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"The inability of VEGFR2 neutralization to affect flow induced Akt phosphorylation despite attenuating eNOS phosphorylation is consistent with the findings by Jo and colleagues, who demonstrated that shear stress stimulates phosphorylation of eNOS by an Akt independent mechanism [XREF_BIBR]."
"The phosphorylation of both S617 and S635 have also been shown to promote increased eNOS-derived NO release (Michell et al., 2002). The phosphorylaiton of S617 can be induced by PKA or Akt activity, and may serve to sensitize eNOS to calmodulin binding and modulate the phosphorylation of other eNOS sites"
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"However, Dimmeler et al. [XREF_BIBR] previously observed via eNOS immunoprecipitation and phosphoamino acid analysis a significant increase in Akt phosphorylation following exposure to a shear stress magnitude of 5 dyn/cm 2 (i.e., 0.5 Pa), and determined Akt phosphorylation significantly increased eNOS phosphorylation."
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"We tested the hypothesis that impaired nitric oxide (NO)-mediated, endothelium dependent dilation in aged soleus muscle feed arteries (SFA) is due to an age related decline in the potential for PI3-kinase (PI3K)/protein kinase B (Akt)-dependent phosphorylation of endothelial NO synthase (eNOS) on serine residue 1177 (p-eNOS (ser1177))."
"Although AKT can phosphorylate several proteins4, we focused on BAD, FOXO, IKKa, TSC2 and eNOS, as the consequence of AKT phosphorylation of these proteins is not redundant with the functions of the oncoproteins expressed in cells used in the cellmixing assay of tumour maintenance5 (Supplementary Fig. 1)."
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"Decreased expression of endothelial NO synthase (eNOS) protein, decreased phosphorylation of eNOS by the serine threonine kinase AKT, the presence of inhibitory substances (e.g., asymmetric dimethylarginine, ADMA), and hyporesponsiveness to NO underlie this endothelial dysfunction [XREF_BIBR - XREF_BIBR]."
"Shear stress, via G proteins (Gs), can activate several signal transduction pathways, including the phosphoinoside 3-kinase (PI3K) and adenylate cyclase (AC) pathways, leading to eNOS activation via phosphorylation of serine residues (S617 and S1179 for Akt, and S635 and S1179 for PKA), which promote eNOS activation."