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Abstract
G-protein coupled receptors (GPCRs) mediate a wide variety of cellular functions related to cell proliferation and survival. Regulators of G-protein Signaling (RGS) proteins that are important negative regulators of both G-proteins and GPCR products. The focus of this thesis involves two human protein variants of RGS10 and their effects on cytokine levels. RGS proteins are GTPase Accelerating Proteins (GAPs) which can facilitate an increased rate of GTP hydrolysis to drive inactivation of GPCR signaling. Based on their ability to regulate GPCRs, RGS proteins are implicated in multiple disease states including cancer and neuro-inflammation. The aim of this study was to define the similarities or differences among RGS10 protein isoforms, and help understand their non-canonical function. Particularly, differences in primary sequence of RGS10 protein variants and their ability to mediate inflammatory cytokines in human embryonic kidney (HEK) cells was investigated.