中文摘要：

FHC和Bim参与细胞铁代谢和由ROS引起的细胞凋亡过程．但是其具体的分子机制还未阐明．用pLexA．BimL作为诱饵，筛选了一个基于pBD42AD的胎脑cDNA文库，发现FHC是一个新的Bim相互作用蛋白．酵母杂交实验发现Bim的相互作用片段为BH3功能域．上述相互作用进一步用免疫共沉淀和荧光共定位得以证实．在HEK293细胞过表达FHC可以减轻由Bim过表达或ROS所引起的细胞凋亡，而用FHC特异性siRNA调低FHC表达，则增加Bim过表达或ROS引起的细胞凋亡．研究首次报道了Bim和FHC的相互作用以及对细胞凋亡和氧化应激的影响，为进一步阐明FHC和Bim参与凋亡和ROS反应提供了新的线索．

英文摘要：

It is known that both FHC and Bim is involved in the regulation of intracellular iron metabolism, and plays a role in cellular apoptosis caused by ROS. However, the molecular mechanisms of FHC regulating apoptosis are remaining unknown. Using pLexA-Bim L as bait, a pB42AD based eDNA library was screened and FHC was identified as a Bim interacting protein. The interaction domain on Bim was located to BH3 domain. The interaction between FHC and Bim was further verified by co-immunoprecipitation. The subcellular location assay revealed that both Bim and FHC are located to cytoplasm and partially overlap. Over expression of FHC in HEK293 protects the cells from cytotoxity caused by over expressing Bim L. Both over-expression and knock-down analysis of FHC suggest that FHC protects HEK293 cells from hydrogen peroxide treatment. A novel Bim interacting protein, FHC was identified and it was suggested that FHC play a role in Bim mediated apoptosis and oxidative stress.