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Fig. 6 | Molecular Brain

Fig. 6

From: MLKL regulates Cx43 ubiquitinational degradation and mediates neuronal necroptosis in ipsilateral thalamus after focal cortical infarction

Fig. 6

Schematic 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 VPN

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Molecular Brain

ISSN: 1756-6606