CTR1 与 ATP7A/B 是关键铜转运蛋白  ，在铜的调控中扮演重要角色 。CTR1的水平受到铜浓度的负反馈调节作用  ，铜缺乏时  ，肠和肝中 CTR1上调  ，增强细胞对铜的吸收  ，同时肝脏会进行铜保存以减少铜的流失；当铜超载时  ，肠和肝的 CTR1和金属硫蛋白转录增加  ，与过量的铜结合降低铜的毒性 。ATP7A在全身中普遍表达（肝脏处于正常状态除外）   ，而ATP7B主要在肝脏和大脑、胎盘的某些区域表达 。ATP7A/B也有类似CTR1的作用  ，在铜不足时  ，ATP7A/B 将铜从细胞质转运到高尔基体  ，且ATP7A还能将铜从血-脑脊液屏障运输到脑实质内  ，增加铜含量；铜过多时  ，ATP7A/B与动力蛋白的 p62亚基相互作用  ，并运输到囊泡通过质膜将多余的铜排出细胞  ，或进入肝脏的胆汁  ，经消化道排出  ，降低铜水平 。

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抗坏血酸锰Manganese Ascorbate、抗坏血酸亚铁Ferrous Ascorbate、赖氨酸甘氨酸镁Magnesium Lysinate Glycinate、甘氨酸谷氨酰胺镁Magnesium Glycinate Glutamine、柠檬酸苹果酸镁Magnesium Citrate Malate、柠檬酸锶Strontium Citrate、柠檬酸锰Manganese Citrate、柠檬酸铜Copper Citrate、天门冬氨酸锂Lithium Aspartate、牛磺酸硒Selenium Taurate.

CTR1 and ATP7A/B: key transport proteins in copper homeostasis and their regulatory mechanisms (Copper Malate, Copper Glutamate).

CTR1 and ATP7A/B are key copper transport proteins and play an important role in copper regulation. The level of CTR1 is negatively regulated by copper concentration. When copper is deficient, CTR1 in the intestine and liver is upregulated, enhancing the absorption of copper by cells, while the liver conserves copper to reduce copper loss; when copper is overloaded, CTR1 and metallothionein transcription in the intestine and liver increases, binding to excess copper to reduce copper toxicity. ATP7A is widely expressed throughout the body (except when the liver is in a normal state), while ATP7B is mainly expressed in the liver and certain areas of the brain and placenta. ATP7A/B also has a similar effect to CTR1. When copper is insufficient, ATP7A/B transports copper from the cytoplasm to the Golgi apparatus, and ATP7A can also transport copper from the blood-cerebrospinal fluid barrier to the brain parenchyma to increase the copper content; when copper is excessive, ATP7A/B interacts with the p62 subunit of dynein and transports it to vesicles to excrete excess copper from cells through the plasma membrane, or enter the bile of the liver and excrete it through the digestive tract to reduce copper levels.

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