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人肝癌细胞系HepG2中转铁蛋白合成的铁调节

Iron regulation of transferrin synthesis in the human hepatoma cell line HepG2.

作者信息

Barnum-Huckins K, Adrian G S

机构信息

Department of Cellular and Structural Biology, The University of Texas Health Science Center, 7703 Floyd Curl Drive, San Antonio, TX 78284, USA.

出版信息

Cell Biol Int. 2000;24(2):71-7. doi: 10.1006/cbir.1999.0456.

Abstract

In human beings, serum transferrin levels increase during iron deficiency and decrease with iron overload. Yet, whether or not iron levels actually affect the synthesis of transferrin in human liver cells is not known. In previous studies, iron was shown to suppress the expression of chimeric human transferrin genes in livers of transgenic mice. The goal of this study was to determine if iron suppresses intact endogenous human transferrin synthesis by testing the effects of changes in iron levels on synthesis of transferrin in a human hepatoma cell line HepG2. In HepG2 cells, normalized(35)S-metabolically labeled transferrin synthesis was consistently less following iron treatment with hemin or ferric citrate, than following treatment with an iron-chelator deferroxamine. Thus, this study provides new evidence that iron can regulate synthesis of intact endogenous human transferrin.

摘要

在人类中,血清转铁蛋白水平在缺铁时升高,在铁过载时降低。然而,铁水平是否真的会影响人类肝细胞中转铁蛋白的合成尚不清楚。在先前的研究中,铁被证明可抑制转基因小鼠肝脏中嵌合型人类转铁蛋白基因的表达。本研究的目的是通过测试铁水平变化对人肝癌细胞系HepG2中转铁蛋白合成的影响,来确定铁是否会抑制完整内源性人类转铁蛋白的合成。在HepG2细胞中,用血红素或柠檬酸铁进行铁处理后,经归一化的(35)S-代谢标记转铁蛋白合成始终低于用铁螯合剂去铁胺处理后的水平。因此,本研究提供了新的证据,表明铁可以调节完整内源性人类转铁蛋白的合成。

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