Fig. 6From: MLKL regulates Cx43 ubiquitinational degradation and mediates neuronal necroptosis in ipsilateral thalamus after focal cortical infarctionSchematic illustration of the mechanism by which MLKL regulates Cx43 ubiquitination and degradation to mediate necroptosis in ipsilateral thalamic neurons after focal cerebral infarction. The RIP1-RIP3-MLKL pathway was activated in the VPN of ipsilateral thalamus after focal cerebral ischemia. MLKL was up-regulated and translocated to the plasma membrane and then interacted with Cx43 at Lys 303, thereby inhibiting the ubiquitination of Cx43 at Lys 303 by VHL and the ubiquitin-proteasomal degradation of Cx43, promoting opening of Cx43 hemichannels, overloading intracellular calcium, and eventually leading to neuronal necroptosis in VPNBack to article page