https://www.selleckchem.com/pr....oducts/cftrinh-172.h
Upon exposure to amyloid-β oligomers (Aβ1-42), glial cells start expressing proinflammatory cytokines, despite an increase in levels of repressive microRNAs (miRNAs). Exploring the mechanism of this potential immunity of target cytokine mRNAs against repressive miRNAs in amyloid-β-exposed glial cells, we have identified differential compartmentalization of repressive miRNAs in glial cells that explains this aberrant miRNA function. In Aβ1-42-treated cells, whereas target mRNAs were found to be associated with polysomes attached to e