Background: Oxidation of KCNB1 channels leads to oligomerization and apoptosis. Results: KCNB1 oligomers aggregate in and disrupt glycolipid raft organization, promoting the activation of the Src/JNK pro-apoptotic pathway. Conclusion: KCNB1 aggregates initiate an apoptotic cascade mediated by c-Src/JNK kinases. Significance: Oxidized KCNB1 channels increase in aging mammalian brain. As such, this mechanism contributes to neuronal aging and neurodegeneration.
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