A database built with INDRA combining content from numerous readers and databases. This page allows you to curate the loaded statements. For more information please see the manual.

IndraLab

Statements

databases
phosphosite cbn pc11 biopax bel_lc signor biogrid tas lincs_drug hprd trrust | geneways tees isi trips rlimsp medscan sparser reach
reading

EGF activates AKT1. 2 / 66
| 6 16
reach
"It is unknown whether C. elegans LIN-3 and EGF signaling activates PI3K (AAP-1, PDK-1, and AGE-1 in C. elegans) or Akt (AKT-1 and AKT-2 in C. elegans); however, Insulin and IGF Signaling (IIS) has been implicated in regulating longevity through PI3K and Akt [XREF_BIBR]."
sparser
"However, while LY294002 inhibited Akt-1 activation by EGF, neither FTI nor RhoB-GG were effectual in blocking this activity (see Fig. 4A )."
EGF activates AKT1. 3 / 3
3 |
bel
"Modified assertion"
bel
"Figure 4 shows the inhibitory effect of gefitinib on EGFinduced autophosphorylation of EGFR, and phophorylation of Akt and ERK1/2 in three of the NSCLC cell lines. EGF stimulated EGFR autophosphorylation and activation of Akt and ERK1/2 in PC9 (A), A549 (B), and QG56 (C) cells, and activation was blocked to different extents by gefitinib."
bel
"Western blotting with the anti-phospho-Akt1 antibody, which recognizes only phosphorylated Ser-473 residue, was performed in human esophageal cancer cell lines (TE-2, TE-5, TE-8, TE-9, TE-10, and TE-12 cells) (top panel). PDGF-treated NIH3T3 cells served as a positive control. The phospho-Akt antibody demonstrated two bands at 60 kDa. The phosphorylation of Akt was enhanced by EGF stimulation in all the esophageal cancer cell lines examined, although TE-5 cells showed high basal phosphorylation of Akt."