The bacterium Salmonella causes a spectrum of foodborne diseases ranging from acute gastroenteritis to systemic bloodstream infections. To outcompete the gut microbiota and subvert the host response, Salmonella uses two distinct type three secretion systems to translocate over 40 different effector proteins into host cells. These effectors interact with specific human proteins to subvert normal cellular processes, thus impairing the ability of host cells to respond to the invading bacteria. Our research focuses on the SseK family of Salmonella effectors, which have unknown function and play an unknown role in Salmonella infection. The SseK effectors show strong sequence similarity to NleB1, a unique glycosyltransferase effector of enteropathogenic E. coli, and therefore we predict the SseK effectors may also function as glycosyltransferases. NleB1 catalyses a unique post-translational modification in which the sugar N-acetylglucosamine is transferred to arginine residues of several host immune signalling proteins. We predict the SseK effectors have a similar biochemical activity, though they appear to target different host proteins. Therefore, the aim of our work is to identify the host substrates of the SseK family, to determine the biochemical modification mediated by these effectors, and to determine the contribution of this activity to Salmonella infection. We have found that each of the SseK effectors have different subcellular localisations when translocated into host cells, and have seen evidence that SseK2 and SseK3 co-localise with the host Golgi. Further, we have used an antibody raised against N-acetylglucosamine-modified arginine to probe infected cell lysates, and found that the SseKs are active as glycosyltransferases and modify several host proteins. We are currently identifying these modified proteins by combining immunoprecipitation with quantitative mass spectrometry. Ultimately, determining the activity of the SseK effectors will contribute to an understanding of how Salmonella is able to survive within host cells and achieve infection.