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Process Backtracking and Reconstruction based on Task Chain Model
Jing Chen,Dewen Seng,Xujian Fang 보안공학연구지원센터 2016 International Journal of Grid and Distributed Comp Vol.9 No.4
Fundamental information of the design unit is described using the correlation between the nodes in the task chain. Data transfer between design units is formulated as fundamental data transfer, design rule transfer and path scheme transfer, respectively. The design process is stored with the node as the unit by using the algorithm for decomposing correlated nodes. The reconstruction method is employed to eliminate the redundant nodes that exist in various previous design processes, alleviating the degree of coupling. The performance of the proposed scheme is verified by applying it to the development of the low-voltage appliance.
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Zhou Zhongcheng,Wu Bin,Chen Jing,Shen Yiyu,Wang Jing,Chen Xujian,Fei Faming,Li Liang 한국유전학회 2023 Genes & Genomics Vol.45 No.11
Background Metastasis of liver cancer (LC) is the main cause of its high mortality. ETV4 is a critical regulatory factor in promoting LC progression, but the mechanism that ETV4 impacts LC proliferation, migration, and invasion is poorly understood. Objective Investigation of the molecular mechanism of LC metastasis is conducive to developing effective drugs that prevent LC metastasis. Methods Expression of ETV4 and its target gene B3GNT3 in LC tissue was analyzed by bioinformatics, and the result was further verified in LC cells by qRT-PCR. In vitro cellular assays evaluated the impact of ETV4 on the proliferation, migration, and invasion of LC cells. Chromatin immunoprecipitation (ChIP) and dual-luciferase reporter gene assay were conducted to analyze the interaction between B3GNT3 and ETV4. SB525334 suppressor was used to treat and access the activation of ETV4 on the TGF-β pathway. Results We discovered that ETV4 and B3GNT3 were evidently up-regulated in LC, and high expression of ETV4 was coupled to the increase of proliferation, migration, and invasion of LC cells and epithelial-mesenchymal transition ability. Besides, ETV4 could bind to the B3GNT3 promoter and activate its transcription. Knockdown of B3GNT3 could prominently suppress the effect of up-regulated ETV4 on LC cells. Meanwhile, ETV4 could activate the TGF-β signaling pathway via B3GNT3, while SB525334 treatment notably repressed the functions of ETV4. Conclusion ETV4 emerges as a driven oncogene in LC, and the ETV4/B3GNT3-TGF-β pathway promotes proliferation, migration, invasion, and epithelial-mesenchymal transition progress of LC. Inhibition of the pathway may provide an underlying method for the prevention and treatment of LC metastasis.
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