A novel mammalian iron-regulated protein involved in intracellular iron metabolism
A novel mammalian iron-regulated protein involved in intracellular iron metabolism
复制标题
DOI：
10.1074/jbc.m000713200
复制
发表时间：
2000-06-30
影响因子：
4.8
通讯作者：
Haile, DJ
中科院分区：
文献类型：
--
作者：
Abboud, S;Haile, DJ
我们已经分离并鉴定了一个新的铁调控基因，该基因与金属转运蛋白1家族的二价金属转运蛋白同源。该基因被称为金属转运蛋白(Mtp1)，在参与体内铁稳态的组织中表达，包括发育和成熟的网状内皮系统、十二指肠和妊娠子宫。MTP1在胚胎的肌肉和中枢神经系统细胞中也有表达。在亚细胞水平上，MTP1定位于十二指肠上皮细胞的基底膜和网状内皮细胞的胞浆室。在组织培养细胞中过表达MTP1会导致细胞内铁耗竭。在成年小鼠中，MTP1在肝脏和十二指肠中的表达是相互调节的。缺铁诱导MTP1在十二指肠的表达，但下调肝脏的表达。这些数据表明，MTP1是一种铁调节的跨膜蛋白，参与细胞内的铁代谢。
We have isolated and characterized a novel iron-regulated gene that is homologous to the divalent metal transporter 1 family of metal transporters. This gene, termed metal transporter protein (mtp1), is expressed in tissues involved in body iron homeostasis including the developing and mature reticuloendothelial system, the duodenum, and the pregnant uterus. MTP1 is also expressed in muscle and central nervous system cells in the embryo. At the subcellular level, MTP1 is localized to the basolateral membrane of the duodenal epithelial cell and a cytoplasmic compartment of reticuloendothelial system cells. Overexpression of MTP1 in tissue culture cells results in intracellular iron depletion. In the adult mouse, MTP1 expression in the liver and duodenum are reciprocally regulated. Iron deficiency induces MTP1 expression in the duodenum but down-regulates expression in the liver. These data indicate that MTP1 is an iron-regulated membrane-spanning protein that is involved in intracellular iron metabolism.