Fig. 9

CD133 regulates cholesterol metabolism and peripheral axon regeneration through TGF-β/Smad2 signaling. Mouse dorsal root ganglion crush injury induces the formation of functional ALK4, a TGF-β type I receptor that binds to its ligand activin, a TGF-β superfamily member and a determinant of axon regenerative capacity. At the plasma membrane, the interaction of ALK4 with CD133 stimulates the phosphorylation of Smad2, which inhibits, after translocation into the nuclear compartment, the expression of genes involved in cholesterol metabolism, thereby promoting a positive effect on axon regeneration. Illustration is based on data presented in Ref [371]