Fig. 11From: Roles of Rufy3 in experimental subarachnoid hemorrhage-induced early brain injury via accelerating neuronal axon repair and synaptic plasticitySchematic diagram of the potential neuroprotective mechanisms of Rufy3 after SAH. Following SAH, the inhibition of Rufy3 expression resulted in an increase in neuronal axon and synaptic damage accompanied by hindered Rufy3/Rap1 complex formation. In addition, Rufy3 overexpression contributed to Rufy3/Rap1 complex formation and accelerated neuronal axon repair via activating the Rap1/Arap3/Rho/Fascin signaling axis. It also accelerated synaptic plasticity by activating the Rap1/MEK/ERK/Synapsin I signaling axis after experimental SAHBack to article page