The Steel factor/Kit signaling pathway plays an important role in the migration of many types of cells during development as well as in the adult animal. Not surprisingly, loss-of-function mutations in Steel factor result in cell migration defects. Selective inactivation in these cells of which of the following proteins might be expected to rescue (i.e. partially restore to normal) the defective phenotype of Steel loss-of-function mutants?
A) Kit, the receptor for Steel B) Bax, an essential apoptotic protein C) Endothelin-3, a survival factor for neural crest cells D) Fibronectin, a multi-adhesive protein of the extracellular matrix E) FGF4, a growth factor