My project researched the effects of copper on the integrated stress response (ISR), specifically its effect on PKR-like endoplasmic reticulum kinase (PERK), one of the four kinases that activates the ISR. PERK is activated in response to misfolded proteins within the cell and is activated chronically in many neurodegenerative diseases. Previous research showed that PERK has a copper-binding domain, so my project’s goal was to determine if PERK activation is copper-dependent. By treating Mouse Embryonic Fibroblast cells (MEFs) with two drugs that activate the ISR either through PERK or through other mechanisms in combination with a copper chelator to reduce the amount of copper in the cells, I was able to establish that PERK behavior does depend on copper levels within the cell.