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Early formation of ROS promoted cell survival through NF-κB activation via c-Src-mediated phosphorylation of IκBα and stabilization of HIF1α, while excessive ROS production stimulated cyt c and Smac/Diablo release, mitochondrial membrane potential loss and apoptotic signalling [77]
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Pancreatic transcripts of AKT1 , and FOXA2 , muscle transcripts of AKT1 , and INSR in the chicks were downregulated by the Se supranutrition and deficiency in the same direction
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