Cellular copper transport.
Cellular copper transport.
复制标题
DOI：
10.1146/annurev.nu.15.070195.001453
复制
发表时间：
1995
影响因子：
8.9
通讯作者：
Chris D. Vulpe;Seymour Packman
中科院分区：
文献类型：
--
作者：
Chris D. Vulpe;Seymour Packman
细胞铜转运过程是所有生物体在细胞生化过程中正确利用和避免铜过量毒性所必需的。铜输入到细菌，酵母和哺乳动物细胞中需要在介导的运输步骤中具有金属结合和催化结构域的蛋白质的协调功能。在进入后，跨物种发现的解毒机制包括铜与特定蛋白质（例如金属硫蛋白）的结合以及铜转移到隔离的细胞区室（例如周质空间，溶酶体）。多种蛋白质介导细菌的细胞内转移，谷胱甘肽可能在哺乳动物细胞胞质铜传递到铜酶中发挥重要作用。对两种人类铜转运障碍的研究，门克斯病和威尔逊病，导致鉴定了一类重要的介导细胞铜输出的蛋白质。门克斯和威尔逊病基因产物是P型铜转运ATP酶，具有ATP酶结构域和N-末端金属结合氨基酸基序，这些基序在单细胞和哺乳动物生物中进化上保守。这些观察结果表明，酵母和细菌铜转运蛋白，或这些蛋白质的个别域，通常可能有同源物在哺乳动物系统。
Cellular copper transport processes are required by all organisms for correct utilization in cell biochemical processes and avoidance of the toxicity of copper excess. Copper import into bacterial, yeast, and mammalian cells requires the coordinate function of proteins with both metal-binding and catalytic domains in mediated transport steps. Following entry, detoxification mechanisms found across species include the binding of copper to specific proteins (e.g. metallothioneins) and the transfer of copper into isolated cell compartments (e.g. periplasmic space, lysosome). Multiple proteins mediate intracellular transfers in bacteria, and glutathione may play a major role in cytosolic copper delivery to cuproenzymes in mammalian cells. Study of two human disorders of copper transport, Menkes disease and Wilson disease, led to the identification of an important category of proteins mediating cell copper export. The Menkes and Wilson disease gene products are copper-transporting ATPases of the P type, with ATPase domains and N-terminal metal-binding amino acid motifs that are evolutionarily conserved in unicellular and mammalian organisms. These observations suggest that yeast and bacterial copper transport proteins, or individual domains of these proteins, may generally have homologues in mammalian systems.