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• W1972790911 abstract "We have shown previously that endothelin-1 (ET-1) induction of Glut1 transcription is mediated by ET-1 responsive elements on enhancer 2, via both protein kinase Cepsilon (PKCepsilon)- and p42/p44 mitogen-activated protein kinase (MAPK)-dependent pathways. In the present study, we further explored the molecular mechanism involved. By using mutation constructs of luciferase reporter driven by Glut1 promoter/enhancers, chromatin immunoprecipitation and co-immunoprecipitation experiments, we were able to demonstrate that cooperative interaction between NF-kappaB and Sp1 were required to enhance Glut1 transcription in response to ET-1. While ET-1 may induce Sp1 expression via both PKC-and MAPK-dependent pathways, activation of NF-kappaB by ET-1 is mediated by a PKCepsilon/reactive oxygen species (ROS) cascade. Taken together, these results suggest that by activating NF-kappaB via PKCepsilon/ROS cascade and increasing Sp1 expression through both PKCepsilon- and MAPK-dependent pathways, ET-1 may activate Glut1 transcription by enhancing interaction between nuclear NF-kappaB and Sp1 as well as their binding to enhancer 2." @default.
• W1972790911 created "2016-06-24" @default.
• W1972790911 creator A5032443785 @default.
• W1972790911 creator A5068645529 @default.
• W1972790911 date "2008-04-01" @default.
• W1972790911 modified "2023-09-25" @default.
• W1972790911 title "Endothelin-1 induces glut1 transcription through enhanced interaction between Sp1 and NF-κB transcription factors" @default.
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• W1972790911 doi "https://doi.org/10.1016/j.cellsig.2007.12.012" @default.
• W1972790911 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/18249093" @default.
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