Title : Sodium tanshinone IIA sulfonate suppresses heat stress-induced endothelial cell apoptosis by promoting NO production through upregulating the PI3K/AKT/eNOS pathway.

Pub. Date : 2017 Aug

PMID : 28627664






5 Functional Relationships(s)
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1 The results presented in the present study demonstrated that the PI3K/AKT pathway was stimulated by STS treatment and that eNOS phosphorylation at Ser-1177 was also upregulated, resulting in increased nitric oxide production in HUVECs under heat stress. Serine nitric oxide synthase 3 Homo sapiens
2 Using specific inhibitors, the authors confirmed that STS-induced endothelial nitric oxide synthase (eNOS) phosphorylation at Ser-1177 was activated by protein kinase B phosphorylation at Ser-473, involving activation of phosphatidylinositol-3 kinase (PI3K). Serine nitric oxide synthase 3 Homo sapiens
3 Using specific inhibitors, the authors confirmed that STS-induced endothelial nitric oxide synthase (eNOS) phosphorylation at Ser-1177 was activated by protein kinase B phosphorylation at Ser-473, involving activation of phosphatidylinositol-3 kinase (PI3K). Serine nitric oxide synthase 3 Homo sapiens
4 Using specific inhibitors, the authors confirmed that STS-induced endothelial nitric oxide synthase (eNOS) phosphorylation at Ser-1177 was activated by protein kinase B phosphorylation at Ser-473, involving activation of phosphatidylinositol-3 kinase (PI3K). Serine nitric oxide synthase 3 Homo sapiens
5 Using specific inhibitors, the authors confirmed that STS-induced endothelial nitric oxide synthase (eNOS) phosphorylation at Ser-1177 was activated by protein kinase B phosphorylation at Ser-473, involving activation of phosphatidylinositol-3 kinase (PI3K). Serine nitric oxide synthase 3 Homo sapiens