# |
PMID |
Sentence |
1 |
26278786
|
We herein report that pro-inflammatory cytokines, IFNG and TNFA, synergistically activated transcription of RNF213 both in vitro and in vivo.
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2 |
26278786
|
Using various chemical inhibitors, we found that AKT and PKR pathways contributed to the transcriptional activation of RNF213.
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3 |
26278786
|
Chemical inhibitors for AKT (LY294002) and PKR (C16) disrupted their angiogenic potentials, suggesting that RNF213 and its upstream pathways cooperatively organize the process of angiogenesis.
|
4 |
26278786
|
We herein report that pro-inflammatory cytokines, IFNG and TNFA, synergistically activated transcription of RNF213 both in vitro and in vivo.
|
5 |
26278786
|
Using various chemical inhibitors, we found that AKT and PKR pathways contributed to the transcriptional activation of RNF213.
|
6 |
26278786
|
Chemical inhibitors for AKT (LY294002) and PKR (C16) disrupted their angiogenic potentials, suggesting that RNF213 and its upstream pathways cooperatively organize the process of angiogenesis.
|
7 |
26278786
|
We herein report that pro-inflammatory cytokines, IFNG and TNFA, synergistically activated transcription of RNF213 both in vitro and in vivo.
|
8 |
26278786
|
Using various chemical inhibitors, we found that AKT and PKR pathways contributed to the transcriptional activation of RNF213.
|
9 |
26278786
|
Chemical inhibitors for AKT (LY294002) and PKR (C16) disrupted their angiogenic potentials, suggesting that RNF213 and its upstream pathways cooperatively organize the process of angiogenesis.
|