Vanesa Vinciauskaite

The paper identifies three GCN2 activators, one of which works independently of GCN1, and describes its unique binding mechanism.

This paper shows that DELE1CTD binds to HRI's N-terminal region, displacing haem and activating HRI through competition for the haem-binding site.

This study shows WEE1 inhibitors work better with mRNA translation defects by activating GCN2, and suggests ways to reduce off-target effects.

This study shows heme binding to HRI causes structural changes that inhibit its autophosphorylation, affecting eIF2 kinase activity.

The paper shows ATP-competitive inhibitors paradoxically activate GCN2 through allosteric activation and autophosphorylation, suggesting alternative strategies for GCN2 inhibition.