脂肪酸代谢在生成活性氧自由基的同时具有激活抗氧化的能力，然而这一分子机制仍不清楚。我们新的研究发现FABP5蛋白可以结合细胞抗氧化NRF2信号通路中的TRIM21蛋白，为研究脂肪酸代谢和抗氧化机制的关系提供了线索。我们提出脂肪酸代谢相关蛋白FABP5通过TRIM21调节NRF2信号通路，进而调节了细胞抗氧化的活性。本项目拟利用免疫共沉淀、体外酶活实验、免疫荧光等技术探索FABP5与TRIM21相互作用的关键结合位点，脂肪酸代谢对FABP5-TRIM21相互作用的影响，相互作用对NRF2信号通路的调节以及FABP5蛋白的缺失对脂肪酸代谢激活细胞抗氧化的影响。本项目将揭示FABP5蛋白是协调脂肪酸代谢水平与细胞抗氧化水平的关键蛋白，为脂肪酸代谢过程中细胞抵御氧化损伤的研究提供一种新的机制，同时也为理解与脂肪酸代谢有关的氧化应激导致的疾病的分子机制供了思路。

Fatty acid metabolism has the ability to activate anti-oxidant response while producing reactive oxygen species. However, the molecular mechanism remains unclear. Our latest study found that FABP5 protein can bind TRIM21 protein, a regulator in NRF2 signaling pathway, which provides clues for the study of the relationship between fatty acid metabolism and anti-oxidant response. We propose that FABP5 regulates NRF2 signaling pathway through TRIM21, thereby regulating cell anti-oxidant activity. By immunoprecipitation, in vitro enzymatic activity assay and immunofluorescence techniques, the project aims to identify the key interaction sites between FABP5 and TRIM21, the regulatory effects of fatty acid metabolism on the interaction of FABP5-TRIM21, the regulatory effect of FABP5-TRIM21 on the activation of NRF2 signaling pathway, and the impact of deficiency of FABP5 on the activation of NRF2 signaling pathway during the fatty acid metabolism. This project is to uncover that FABP5 protein is the key protein to coordinate the level of fatty acid metabolism and the level of antioxidant activity in cells. It will provide a new mechanism for the research about how cell avoids oxidative damage in the process of fatty acid metabolism, and also provide ideas for understanding the molecular mechanism of diseases caused by oxidative stress related to fatty acid metabolism.