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| 1 | 15-deoxy-△12,14-prostaglandin J2 ameliorates endotoxin-induced acute lung injury in rats显示文摘 | Geng Zhilong Zhu Wankun Wang Huiwen Chen Ye Liang Juan Liu Dong | 2014 | Chinese Medical Journal2014，，5： | 7 |
| 2 | Nalmefene attenuates malignant potential in colorectal cancer cell via inhibition of opioid receptor显示文摘吗啡被要求在在外科手术前的时期期间支持肿瘤生长和转移的一个风险因素,和肿瘤房间的高 glycolysis 被证明加速肿瘤前进。在这研究,我们调查了是否 nalmefene,一个 opioid 受体禁止者,能通过影响细胞 glycolysis 禁止 CT26 结肠癌细胞生长。CCK8 和 transwell 迁居试金证明 nalmefene 以一种集中依赖者方式禁止了 CT26 房间生存能力和移植。细胞外的使发酸率和氧消费率证明 nalmefene 禁止了 CT26 房间的 glycolysis。而且,西方的污点分析和量的即时 PCR 表明 nalmefene 减少了与 glycolysis 有关的酶的表情。流动 cytometry 结果揭示了那细胞内部的钙(Ca 2+) 水平被 nalmefene 改变,西方的污点分析证明 nalmefene 减少了 calmodulin 表示和 calcium/calmodulin 依赖者蛋白质 kinases II (CaMK II ) phosphorylation,因此禁止 serine/threonine kinase (AKT ) 肝糖 synthase kinase-3 (GSK-3 ) 小径。而且, KN93 的效果, CaMK II 的一个禁止者,类似于 nalmefene,和 nalmefene 的反肿瘤效果的效果能被吗啡抵抗。在结论, nalmefene 的反肿瘤效果可以被禁止 opioid 受体和下面调整的 calmodulin 表示和 CaMK II phosphorylation 完成,因此禁止 AKT-GSK-3 小径和 CT26 房间的 glycolysis。 | Qichao Wu Xiangyuan Chen Jiaqiang Wang Pengfei Sun Meilin Weng Wankun Chen Zhirong Sun Minmin Zhu Changhong Miao | 2018 | Acta Biochimica et Biophysica Sinica2018，50，2： | 2 |
| 3 | PTMD: A Database of Human Disease-associated Post-translational Modifications显示文摘Various posttranslational modifications(PTMs) participate in nearly all aspects of biological processes by regulating protein functions, and aberrant states of PTMs are frequently implicated in human diseases. Therefore, an integral resource of PTM–disease associations(PDAs)would be a great help for both academic research and clinical use. In this work, we reported PTMD,a well-curated database containing PTMs that are associated with human diseases. We manually collected 1950 known PDAs in 749 proteins for 23 types of PTMs and 275 types of diseases from the literature. Database analyses show that phosphorylation has the largest number of disease associations, whereas neurologic diseases have the largest number of PTM associations. We classified all known PDAs into six classes according to the PTM status in diseases and demonstrated that the upregulation and presence of PTM events account for a predominant proportion of diseaseassociated PTM events. By reconstructing a disease–gene network, we observed that breast cancershave the largest number of associated PTMs and AKT1 has the largest number of PTMs connected to diseases. Finally, the PTMD database was developed with detailed annotations and can be a useful resource for further analyzing the relations between PTMs and human diseases. PTMD is freely accessible at http://gffzz7d3e84778ac14081honxv59wf0nbu6oxv.ffgz.tsg.suse.edu.cn. | Haodong Xu Yongbo Wang Shaofeng Lin Wankun Deng Di Peng Qinghua Cui Yu Xue | 2018 | Genomics, Proteomics & Bioinformatics2018，16，4： | 2 |
| 4 | High glucose inhibits vascular endothelial Keap1/Nrf2/ARE signal pathway via downregulation of monomethyltransferase SET8 expression显示文摘Hyperglycemia-mediated reactive oxygen species(ROS)accumulation plays an important role in hyperglycemia-induced endothelial injury.Kelch-like ECH-associated protein 1(Keap1)/nuclear factor erythroid 2-related factor 2(Nrf2)/antioxidant response element(ARE)pathway inhibition participates in hyperglycemia-induced ROS accumulation.Our previous study indicated that SET8 overexpression inhibits high glucose-mediated ROS accumulation in human umbillical vein endothelial cells(HUVECs).In the present study,we hypothesize that SET8 may play a major role in high glucose-induced ROS accumulation via modulation of Keap1/Nrf2/ARE pathway.Our data indicated that high glucose mediated cell viability reduction,ROS accumulation,and Nrf2/ARE signal pathway inhibition via upregulation of Keap1 expression in HUVECs.Moreover,high glucose inhibited the expressions of SET8 and H4K20me1(a downstream target of SET8).SET8 overexpression improved high glucose-mediated Keap 1/Nrf2/ARE pathway inhibition and endothelial oxidation.Consistently,the effects of sh-SET8 were similar to that of high glucose treatment and were reversed by si-Keap1.A mechanistic study found that H4K20me1 was enriched at the Keap1 promoter region.SE T8 overexpression attenuated Keap1 promoter activity and its expression,while mutant SET8 R259G did not affect Keap1 promoter activity and expression.The results of this study demonstrated that SET8 negatively regulates Keap1 expression,thus participating in high glucose-mediated Nrf2/ARE signel pathway inhibition and oxidative injury in HUVECs. | Xiangyuan Chen Jie Qi Qichao Wu Hui Jiang Jing Wang Wankun Chen Anrong Mao Minmin Zhu | 2020 | Acta Biochimica et Biophysica Sinica2020，52，5： | 2 |
| 5 | Innovative process of leaching of nickel supported activated carbon inammonium sulfate显示文摘 | ZHANG Zebiao WANG Wankun PENG Jinhui | 2011 | Advanced Manufacturing Systems2011，2，： | 1 |
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