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Against this background, it is important to understand: (1) how is IFN signaling regulated at the pancreatic beta cell level; (2) how can this regulation modulate beta cell death and the generation of signals that contribute to trigger and amplify the local inflammation (insulitis); and (3) how can this regulation nike air max cheap cross talk with relevant candidate genes for T1D. Our findings indicate that USP18 inhibition increases IFN induced beta cell apoptosis via the mitochondrial pathway of cell death and increases inflammation by exacerbating the STAT signaling pathway and the expression of the T1D candidate gene MDA5 (melanoma differentiation associated protein 5). These data clarify the role of USP18 as a master regulator of type I IFN signaling in beta cells and underlines the importance of this pathway in beta cell inflammation and death in T1D..may1.6
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