基因敲除
调节器
泛素
细胞生物学
氧化应激
线粒体融合
细胞凋亡
蛋白酶体
线粒体
化学
肾
融合蛋白
再灌注损伤
活性氧
缺血
生物
医学
生物化学
基因
线粒体DNA
内科学
内分泌学
重组DNA
作者
Yang Du,Chuanmin Chu,Dong Zhuo,Jinzhuo Ning
标识
DOI:10.1016/j.ijbiomac.2022.04.054
摘要
Tripartite motif 35 (TRIM35) is a member of the tripartite motif protein family and has been recognized to play a key role in immune-inflammatory diseases. However, the role of TRIM35 in renal ischemia-reperfusion injury (IRI) remains unclear. Our study proved that knockdown of TRIM35 alleviates kidney IRI by inhibiting oxidative stress and enhancing mitochondrial fusion. In addition, our experimental results found that TRIM35 interacts with TP53-induced glycolysis and apoptosis regulator (TIGAR) and promotes the polyubiquitination of TIGAR and induces its degradation in the proteasome pathway. Furthermore, TIGAR knockdown significantly inhibited mitochondrial fusion. These results indicate that TRIM35 is a potential therapeutic target for renal IRI.
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