Gene interactions and pathways from curated databases and text-mining

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AKT1 — PECAM1

Pathways - manually collected, often from reviews:

  • OpenBEL Selventa BEL large corpus: PECAM1 → AKT1 (increases, PECAM1 Activity)
    Evidence: the expressions of KDR and CD31 were sharply enhanced in Akt-CA EPCs

Text-mined interactions from Literome

Limaye et al., Blood 2005 : Sphingosine kinase-1 enhances endothelial cell survival through a PECAM-1 dependent activation of PI-3K/Akt and regulation of Bcl-2 family members
Tai et al., J Biol Chem 2005 : Tie2 and PECAM1 expression decreased > 80 % after siRNA treatment, and flow stimulated phosphorylation of ERK1/2, Akt , and endothelial nitric oxide synthase was significantly inhibited by Tie2 and PECAM1 siRNA
Fleming et al., J Cell Sci 2005 : Role of PECAM-1 in the shear-stress induced activation of Akt and the endothelial nitric oxide synthase (eNOS) in endothelial cells ... Down-regulation of PECAM-1 using a siRNA approach attenuated the shear-stress induced phosphorylation of Akt and eNOS, as well as the shear-stress induced accumulation of cyclic GMP levels while the shear-stress induced phosphorylation of AMPK remained intact
Chen et al., Arterioscler Thromb Vasc Biol 2009 (Coronary Restenosis...) : Inward remodeling was associated with PECAM-1 dependent NFkappaB activation, surface adhesion molecule expression, and leukocyte infiltration as well as Akt activation and vascular cell proliferation
He et al., Cancer Chemother Pharmacol 2013 (Carcinoma, Non-Small-Cell Lung...) : EGCG inhibited HPV-16 oncoprotein induced angiogenesis conferred by NSCLC through the inhibition of HIF-1a protein expression and HIF-1a dependent expression of VEGF, IL-8, and CD31 as well as activation of Akt , suggesting that HIF-1a may be a potential target of EGCG against HPV related NSCLC angiogenesis