硒蛋白F（SELENOF）与视黄醇脱氢酶11（RDH11）的相互作用表明SELENOF在维生素A代谢中发挥作用。
The interaction of selenoprotein F (SELENOF) with retinol dehydrogenase 11 (RDH11) implied a role of SELENOF in vitamin A metabolism.
作者信息
Tian Jing, Liu Jiapan, Li Jieqiong, Zheng Jingxin, Chen Lifang, Wang Yujuan, Liu Qiong, Ni Jiazuan
机构信息
1College of Life Sciences and Oceanography, Shenzhen Key Laboratory of Marine Bioresources and Eco-environmental Science, Shenzhen University, Shenzhen, 518060 China.
2College of Life Sciences and Oceanography, Shenzhen Key Laboratory of Microbial Genetic Engineering, Shenzhen University, Shenzhen, 518060 China.
出版信息
Nutr Metab (Lond). 2018 Jan 22;15:7. doi: 10.1186/s12986-017-0235-x. eCollection 2018.
BACKGROUND
Selenoprotein F (SELENOF, was named as 15-kDa selenoprotein) has been reported to play important roles in oxidative stress, endoplasmic reticulum (ER) stress and carcinogenesis. However, the biological function of SELENOF is still unclear.
METHODS
A yeast two-hybrid system was used to screen the interactive protein of SELENOF in a human fetal brain cDNA library. The interaction between SELENOF and interactive protein was validated by fluorescence resonance energy transfer (FRET), co-immunoprecipitation (co-IP) and pull-down assays. The production of retinol was detected by high performance liquid chromatograph (HPLC).
RESULTS
Retinol dehydrogenase 11 (RDH11) was found to interact with SELENOF. RDH11 is an enzyme for the reduction of all-trans-retinaldehyde to all-trans-retinol (vitamin A). The production of retinol was decreased by SELENOF overexpression, resulting in more retinaldehyde.
CONCLUSIONS
SELENOF interacts with RDH11 and blocks its enzyme activity to reduce all-trans-retinaldehyde.
背景
硒蛋白F（SELENOF，曾被命名为15 kDa硒蛋白）据报道在氧化应激、内质网（ER）应激和致癌过程中发挥重要作用。然而，SELENOF的生物学功能仍不清楚。
方法
利用酵母双杂交系统在人胎脑cDNA文库中筛选SELENOF的相互作用蛋白。通过荧光共振能量转移（FRET）、免疫共沉淀（co-IP）和下拉实验验证SELENOF与相互作用蛋白之间的相互作用。通过高效液相色谱（HPLC）检测视黄醇的产生。
结果
发现视黄醇脱氢酶11（RDH11）与SELENOF相互作用。RDH11是一种将全反式视黄醛还原为全反式视黄醇（维生素A）的酶。SELENOF过表达导致视黄醇产生减少，从而产生更多的视黄醛。
结论
SELENOF与RDH11相互作用并阻断其将全反式视黄醛还原的酶活性。
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