CTR1與ATP7A/B:銅穩(wěn)態(tài)中的關(guān)鍵轉(zhuǎn)運(yùn)蛋自及其調(diào)控機(jī)制（蘋(píng)果酸銅Copper Malate、谷氨酸銅Copper Glutamate）。發(fā)表時(shí)間：2024-12-04 17:57 CTR1 與 ATP7A/B 是關(guān)鍵銅轉(zhuǎn)運(yùn)蛋白，在銅的調(diào)控中扮演重要角色。CTR1的水平受到銅濃度的負(fù)反饋調(diào)節(jié)作用，銅缺乏時(shí)，腸和肝中 CTR1上調(diào)，增強(qiáng)細(xì)胞對(duì)銅的吸收，同時(shí)肝臟會(huì)進(jìn)行銅保存以減少銅的流失；當(dāng)銅超載時(shí)，腸和肝的 CTR1和金屬硫蛋白轉(zhuǎn)錄增加，與過(guò)量的銅結(jié)合降低銅的毒性。ATP7A在全身中普遍表達(dá)（肝臟處于正常狀態(tài)除外），而ATP7B主要在肝臟和大腦、胎盤(pán)的某些區(qū)域表達(dá)。ATP7A/B也有類(lèi)似CTR1的作用，在銅不足時(shí)，ATP7A/B 將銅從細(xì)胞質(zhì)轉(zhuǎn)運(yùn)到高爾基體，且ATP7A還能將銅從血-腦脊液屏障運(yùn)輸?shù)侥X實(shí)質(zhì)內(nèi)，增加銅含量；銅過(guò)多時(shí)，ATP7A/B與動(dòng)力蛋白的 p62亞基相互作用，并運(yùn)輸?shù)侥遗萃ㄟ^(guò)質(zhì)膜將多余的銅排出細(xì)胞，或進(jìn)入肝臟的膽汁，經(jīng)消化道排出，降低銅水平。 公司官網(wǎng)：www.wilincare.net歡迎選購(gòu)！ 抗壞血酸錳Manganese Ascorbate、抗壞血酸亞鐵Ferrous Ascorbate、賴(lài)氨酸甘氨酸鎂Magnesium Lysinate Glycinate、甘氨酸谷氨酰胺鎂Magnesium Glycinate Glutamine、檸檬酸蘋(píng)果酸鎂Magnesium Citrate Malate、檸檬酸鍶Strontium Citrate、檸檬酸錳Manganese Citrate、檸檬酸銅Copper Citrate、天門(mén)冬氨酸鋰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. Company website: www.wilincare.net Welcome to purchase! Manganese Ascorbate, Ferrous Ascorbate, Magnesium Lysinate Glycinate, Magnesium Glycinate Glutamine, Magnesium Citrate Malate, Strontium Citrate, Manganese Citrate, Copper Citrate, Lithium Aspartate, Selenium Taurate. |