Wolf G
Department of Nutritional Sciences, University of California, Berkeley 94720, USA.
Nutr Rev. 1995 Apr;53(4 Pt 1):98-9. doi: 10.1111/j.1753-4887.1995.tb01528.x.
Mice were made deficient in transthyretin (TTR), the protein that normally transports plasma retinol complexed with retinol-binding protein (RBP), by targeted mutagenesis (TTR-knockout mice). The TTR- mice were healthy and fertile, despite extremely low plasma retinol and RBP levels (6% of wild type). Circulating retinoic acid was 2.3 times that of wild-type controls. Liver levels of RBP were 60% higher in the TTR-mutants compared to wild-type mice, suggesting that lack of TTR may block secretion of RBP-retinol from liver.
通过靶向诱变使小鼠缺乏转甲状腺素蛋白(TTR),该蛋白通常运输与视黄醇结合蛋白(RBP)复合的血浆视黄醇(TTR基因敲除小鼠)。尽管血浆视黄醇和RBP水平极低(为野生型的6%),TTR基因敲除小鼠仍健康且可育。循环视黄酸是野生型对照的2.3倍。与野生型小鼠相比,TTR突变体肝脏中的RBP水平高60%,这表明缺乏TTR可能会阻止肝脏中RBP - 视黄醇的分泌。