Fig. 1From: Targeted BRD4 protein degradation by dBET1 ameliorates acute ischemic brain injury and improves functional outcomes associated with reduced neuroinflammation and oxidative stress and preservation of blood–brain barrier integrityBRD4 protein degradation in the mouse brain by dBET1. A Schematic illustration of BRD4 PROTAC dBET1 mechanism-induced BRD4 protein degradation through the ubiquitin–proteasome system. With dBET1, E3 ligase recognizes, binds, and ubiquitinates BRD4 protein, making it available for subsequent proteasomal degradation. B Representative western blot depicts dBET1 (30 mg/kg; i.p. at 4 and 24 h) induces significant BRD4 degradation in the whole hemisphere and cerebral cortex of mice at 48 h after sham surgery. n = 4–5 per group, **P < 0.01, ***P < 0.001. C Representative western blot shows the BRD4 protein levels in the cerebral cortex of sham and stroke mice at 48 h after surgery. n = 5 per group. ***P < 0.001. D Representative western blot depicts dBET1 (30 mg/kg; i.p. at 4 and 24 h after stroke) reduces the protein level of BRD4 in the cerebral cortex under the condition of stroke by tMCAO. ***P < 0.001. Ub, ubiquitin; E1, E2, E3, ubiquitin-activating enzyme E1, E2, E3; BET, bromodomain and extra-terminal domain proteinBack to article page