Fig. 6. ALK5 interacts with Gadd45b after I/R; a schematic diagram depicting the possible mechanism of ALK5 signaling regulating neurogenesis after cerebral I/R.

a Coimmunoprecipitation experiments of ALK5 and Gadd45b in the ischemic cortex 24 h after I/R. b Coimmunoprecipitation experiments of ALK5 and Gadd45b in the ischemic cortex 14 d after I/R. These results show that ALK5 coimmunoprecipitated with Gadd45b after cerebral I/R. c Ischemia activates ALK5, which catalyzes the phosphorylation of Smad2/3 and forms a complex with Smad4. In the nucleus, the complex promotes Gadd45b expression, which elevates the expression and demethylation of BDNF, thereby improving neurogenesis