Lactylation-mediated degradation of ANKS1B mitigates ischemic excitotoxicity by impairing GluN2B trafficking

Puntos clave

• ANKS1B degradation alleviates excitotoxicity caused by ischemia, enhancing cell survival.
• Lactylation modifies ANKS1B, leading to impaired trafficking of the GluN2B receptor.
• Observational analysis reveals significant impacts of degradation on neuron responses to ischemic conditions.
• These findings highlight lactylation as a potential regulatory mechanism in neuroprotection against excitotoxicity.