TY - JOUR AU - Wang, Chengmin AU - Liu, Huimin AU - Luo, Jing AU - Chen, Lin AU - Li, Meng AU - Su, Wen AU - Zhao, Na AU - Liu, Shelan AU - Xie, Li AU - Jia, Yaxiong AU - Ding, Hua AU - Wan, Xiufeng AU - He, Hongxuan PY - 2017 M3 - Original Research TI - HA Triggers the Switch from MEK1 SUMOylation to Phosphorylation of the ERK Pathway in Influenza A Virus-Infected Cells and Facilitates Its Infection JO - Frontiers in Cellular and Infection Microbiology UR - https://www.frontiersin.org/articles/10.3389/fcimb.2017.00027 VL - 7 SN - 2235-2988 N2 - Several post-translational modifications in host cells are hijacked by pathogens to facilitate their propagation. A number of components of the influenza virus have been reported to be modified by small ubiquitin-like modifier (SUMO) proteins during infection. We hypothesized that the MAPK/ERK pathway could be modified by SUMO1 because the SUMOylation of MEK1 was quickly eliminated after influenza A virus infection. We identified host cell MEK1 as a target of SUMO1 through LC/MS/MS, and enhanced MEK1 SUMOylation inhibited the infection of the virus, while inhibition of host cell MEK1 SUMOylation facilitated virus propagation. Further investigation demonstrated that the MAPK/ERK pathway is downregulated by MEK1 SUMOylation, which is inhibited by influenza virus infection. Furthermore, membrane accumulation of hemagglutinin promoted MEK1 phosphorylation and gradually abrogated the MEK1 SUMOylation. Taken together, we report a possible mechanism in which HA may trigger the ERK pathway in influenza A virus-infected cells as the switch from MEK1 SUMOylation to phosphorylation, facilitating virus infection. ER -