Roybal et al., J Biol Chem 2004
(Neovascularization, Pathologic) :
These studies indicate that expression of the pro-angiogenic factor VEGF is increased by homocysteine and other thiol containing reductive compounds via ATF4 dependent activation of VEGF transcription
Roybal et al., J Biol Chem 2005
:
Because ATF4 is expressed in response to oxidative stress, we hypothesized that ATF4 was also responsible for increased VEGF transcription in response to arsenite ... Inactivation or loss of ATF4 greatly diminished the VEGF response to arsenite treatment ... Overexpression of ATF4 was sufficient to activate the VEGF promoter, and arsenite cooperated with exogenous ATF4 to further activate the promoter
Chen et al., Diabetologia 2012
(Diabetes Mellitus, Type 1...) :
Suppressing ER stress or inhibiting ATF4 activity markedly attenuated high-glucose induced production of intercellular adhesion molecule 1, TNF-a and vascular endothelial growth factor Seko et al., J Cell Physiol 1998
:
VEGF also caused phosphorylation of the activating transcription factor 2