for studying population genetics and species identification.
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Zhang, Qing-Mei,Shen, Ning,Xie, Sha,Bi, Shui-Qing,Luo, Bin,Lin, Yong-Da,Fu, Jun,Zhou, Su-Fang,Luo, Guo-Rong,Xie, Xiao-Xun,Xiao, Shao-Wen Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.8
Melanoma-associated antigen (MAGE) family genes have been considered as potentially promising targets for anticancer immunotherapy. MAGED4 was originally identified as a glioma-specific antigen. Current knowledge about MAGED4 expression in glioma is only based on mRNA analysis and MAGED4 protein expression has not been elucidated. In the present study, we investigated this point and found that MAGED4 mRNA and protein were absent or very lowly expressed in various normal tissues and glioma cell line SHG44, but overexpressed in glioma cell lines A172,U251,U87-MG as well as glioma tissues, with significant heterogeneity. Furthermore, MAGED4 protein expression was positively correlated with the glioma type and grade. We also found that the expression of MAGED4 inversely correlated with the overall methylation status of the MAGED4 promoter CpG island. Furthermore, when SHG44 and A172 with higher methylation were treated with the DNA demethylating agent 5-aza-2'-deoxycytidine (5-AZA-CdR) reactivation of MAGED4 mRNA was mediated by significant demethylation in SHG44 instead of A172. However, 5-AZA-CdR treatment had no effect on MAGED4 protein in both SHG44 and A172 cells. In conclusion, MAGED4 is frequently and highly expressed in glioma and is partly regulated by DNA methylation. The results suggest that MAGED4 might be a promising target for glioma immunotherapy combined with 5-AZA-CdR to enhance its expression and eliminate intratumor heterogeneity.
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Fan, Hui-Jie,Tan, Zhang-Bin,Wu, Yu-Ting,Feng, Xiao-Reng,Bi, Yi-Ming,Xie, Ling-Peng,Zhang, Wen-Tong,Ming, Zhi,Liu, Bin,Zhou, Ying-Chun The Korean Society of Ginseng 2020 Journal of Ginseng Research Vol.44 No.2
Background: Oxidative stress-induced cardiomyocytes apoptosis is a key pathological process in ischemic heart disease. Glutathione reductase (GR) reduces glutathione disulfide to glutathione (GSH) to alleviate oxidative stress. Ginsenoside Rb1 (GRb1) prevents the apoptosis of cardiomyocytes; however, the role of GR in this process is unclear. Therefore, the effects of GRb1 on GR were investigated in this study. Methods: The antiapoptotic effects of GRb1 were evaluated in H9C2 cells by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, annexin V/propidium iodide staining, and Western blotting. The antioxidative effects were measured by a reactive oxygen species assay, and GSH levels and GR activity were examined in the presence and absence of the GR inhibitor 1,3-bis-(2-chloroethyl)-1-nitrosourea. Molecular docking and molecular dynamics simulations were used to investigate the binding of GRb1 to GR. The direct influence of GRb1 on GR was confirmed by recombinant human GR protein. Results: GRb1 pretreatment caused dose-dependent inhibition of tert-butyl hydroperoxide-induced cell apoptosis, at a level comparable to that of the positive control N-acetyl-L-cysteine. The binding energy between GRb1 and GR was positive (-6.426 kcal/mol), and the binding was stable. GRb1 significantl reduced reactive oxygen species production and increased GSH level and GR activity without altering GR protein expression in H9C2 cells. Moreover, GRb1 enhanced the recombinant human GR protein activity in vitro, with a half-maximal effective concentration of ≈2.317 μM. Conversely, 1,3-bis-(2-chloroethyl)-1-nitrosourea co-treatment significantly abolished the GRb1's apoptotic and antioxidative effects of GRb1 in H9C2 cells. Conclusion: GRb1 is a potential natural GR agonist that protects against oxidative stress-induced apoptosis of H9C2 cells.
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Hui-Jie Fan,Zhang-Bin Tan,Yu-Ting Wu,Xiao-Reng Feng,Yi-Ming Bi,Ling-Peng Xie,Wen-Tong Zhang,Zhi Ming,Bin Liu,Ying-Chun Zhou 고려인삼학회 2020 Journal of Ginseng Research Vol.44 No.2
Background: Oxidative stress-induced cardiomyocytes apoptosis is a key pathological process inischemic heart disease. Glutathione reductase (GR) reduces glutathione disulfide to glutathione (GSH) toalleviate oxidative stress. Ginsenoside Rb1 (GRb1) prevents the apoptosis of cardiomyocytes; however,the role of GR in this process is unclear. Therefore, the effects of GRb1 on GR were investigated in thisstudy. Methods: The antiapoptotic effects of GRb1 were evaluated in H9C2 cells by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, annexin V/propidium iodide staining, and Western blotting. Theantioxidative effects were measured by a reactive oxygen species assay, and GSH levels and GR activitywere examined in the presence and absence of the GR inhibitor 1,3-bis-(2-chloroethyl)-1-nitrosourea. Molecular docking and molecular dynamics simulations were used to investigate the binding of GRb1 toGR. The direct influence of GRb1 on GR was confirmed by recombinant human GR protein. Results: GRb1 pretreatment caused dose-dependent inhibition of tert-butyl hydroperoxide-induced cellapoptosis, at a level comparable to that of the positive control N-acetyl-L-cysteine. The binding energybetween GRb1 and GR was positive ( 6.426 kcal/mol), and the binding was stable. GRb1 significantlyreduced reactive oxygen species production and increased GSH level and GR activity without altering GRprotein expression in H9C2 cells. Moreover, GRb1 enhanced the recombinant human GR protein activityin vitro, with a half-maximal effective concentration of z2.317 mM. Conversely, 1,3-bis-(2-chloroethyl)-1-nitrosourea co-treatment significantly abolished the GRb1’s apoptotic and antioxidative effects of GRb1in H9C2 cells. Conclusion: GRb1 is a potential natural GR agonist that protects against oxidative stresseinducedapoptosis of H9C2 cells.
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