Figure 7. Model of GPR56 function in VEGF production by melanoma cells.
We hypothesize that the free GPRC fragment of GPR56 represents a basal/constitutive “on” state to induce the activation of PKCα, VEGF production, angiogenesis, and melanoma progression. The binding of full-length GPRN switches GPRC to an “off” state and inhibits those processes. The binding of ΔSTP-GPRN, however, activates it and promotes melanoma progression.