Female sex and history of prior pregnancies are associated with favorable melanoma outcomes, and past research from the Ridky Lab has shown that this melanoma protective effect likely results from estrogen signaling through the G protein-coupled estrogen receptor (GPER) on melanocytes. While the signaling mechanism is thought to be through cyclic adenosine monophosphate (cAMP) activation of protein kinase A (PKA), as GPER is thought to be a Gs-coupled receptor, there is still some uncertainty regarding the alpha subunit of GPER’s associated G protein. This project seeks to answer this question through the cloning of GPER into a PRRL vector and the use of bioluminescence resonance energy transfer (BRET) to confirm or reject the idea that GPER is Gs-coupled. Deeper knowledge of the nature of this receptor could lead to better understanding of this melanoma protective effect and, consequently, optimized treatment options for melanoma and other cancers.