Research Perspective Volume 7, Issue 7 pp 469—474

Heterotrimeric G proteins as emerging targets for network based therapy in cancer: End of a long futile campaign striking heads of a Hydra


Figure 1. Activation of G proteins by GIV-GEF modulates multi-receptor signaling and broadly impacts the downstream signaling network. Schematic showing the diverse classes of receptors (upper half) which sense a variety of chemical signals, that converge on GIV. Lower part shows the consequence of non-canonical transactivation of G proteins by GIV (when GIV-GEF is functionally intact or turned "ON") on the multitude of downstream pathways within the signaling network. Green = enhancement; Red = suppression. Shown in the middle are three known ways to either inhibit (PKCθ selectively phosphoinhibits GIV-GEF [27]; SHP-1 dephosphorylates tyrosine-phosphorylated GIV [30]) or activate (CDK5 phosphoactivates GIV-GEF [37]) GIV-dependent signaling.