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Furthermore, we found that the AMPK-mTOR-ULK1 path is associated with Vip3Aa-induced autophagy, that will be associated with the destruction of ATP homeostasis in Vip3Aa-treated cells. Both the elevated p62 level additionally the enhanced amounts of GFP-RFP-Atg8 yellow fluorescent spots demonstrated that autophagy in Sf9 cells had been inhibited at 24 h after Vip3Aa therapy. With the prolongation of Vip3Aa therapy time, this inhibition became more severe and led to autophagosome

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