Gene interactions and pathways from curated databases and text-mining

◀ Back to NOS3

EPX — NOS3

Text-mined interactions from Literome

Wang et al., Hypertension 1999 : The present study was done to determine the effect of EPO on NO production and endothelial NO synthase (eNOS) expression by endothelial cells
Santhanam et al., Stroke 2005 (Subarachnoid Hemorrhage...) : The vascular protective effect of Epo against cerebral vasospasm induced by SAH may be mediated in part by phosphorylation of Akt/eNOS
Desai et al., Lab Invest 2006 (Atherosclerosis...) : In vitro studies revealed that EPO reduces ecNOS expression at both the protein and mRNA levels and that EPO also mediates a reduction in ecNOS enzymatic activity
Wen et al., Scand J Clin Lab Invest 2009 (Cardiomegaly) : EPO enhanced Akt activation and eNOS protein expression, whereas LY294002 or L-NAME partially abolished the anti-hypertrophic effect of EPO , accompanied by a decrease in Akt activation, eNOS protein expression and/or a reduction of NO production
Su et al., J Cell Physiol 2011 : We investigated the role of ßCR in EPO induced endothelial NO synthase (eNOS) activation in bovine aortic ECs ( BAECs ) and the molecular mechanisms involved ... Additionally, blockage of ßCR abrogated the EPO induced increase in the phosphorylation of eNOS , Akt, Src, or Janus kinase 2 (JAK2) ... Moreover, in vivo experiments showed that EPO increased the level of phosphorylated eNOS , Src, JAK2, and Akt, as well as ßCR-eNOS association in aortas and promoted the angiogenesis in Matrigel plug, which was diminished by ßCR or EPOR neutralizing antibodies
Patel et al., Mol Med 2012 (Acute Kidney Injury) : Interestingly, the phosphorylation of endothelial nitric oxide synthase was enhanced by EPO and, to a much lesser extent, by pHBSP, suggesting that the signaling pathways activated by EPO and pHBSP may not be identical
Nandra et al., Dis Model Mech 2013 (Disease Models, Animal...) : In livers from rats subjected to HS, EPO enhanced the phosphorylation of Akt ( activation ), glycogen synthase kinase-3ß ( GSK-3ß ; inhibition ) and endothelial nitric oxide synthase ( eNOS ; activation )