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在HeLa细胞中,铁螯合作用可增强铁转运刺激因子(SFT)的表达;在肝脏中,血色素沉着症可增强SFT的表达。

Expression of SFT (stimulator of Fe transport) is enhanced by iron chelation in HeLa cells and by hemochromatosis in liver.

作者信息

Yu J, Yu Z K, Wessling-Resnick M

机构信息

Department of Nutrition, Harvard School of Public Health, Boston, Massachusetts 02115, USA.

出版信息

J Biol Chem. 1998 Dec 25;273(52):34675-8. doi: 10.1074/jbc.273.52.34675.

Abstract

SFT (stimulator of Fe transport) is a novel transport protein that has been found to facilitate uptake of iron presented to cells as either Fe(II) or Fe(III). When HeLa cells are exposed to the iron chelator desferrioxamine, levels of SFT mRNA increase in an actinomycin D-sensitive manner. In contrast, cells exposed to high levels of iron down-regulate SFT expression in a time-dependent and reversible fashion. Thus, homeostatic regulation of SFT expression not only ensures that sufficient levels of iron are maintained but also limits excessive assimilation to prevent potentially harmful effects of this toxic metal. The unexpected observation that SFT transcript levels are up-regulated in hemochromatosis patients therefore suggests that enhanced SFT expression contributes to the etiology of this iron overload disorder.

摘要

铁转运刺激因子(SFT)是一种新型转运蛋白,已发现它能促进细胞摄取以Fe(II)或Fe(III)形式呈现的铁。当HeLa细胞暴露于铁螯合剂去铁胺时,SFT mRNA水平以放线菌素D敏感的方式增加。相反,暴露于高水平铁的细胞以时间依赖性和可逆方式下调SFT表达。因此,SFT表达的稳态调节不仅确保维持足够的铁水平,还限制过度吸收以防止这种有毒金属的潜在有害影响。血色病患者中SFT转录水平上调这一意外观察结果因此表明,SFT表达增强促成了这种铁过载疾病的病因。

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