GIPC proteins negatively modulate Plexind1 signaling during vascular development.

By potency, do the authors mean that PlxnD1ΔGBM is insensitive to inhibition and therefore more active? What phenotype would a 'more active' PlxnD1 mutant have? For the second hypothesis, do the authors mean that while GIPC binds PlxnD1, it has no influence on activity? Also, and importantly, when comparing the influence of PlxnD1-WT and PlxnD1ΔGBM on "angiogenic potential", the authors speculate on the meaning of an observed trend that is not statistically significant.

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