VEGF amplifies transcription through ETS1 acetylation to enable angiogenesis
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Author
Chen, Jiahuan
Fu, Yi
Day, Daniel S.
Wang, Shiyan
Liang, Xiaodong
Gu, Fei
Zhang, Fang
Stevens, Sean M.
Zhou, Pingzhu
Li, Kai
Zhang, Yan
Lin, Ruei-zeng
Zhang, Jin
Sun, Kun
Han, Zeguang
Zhang, Bing
Note: Order does not necessarily reflect citation order of authors.
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https://doi.org/10.1038/s41467-017-00405-xMetadata
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Chen, J., Y. Fu, D. S. Day, Y. Sun, S. Wang, X. Liang, F. Gu, et al. 2017. “VEGF amplifies transcription through ETS1 acetylation to enable angiogenesis.” Nature Communications 8 (1): 383. doi:10.1038/s41467-017-00405-x. http://dx.doi.org/10.1038/s41467-017-00405-x.Abstract
Release of promoter-proximally paused RNA polymerase II (RNAPII) is a recently recognized transcriptional regulatory checkpoint. The biological roles of RNAPII pause release and the mechanisms by which extracellular signals control it are incompletely understood. Here we show that VEGF stimulates RNAPII pause release by stimulating acetylation of ETS1, a master endothelial cell transcriptional regulator. In endothelial cells, ETS1 binds transcribed gene promoters and stimulates their expression by broadly increasing RNAPII pause release. 34 VEGF enhances ETS1 chromatin occupancy and increases ETS1 acetylation, enhancing its binding to BRD4, which recruits the pause release machinery and increases RNAPII pause release. Endothelial cell angiogenic responses in vitro and in vivo require ETS1-mediated transduction of VEGF signaling to release paused RNAPII. Our results define an angiogenic pathway in which VEGF enhances ETS1–BRD4 interaction to broadly promote RNAPII pause release and drive angiogenesis.Other Sources
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5575285/pdf/Terms of Use
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