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Expression of influenza virus M2 inhibits epithelial sodium channel (ENaC) activity. Influenza M2 expression increases cellular reactive oxygen species (ROS) either through mitochondrial dysfunction or through activation of the NADPH oxidases. ROS activates PKC, which increases ENaC ubiquitination via the E3 ubiquitin ligase Nedd4-2. Ubiquitinated ENaC is proteasomally degraded, leading to decreased ENaC-mediated sodium transport. This is based on conclusions published previously (54).
