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

Kinase-active AKT activates MTOR. 7 / 7
7 |
bel
"growth factors, cytokines and other signalling molecules stimulate HIF-1a synthesis via activation of the phosphatidylinositol 3-kinase (PI3K) or mitogen- activated protein kinase (MAPK) pathways (FIG. 1)."
bel
"mechanical strain of HASM induced a significant increase in hypoxia-inducible factor-1alpha (HIF-1alpha) mRNA and protein, a transcription factor required for VEGF gene transcription; and 5) mechanical strain of HASM induced HIF-1alpha/VEGF through dual phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) and ERK pathways."
bel
"Akt suppresses TSC1/2, leading to the activation of mTOR."
bel
"The mechanism involves the ability of this integrin to stimulate the phosphorylation and inactivation of 4E-binding protein (4E-BP1), a translational repressor that inhibits the function of eukaryotic translation initiation factor 4E (eIF-4E). The regulation of 4E-BP1 phosphorylation by alpha 6 beta 4 derives from the ability of this integrin to activate the PI-3K-Akt pathway and, consequently, the rapamycin-sensitive kinase mTOR that can phosphorylate 4E-BP1."
bel
"Modified assertion"
bel
"Modified assertion"
bel
"Modified assertion"