目的探讨泛素-蛋白酶体通路(UPP)在实验性视网膜脱离(RD)中对视网膜细胞凋亡的调控作用。
Objective to investigate the role of ubiquitin-proteasome pathway (UPP) in the regulation of retinal cell apoptosis after experimental retinal detachment (RD).
CHIP的特殊结构特征使其成为沟通分子伴侣与泛素-蛋白酶体通路之间的桥梁，是蛋白质量控制系统的重要中介分子。
The special characteristics of CHIP make it become the bridge of molecular chaperone system and ubiquitin-proteasome pathway.
泛素- 蛋白酶体通路介导细胞蛋白质的降解，在细胞周期、基因转录及表达、 抗原提呈和炎症演进等方面发挥调控作用。
Ubiquitin-proteasome pathway mediates the degradation of cell protein and modulates cell cycle, gene translation and expression, antigen presentation and inflammation development.
蛋白酶体的抑制在肿瘤的信号通路定向治疗方面已经成为一个极其有希望的途径。
Inhibition of proteasome has been emerging as a promising approach in pathway-directed cancer therapy.
蛋白酶体抑制剂MG- 132可以减轻高氧引起的肺损伤，可能对p 38 MAPK信号通路有抑制作用。
The proteasome inhibitor MG-132 can reduce the lung injury induced by hyperoxia and inhibit P38MAPK signaling pathway.
蛋白酶体抑制剂MG- 132可以减轻高氧引起的肺损伤，可能对p 38 MAPK信号通路有抑制作用。
The proteasome inhibitor MG-132 can reduce the lung injury induced by hyperoxia and inhibit P38MAPK signaling pathway.
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