In contrast, we observed a slight increase in IRS1 expression levels when silencing JNK1. The viral M2 protein, a tetrameric proton channel, conducts protons from the endosomal lumen into the virion. In the trans-Golgi network of infected cells, M2 also prevents lowpH inactivation of HA following activation of the precursor, HA0, by furin cleavage to HA1 and HA2, and it appears to have yet a Neosperidin-dihydrochalcone further role during membrane scission, the final step of virus budding. A small effect of M2 activity on the kinetics of hemifusion has led to the proposal that internal virion acidification can accelerate membrane remodeling driven by HA conformational rearrangements in the context of an intact virion. Those observations suggest that the effect of internal acidification on the kinetics of fusion-pore formation might be more substantial, but this possibility has not been explored. Molecular dynamics simulations have led to 2-O-beta-L-galactopyranosylorientin opposing models, describing M2 either as a simple proton channel or as a proton transporter. Measurements of the kinetics of proton transfer through M2 channels reconstituted in liposomes have offered support to the transporter model. To study M2 activity in the context of an intact virion, to determine whether M2 activity influences fusion, and to determine the relative rates of internal acidification and fusion-pore formation, we have adapted our single-virion fusion assay to include measurements of the kinetics of internal acidification. Associated changes in intestinal inflammatory parameters include higher densities of lymphocyte populations, aberrant cytokine profiles, and deposition of immunoglobulin and complement C1q on the basolateral enterocyte membrane. In addition, Proteobacteria and Betaproteobacteria abundance were not significantly different between AUT-GI and Control-GI children after adjusting for the expression of all disaccharidases and transporters. However, as ASD status remained a significant predictor of disaccharidase mRNA expression even after adjusting for CDX2 and villin, additional factors must also contribute.