Copper redistribution in Atox1-deficient mouse fibroblast cells
Copper redistribution in Atox1-deficient mouse fibroblast cells
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DOI：
10.1007/s00775-009-0598-1
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发表时间：
2010-01-01
影响因子：
3
通讯作者：
Fahrni, Christoph J.
中科院分区：
文献类型：
--
作者：
McRae, Reagan;Lai, Barry;Fahrni, Christoph J.
对缺乏抗氧化剂 1 (Atox1) 的贴壁小鼠成纤维细胞进行定量同步加速器 X 射线荧光 (SXRF) 成像，揭示了与野生型细胞相比，亚细胞铜分布的显着差异。抗氧化剂 1 是一种金属伴侣蛋白，负责将铜传递给反式高尔基体网络中的铜酶。后者显示出明显的 Cu 核周定位，而 Atox1 缺陷细胞则显示出在整个细胞体内的大部分非结构化和弥漫性分布。相同样品中 Zn 和 Fe 的 SXRF 元素图的比较表明，两种细胞系之间没有显着差异。这些数据强调了 Atox1 的重要性，它不仅作为将铜传递给铜酶的金属伴侣，而且作为维持铜在细胞水平上的正确分布和组织的关键角色。
Quantitative synchrotron X-ray fluorescence (SXRF) imaging of adherent mouse fibroblast cells deficient in antioxidant-1 (Atox1), a metallochaperone protein responsible for delivering Cu to cuproenzymes in the trans-Golgi network, revealed striking differences in the subcellular Cu distribution compared with wild-type cells. Whereas the latter showed a pronounced perinuclear localization of Cu, the Atox1-deficient cells displayed a mostly unstructured and diffuse distribution throughout the entire cell body. Comparison of the SXRF elemental maps for Zn and Fe of the same samples showed no marked differences between the two cell lines. The data underscore the importance of Atox1, not only as a metallochaperone for delivering Cu to cuproenzymes, but also as a key player in maintaining the proper distribution and organization of Cu at the cellular level.