AI Article Synopsis
- Copper is important for cells, helping them work properly, but too much of it can be harmful.
- Researchers discovered that a protein called Refrex1 helps control how much copper gets into cells, especially when there's a lot of it outside.
- If levels of Refrex1 are lowered, cells can get too much copper, leading to damage and cell death, but this can be stopped with a special treatment that removes copper.
Article Abstract
Copper is a critical element for eukaryotic life involved in numerous cellular functions, including redox balance, but is toxic in excess. Therefore, tight regulation of copper acquisition and homeostasis is essential for cell physiology and survival. Here, we identify a different regulatory mechanism for cellular copper homeostasis that requires the presence of an endogenous retroviral envelope glycoprotein called Refrex1. We show that cells respond to elevated extracellular copper by increasing the expression of Refrex1, which regulates copper acquisition through interaction with the main copper transporter CTR1. Downmodulation of Refrex1 results in intracellular copper accumulation leading to reactive oxygen species (ROS) production and subsequent apoptosis, which is prevented by copper chelator treatment. Our results show that Refrex1 has been co-opted for its ability to regulate copper entry through CTR1 in order to limit copper excess, redox imbalance, and ensuing cell death, strongly suggesting that other endogenous retroviruses may have similar metabolic functions among vertebrates.
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| http://dx.doi.org/10.1016/j.celrep.2023.113065 | DOI Listing |
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