Rouault T, Rao K, Harford J, Mattia E, Klausner R D
J Biol Chem. 1985 Nov 25;260(27):14862-6.
We have examined the mechanism by which hemin regulates the expression of the human transferrin receptor. Previous work led to the suggestion that the regulatory signal is provided by heme (Ward J. H., Jordan, I., Kushner, J. P., and Kaplan, J. (1984) J. Biol. Chem. 259, 13235-13240). We demonstrated that hemin regulates the expression of the receptor via alterations in the rate of receptor biosynthesis. However, this effect can be completely abolished by addition of desferrioxamine, an intracellular iron chelator. Competition curves demonstrate that desferrioxamine and hemin affect the same intracellular iron pool. Since the chelator cannot remove iron from heme, we propose that hemin acts simply by delivering iron to a chelatable iron pool and that levels of chelatable iron provide the regulatory signal for expression of the transferrin receptor gene.
我们研究了血红素调节人类转铁蛋白受体表达的机制。先前的研究表明调节信号由血红素提供（沃德·J·H、乔丹、I、库什纳、J·P和卡普兰、J（1984年）《生物化学杂志》259卷，13235 - 13240页）。我们证明血红素通过改变受体生物合成速率来调节受体表达。然而，添加去铁胺（一种细胞内铁螯合剂）可完全消除这种效应。竞争曲线表明去铁胺和血红素影响同一个细胞内铁池。由于螯合剂不能从血红素中去除铁，我们提出血红素只是通过将铁传递到可螯合铁池来发挥作用，并且可螯合铁的水平为转铁蛋白受体基因的表达提供调节信号。
