Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
5905145 | Gene | 2016 | 6 Pages |
Abstract
Leptin receptor overlapping transcript (LepROT) is co-transcribed with the leptin receptor (LepR). However, the function and mechanism of LepROT in insulin pathway is unclear. In this study, we report the function of LepROT in maintaining consistent FoxO transcription. LepROT is constitutively expressed during larval development. 20-Hydroxyecdysone, methoprene, and insulin have no effect on the transcription of LepROT. However, the knockdown of LepROT by dsRNA injection in larvae causes delay of the development of Helicoverpa armigera. Knockdown of LepROT results in the upregulation of FoxO and downregulation of PI3K. The knockdown of LepROT also results in the subcellular translocation of FoxO from cytoplasm to nuclei. By contrast, overexpression of LepROT in the HaEpi cell line inhibits FoxO expression. Results suggest that LepROT participates in insulin signaling.
Keywords
JAK220Einsulin/insulin-like growth factor20-HydroxyecdysoneJanus Kinase 2LEPRSTAT-3IRSORFPI3KIGFFBSH. armigerainsulin receptor substrateDimethyl sulfoxideDevelopmentfetal bovine serumFoxOphosphoinositide-3 kinaseopen reading frameInsulin signaling pathwaypolymerase chain reactionPCRHelicoverpa armigerainsulin receptorLeptin receptor
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Authors
Chuan-Xu Wang, Ai-Hua Zhao,