Gene interactions and pathways from curated databases and text-mining

◀ Back to AKT1

AKT1 — HBEGF

Pathways - manually collected, often from reviews:

  • OpenBEL Selventa BEL large corpus: AKT1 → HBEGF (increases, HBEGF Activity)
    Evidence: HB-EGF induced AKT phosphorylation but not STAT3 phosphorylation (Figure 5A Figure 5 , lane 3).

Text-mined interactions from Literome

Reynolds et al., Hypertension 2002 : PD98059 inhibited HB-EGF induced ERK activation, whereas it had no effect on Akt activation by HB-EGF ... By contrast, LY294002 inhibited HB-EGF induced Akt and p70S6K activation without effecting ERK activation by HB-EGF
Mukai et al., Atherosclerosis 2004 : HB-EGF induced phosphorylation of ERK, p38 MAPK and Akt , which were suppressed by ZD1839
Jin et al., J Neurosci Res 2005 (MAP Kinase Signaling System) : The phosphatidylinositol 3'-kinase (PI3K) inhibitors LY294002 and wortmannin, and the MAPK/extracellular signal regulated kinase ( ERK ) kinase ( MEK ) inhibitors U0126 and PD98059, reduced HB-EGF induced BrdU incorporation into cultures, and HB-EGF enhanced phosphorylation of Akt and ERK, implying a role for PI3K/Akt and MEK/ERK signaling in HB-EGF stimulated cell proliferation
Mehta et al., J Immunol 2005 (MAP Kinase Signaling System) : In this report, we show that in intestinal epithelial cells, HB-EGF triggered PI3K dependent phosphorylation of Akt
Xu et al., Invest Ophthalmol Vis Sci 2006 : On the other hand, AKT phosphorylation was much more sensitive to PP2 than ERK or EGFR phosphorylation because 3.13 microM PP2 effectively inhibited wound- or HB-EGF induced AKT phosphorylation
Cao et al., Science signaling 2009 : Loss of Galpha ( i1 ) and Galpha ( i3 ) severely impaired the activation of Akt and of p70 S6 kinase and 4E-BP1, downstream targets of mTORC1, in response to EGF, heparin binding EGF-like growth factor , and transforming growth factor alpha, but not insulin, insulin-like growth factor, or platelet derived growth factor
Nakai et al., J Dermatol Sci 2009 : Finally, the HB-EGF induced activation of Akt and eNOS was suppressed by VEGF competitive antagonist, CBO-P11
Lian et al., PloS one 2012 (Fibrosis) : Furthermore, HB-EGF significantly increased phosphorylation levels of Akt , mTor and p70s6k and increased expression of type I collagen in cultured primary cardiac fibroblasts