Utilization of cellular kinase serine-threonine kinase 11 interacting protein (STK11IP) to promote virus replication 3682

Abstract Description Viruses utilize host factors to control the cellular environment for successful replication. We have shown that STK11IP expression is increased during viral infection using rotavirus as a model. STK11IP regulates the function of STK11, a kinase that plays multiple roles in cell biology. The objective was to elucidate the STK11-independent mechanism by which STK11IP functions to promote replication. RNAi-mediated knockdown determined the independent/dependent relationship of the interacting protein to the downstream regulator during infection. RNAi-mediated knockdown suggested that STK11IP can act independently of STK11 during rotavirus infection, despite their co-expressive relationship. The Class, Architecture, Topology, and Homology database found that STK11IP homology matched with six different structural domains and 38 different functional families. Two functional families identified were ribonuclease inhibitor 1 and Toll-like receptor 7 because of their function in preventing RNA degradation and facilitating intra-cellular pathogen immune response respectively. These findings suggest that STK11IP may serve as a potential therapeutic target across different viral families, offering insights into viral replication mechanisms and host cell interactions. Funding Sources NIH/NIGMS Award Number 5U54GM104942-04 Topic Categories Viral Immunology (VIR)